HANDOUTS.

SEMINAR II

First aid in maxillo-facial injury. Technic and indication for tracheotomy.

Statistic data Frequency of the faces bone fractures: Mandible 68% Zygomatic bone with orbit 17% Nos with ethmoid bones 9% Maxilla 6% Statistic data Reasons of the trauma: Beating Communication cases Accidents at work Sport injures Gunshots & another 40% 29% 21% 7% 3%

Statistic data Depending on sex

men women children

87% 8,5% 4,5%

Statistic data Predominatig group of the patients are present by people in the medium age. Systemic complikations of the trauma Shock Injury of the central nervous system Brain concussion (commotio cerebri) Brain contusion (contusio cerebri) Brain compression (compressio cerebri) - hematoma epimeningeal (haematoma epidurale) - hematoma submeningeal (haematoma subdurale) - subarachnoid hemorrage (haemorrhagia subarahnoidea) Kind of shocks HIPOVOLEMIC SHOCK

SHOCK- KLINICAL COMPLEX OF SYMPTOMS OCCUR, WHEN THE AUTOREGULATION (COMPENSATORY) MECHANISMS OF ORGANISM , ARE NOT ENOUGH TO MAKE A CORRECT PASSAGE OF THE BLOOD BY IMPORTANT FOR A LIFE ORGANS LIKE BRAIN, HEART, LUNGS, LIVER AND KIDNEYS. HIPOVOLEMIC SHOCK REASONS: Loss of whole blood

Loss of blood and plasma Loss of plasma and extracellular fluid

Loss of water and electrolytes HIPOVOLEMIC SHOCK: SCALE OF HEAVINESS: depends on loss of volume of circulating blood.

15-30% midding heavy 30-60% heavy

60% irreversibility shock leading to death HIPOVOLEMIC SHOCK Clinical picture: Patient is pale and apathetic Reacts for pain impuls only Excerbated facial features Dilation of pupils Chill skin Pale lips Jugular venous collapse Cold limbs Cyanosis circuit is visible Low arteriar pressure (70-80 mm Hg) Increased puls 120-130/min. Accelerated respiration Oliguria or anuria HIPOVOLEMIC SHOCK 3 periods of symptoms development :

Despite of decrease circulating blood, volumes, passage by tissue and organs is corectthanks to compensatory mechanism. Decrease pressure and blood passage through the tissue Irreversibility phase organs and tissue are permanent damage by the reason of circulating disturbance and hypoxia General rules of procedure in case of shock Hemostasis - pressure dressing Enabling of correct gas exchange Blood group should be determinated Transfusion of compound electrolyte solution Inserting vesical catherer, and control of fluids balance Transfusion of blood, when the group is determinated Continous control of blood pressure Prevention of metabolic acidosis

 Prevention of infections Traumatic shock Its separatig type of hipovolemic shock. There are many factors taking a role in its occurig-like: pain, fear, extensive damage of tissues. Except of considerable loss of circulatin blood, there are excessive coagulability, and syndrome of disseminated intravascular clotting. Healing is simple like in hipovolemic shock + low-molecular Dextran in amount 1500 ml for decreasing of blood viscosity and correction of conditions in peripheral circulation. Brain concussion Symptoms: Loss of consciousness strong obnubilation after the trauma vomiting Retrograde amnesia (amnesio retrograda) Hypersomnia after recovery of conscious Decreased Achilles tendon reflex, and skin reflex in abdominal area Nystagmus, decreased of pupil reaction on the light, pupillary stenosis at the begining, and than mydriasis Group of syndroms from the brain stem Filiform puls Dismissed heart action Decreased diastolic pressure of blood Skin perspiration Decreased teperature of the body Increased level of glucose in blood (to 320mg%) and glucosuria doesnt react for insulin Brain concussion Three degrees :

I easy loss of consciousness to 10 min., and than headache, hypersomnia

II middling heavy loss of consciousness from 10-30 min., vomiting, veretigo, decreased reflexes, shallow respiration,insignificant bradysphygmia, retrograde amnesia III heavy unconsciousness 30 min., vertigo and heavy headache, reapeating vomite and retrograde amnesia for few days. Brain concussion Treatment: Inconditional lying in bed, and good nursing care

prevention of cerebral edema- for instance: Mannitol Application of dehydrating dugs- furosemid(cautiously)

Control of fluids balance Brain contusion Diferently from brain concussion- here we can distincly ascertain damage of the brain tissue, which is manifested as neurological damages. Diagnosis: symptoms of heavy brain concussion Neurological hypofunction of some regions in brain, which is manifested as paralysis of some peripheral nerves Treatment:

 Symptomatic treatment Prevention of cerebral edema Brain compresion Symptoms: Loss of consciousness imediately after the trauma Regain consciousness- intervallum lucidum (short period is evidence of arterial hemorage however long one about jugular) reconsciousness, sleepines, stupor, coma Three kinds: hematoma epimeningeal (haematoma epidurale) hematoma submeningeal(haematoma subdurale) subarachnoid hemorrage(haemorrhagia subarachnoidea) First aid in maxillo-facial surgery Evaluation of patients general condition after trauma. At first we should treat general symptoms of trauma!!! we should look whether the patients is conscious- if not restoration of airways patency Removing blood, fragments of fractured teeth, prostheses Placement of a patient in lateral recumbent position Perform the Esmarchs maneuver if is needed Intubation or tracheotomy if is needed Evaluation of symptoms from C.N.S. Examination directed on possibility of appearance of shock symptoms, which are sometimes more dangerous for patients than injury. First aid treatment Clearing air passage

Hemostasis Dressing of wound

Temporary immobilization of fractures Clearing air passage Care should be taken that patients can breathe easily. Often dentures are displaced and obstruct the pharynx. In other cases fragment of bone, dislodged teeth, or foreign bodies may obstruct the air passage. The nasal passage is often clogged up with bllood clots and must be cleared, and if tongue shows a tendency to fall back it must be pulled forward by means of tongue forceps or a suture passed through the tip. If this measures dont bring results, a tracheotomy may be indicaed. Hemostasis The arrest of hemorrhage is next in importance. In most facial wounds bleeding can be arrested by pressure applied to the external maxillary artery at the lower border of the mandible. The superficial temporar artery may be compressed where it crosses the zygomatic arch just anterior to the ear. Bleeding from deep wounds and from inside of the face may be controlled by compressing the external carotid artery at the anterior margin of the sternocleidomastoid muscle. In some cases, packing, clamping, and ligating blood vessels are indicated. Dressing of wounds Displaced soft tissue should be secured. Compresse may be placed on the wound so that losse flaps are pressed into position. The bandage is useful for wounds of the chin which are covered with gause.

The wounds should be cleaned and if it possible should be sutured. Temporary immobilization of fractures Temporary immobilization decrease the danger of secondary hemorrhage and infection, relieve pain and shock, and prevent disfigurement. In some instances the fractures can be satisfactorily immobilized by means of bandage. Great care must be taken that the bandages do not cause further displacement by excerting pressure in the wrong direction. The fourtailet bandage, particulary, exerts a backward pressure and should be applied under the chin in mandibular fractures, which are easly displaced, or it will do more harm than good. We can immobilize the fractures by using different kind of dental splints ( Stouda, Hammonda, Tiegertaedta, Wassmunda, made in laboratory, or poroplastic splint). Temporary immobilization of fractures For temporary immobilization of fractures, fractured or luxated teeth, we can use a different wire ligation ( Ivy, simple, Ernsts etc.) That way the patient is protected to the moment of last fixation fragments of fractured bone ( operativ or ortopedical -conservative treatment). We should remember about analgesic treatment, antibiotic therapy, and prophylactic measures to prevent tetanus and gas gangrene. Technic and indication for tracheotomy This is an operation designed to secure a free airway. It may be used for prophylactic reasons or as an emergency operation if there is obstruction above the larynx causing acute respiratory embarrassment. The operation is not without danger, but, when needed, it may be the most important factor in saving life. Before attempting to tracheotomy, other methods for maintaining an airway should be considered, such a proper support of the mandible, protraction of the tongue, insertion of oral, nasal, or endotracheal airways, and artificial respiration. Technic and indication for tracheotomy The following are the principal conditions for which tracheotomy is used: Injury to the posterior part of the tongue Injuries to the pharynx either with or without foreign bodies Large foreign bodies which have entered the air passages but which cannot be removed under direct vision Fractures or resection of the anterior part of the mandible which allows the tongue to fall back Extensive injures and severe fractures of the upper facial regions Postoperative inflammation which may descent to involve the pharynx and the mucous membranes of the air passages Injury to the reccurent laryngeal nerve or the vagus by pressure from hemorrhage, which may cause paralysis of both cords if bilateral, with extreme dyspnea resulting.
-

Technic and indication for tracheotomy Depending on place of entrance to the trachea we distinguish: Upper tracheotomy above of the isthmus of the thyroid gland Middle- in place of intersection of isthmus Lower- below the isthmus Tracheotomy Rules of operation: 1) Emergency trocar technique It must be performed without delay. The trocar used should consist of a curved tube into which is inserted a sharp well-fitting stylet with a cutting point that should protrude about 0,6 cm.

After circothyroid space has been located with the patients head in a flexed positions, the trocar is grasped and thrust through the skin into the trachea. The stylet is removed at ones, and the tube positioned so that it points caudally. Tracheotomy 2) Open tracheotomy technique: After the sandback has been placed under the patients shoulders to render the upper trachea prominent, a 3 cm. transverse incision is made through the skin and platysma over the third tracheal cartilage. This is done under local anesthesia unless the patient ia already anesthetized. The skin is is made tense with the left hand while the incision is made in the midline, starting from the cricoid cartilage downwards through the soft tissue which overlies the trachea and almost as far as the external notch. The pratracheal muscles are separated, and the third, fourth, and fifth rings of the trachea are divided from above downwards. After the trachea is penetrated, a tracheotomy dilator is inserted to spread the cartilaginous margins sufficiently to insert the tracheotomy cannula. The wound is covered with split gauze which should be extend under the shield of the cannula. The latter is held in place by a tape attached to each side and passed arond the neck. Complications of Tracheostomy Complications 5-40%

Mortality <2%

Complications are more frequent in emergency situations, severely ill patients and small children. Complications of Tracheostomy Stoma Stoma site infection Stomal hemorrhage Poor stoma healing after decannulation with scar, keloid, or tracheocutaneous fistula Complications of Tracheostomy Trachea

Granuloma

Tracheoesophageal fistula fewer than 1% of patients as a result of pressure necrosis of the tracheal and esophageal mucosa from the tube cuff risks: high cuff pressures, presence of a nasogastric tube, excessive tube movement, and underlying diabetes mellitus Complications of Tracheostomy Tracheoinnominate fistula: 0.4% with mortality rate of 85% to 90%. Major airway hemorrhage may occur first within several days or as long as 7 months after performance of a tracheostomy. Risk factors : excessive tube movement, low placement of the tracheostomy, sepsis, poor nutritional status, and corticosteroid therapy Tracheal stenosis: can develop from 1 to 6 months after decannulation risk for tracheal stenosis ranges between 0% and 16% Tracheomalacia

SEMINAR III

Temporomandibular Disorders
ANATOMY The temporomandibular joint, or TMJ, is the articulation between the condyle of the mandible and the squamous portion of the temporal bone. The condyle is elliptically shaped with its long axis oriented mediolaterally. The articular surface of the temporal bone is composed of the concave articular fossa and the convex articular eminence. The TMJ is unique because it is capable of 2 types of motion. The mandible initially opens with a hinge (rotational) movement and then glides forward or translates along the temporal bone. The joint is superiorly bound by the glenoid fossa that houses the mandibular condylar head with a fibrous capsule lined with synovium. The articular disk and synovial fluid comprise the joint capsule. The articular disk is composed of fibrocartilage, which also covers the articulating surfaces of the TMJ and the disk is described in three different zones: anterior, posterior, and intermediate measuring approximately 3.0mm, 2.0mm, and 1.0mm in width, respectively.2 The posterior band of the disk, referred to as retrodiscal tissue, is loosely organized and consists of elastic and collagen fibers, nerves, blood, fat, and lymphatics. Several ligaments attach to the disk anteriorly, posteriorly, laterally, medially, and externally. The muscles of mastication (MOM) associated with the TMJ include the temporalis, masseter, lateral pterygoid, and medial pterygoid Muscle attachments of the temporalis, deep masseter, and superior belly of the lateral pterygoid have been observed within portions of the articular disk anteriorly. 1 Accessory MOM includes the digastric, mylohyoid, geniohyoid, buccinator, stylomandibular, and stylohyoid. Cervical muscles commonly associated with TMD are the sternocleidomastoid, splenius capitus and trapezius. Occlusion refers to the maximal intercuspation (intimate contact) of the maxillary and mandibular teeth and can be described as being physiologic ( functional) or pathologic. When the mandible closes completely and/or moves laterally from maximum intercuspation of the teeth, significant forces may be generated. Missing teeth, loss of tooth contacts, and drifting of teeth can all contribute to the development of a pathologic occlusion. The most common causes of temporomandibular disorders (TMDs) are muscular disorders, which are commonly reffered to a myofascial pain and dysfunction. Other causes of temporomandibular pain or dysfunction originate primarily within the temporomandibular join (TMJ). This causes includ internal derangement, osteoartritis, reumatoid artritis, chronic reccurent dislocation, ankylosis, neoplasia, and infection. Although most of these disorders respond to non surgical therapy, some patients may eventually require surgical treatment. EVALUATION- should include: Interview

Examination

Radiographic Evaluation INTERVIEW The patients history may be the most important part of the evaluation.The history begins

with the chief complaint, which is a statement of the patients reasons for seeking consultation or treatment.The history should be comprehensive, and include an accurate description of patients symptoms, chronology of the symptoms, description of how the problem affects the patients and information about any previous treatments (including the patients response to those treatment). EXAMINATION The physical examination consist of an evaluation of the entire masticatory system. The head and neck should be inspected for soft tissue asymmetry or evidence of muscular hypertrophy.The patients should be observed for signs of jaw clenching or other habits.The masticatory muscles should be examinated systematically. The muscles should be palpated for thr presence of tenderness, fasciculation, spasm, or trigger points. The TMJs are examinated for tenderness and noise.The most common forms of joint noise are clicking (a distinct sound), and crepitus (scraping or grating sounds).Many joint sounds can be easily heard without special instrumentation or can be felt during palpation of the joint. Sometimes we need to use the stethoscop The mandibulae range of motion should be determined. Normal range of movement of an adults mandibulae is about 45 mm vertically (intercisally) and 10 mm protrusivelly and laterally. The normal movement is straight and symetric. In some cases tenderness in the join or muscle areas may prevent opening. The clinitian should attempt to ascertain not only the peinless voluntary opening but also the maximum opening that can be achieved with gentle digital presssure.If it is able (normal opening) it may suggest muscular rather than intracapsular problems. Very important is also dental evaluations. Odontogenic sources of pain should be eliminated. The teeth should be examinated for wear facets , soreness, and mobility, which may be evidence of bruxism. Missing teeth should be noted. The clinician should note any centric relation and centric occlusion discrepancy or significant posturing by the patient. RADIOGRAPHIC EVALUATION PANORAMIC RADIOGRAPHY TOMOGRAMS TEMPOROMANDIBULAR JOINT ARTROGRAPHY COMPUTED TOMOGRAPHY MAGNETIC RESONANCE IMAGING NUCLEAR IMAGING PANORAMIC RADIOGRAPHY This is one of the best radiographs for screening evaluation of TMJ.This technique allows visualization of both TMJs on the same film. Many machines are equipped to provide special view of the mandible, focusing primarily on the area of TMJs. This radiograph can often be completed in the open and closed position. TOMOGRAMS The tomographic technique allows a more detailed view of TMJ. This technique allows radigraphic sectioning of the joint at different levels of the condyle and fossa complex, which provides individual views visualizing the joint in slices from the medial to the lateral pole TEMPOROMANDIBULAR JOINT ARTROGRAPHY This method was the first technique available that allowed visualization of the intraarticular disc. Artrography involves the injection of contrast material into the inferior and superior spaces of a joint, after which the joint is radiographed. This allows evaluation of the position and morphology of the articular disc.This technique also demonstrates the presence of perforations and adhesion of the disc or its attachement.

COMPUTED TOMOGRAPHY CT provides a combination o tomographic views of the joint, combined with computer enhancement of hard and soft tissue images. CT scan reconstruction capabilities allow images obtained in one plane of space to be reconstructed so that the images can be evaluated from a different view. Thus evaluation of the joint from the variety of perspectives can be made from a single radiation exposure. MAGNETIC RESONANCE IMAGING This is the most effective diagnostic imaging technique to evaluate TMJ soft tissue. MRI images can be obtained showing dynamic joint function in a cinematic fashion, providing valuable information about the anatomic components of the joint during function. The fact that this technique does not use ionizing radiation is the significant advantage. NUCLEAR IMAGING Nuclear medicine studies involve intravenous injection of technetium-99, -emiting isotope that is concentrated in areas of active bone metabolism. Aproximately 3 hours after injection of the isotop, images are obtained using gamma camera. Single-photon emission computerized tomography images can then be used to determine activ areas of bone metabolism. Although this technique is extremely sensitive, the information obtained may be difficult to interpret. Because bone changes, such as degeneration, may appear identical to repair or regeneration. This technique must be evaluated in combination with clinical findings. PSYCHOLOGICAL EVALUATION Many patients with temporomandibular pain and dysfunction of long-standing duration develop manifestation of chronic pain syndrom behavior.This complex may include gross exaggeration of symptoms and clinical depression. The comorbidity of psychiatric illness and temporomandibular disfunction can be as high as 10-20% of patients seeking treatment. Psychiatric disorders may elicit somatic components through parafunctional habits resulting in dystonia and myalgia, and individuals with chronic pain commonly have a higher incidence of concomitant anxiety disorders. CLASSIFICATION OF TEMPOROMANDIBULAR DISORDERS Myofacial pain Disc Displacement Disorders Degenerative Joint Disease(Arthrosis, Osteoarthritis) Systemic Arthritic Conditions Chronic Reccurent Dislocation Ankylosis Infection MYOFACIAL PAIN REASONS : Myofacial pain and disorders (MPD) is the most common cause of masticatory pain and limited function for which patients seek dental consultation and treatment. The source of the pain and dysfunction is muscular with masticatory muscles developing tenderness and pain as a result of abnormal muscular function or hyperactivity. It is frequently associated with daytime clenching or nocturnal bruxism (resulting from stress and anxiety). MPD may also occure because of internal joint problems, such as disc displcement disorders or degenerative joint disease (DJD). MYOFACIAL PAIN SYMPTOMS: Patients with MPD generally complain of diffuse, poorly localized, preauricular pain that may also involve other muscles of mastcation, such as the temporalis and medial pterygoid m. In patients with nocturnal bruxism, the pain is frequently more severe in the morning. Patients describe decreased jaw opening with pain during functions such as chewing. Headaches, usually bitemporal in location may also be associated with these symptoms.

MYOFACIAL PAIN The range of mandibular movement is may be decreased and is associated with deviation of the mandible toward the affected side.The teeth frequently have wear facets. Radigraph of the TMJs are usually normal. DISK DISPLACEMENT DISORDERS: 1.ANTERIOR DISK DISPLACEMENT WITH REDUCTION 2.ANTERIOR DISK DISPLACEMENT WITHOUT REDUCTION DISK DISPLACEMENT DISORDERS: In normally functioning TMJ the condyle function in a hinge and sliding fashion. During full opening the condyle not only rotates on a hinge axis but also translates forward to a position near the most inferior portion of the articular eminence. During function the biconcave disk remains interpositioned between the condyle and fossa, with the condyle remaining against the thin intermediate zone during all phases of opening and closing. 1.ANTERIOR DISK DISPLACEMENT WITH REDUCTION In anterior disk displacement the disk is positioned anterior and medial to the condyle in the closed position. During opening the condyle moves over the posterior band of the disk and eventually returns to the normal condyle and and disk relationship. Examination of the patient usually reveals joint tenderness and muscle tenderness may also exist.Joint noise (clicking) is comonly heard with opening when the condyle moves from the area posterior to the disk into the thin concave area in the middle of the disk. 2.ANTERIOR DISK DISPLACEMENT WITHOUT REDUCTION In this type of internal derangement the disk displacement cannot be reduced, and thus the condyle is unable to translate to its full anterior extent, which prevent maximal opening and causes deviation of the mandible to the affedted side. In these patients no clicking occurs because they are unable to translate the condyle over the posterior aspect of the disk. DEGENERATIVE JOINT DISEASE (ARTHROSIS, OSTEOARTHRITIS) DJD includes a variety of anatomic findings, including irregular, perforated, or severely damaged disks in association with articular surface abnormalities, such as articular surface flattening, erosion, or osteophyte formation. The mechanism is not clearly understood. Three possible mechanisms:1)direct mehanical trauma, 2)hypoxia reperfusion injury, 3)neurogenic inflammation. DEGENERATIVE JOINT DISEASE (ARTHROSIS, OSTEOARTHRITIS) Patient with DJD frequently experience pain associated with clicking or crepitus located directly over the TMJ.Usually, an obvious limitation of opening is present, and symptoms usually increase with function. SYSTEMIC ARTRITIS CONDITIONS The most common of this is rheumatoid arthritis. Other processes, such as systemic lupus, can also affect the TMJ. In this cases, symptoms are rarely isolated to the TMJs, and several other signs and symptoms of arthritis are usually present in other areas of the body. The inflamatory process result in abnormal proliferation of synovial tissue in so called pannus formation. The symptoms may occure at an earlier age than those associated with DJD. As opposed to DJD , which is usually unilateral, reumatoid arthritis usually affects the TMJ bilaterally. SYSTEMIC ARTRITIS CONDITIONS Radiographic findings show erosive changes in the anterior and posterior aspects of the condylar heads.The changes may progress to large eroded areas that leave the apperence of small, pointed condyle in a large fossa. Eventually, the entire condyle and condylar neck may be destroyed.Laboratory test, such as rheumatoid factor and erythrocyte sedimentation rate, may be helpful in conforming the diagnosis of rheumatoid arthritis.

CHRONIC RECCURENT DISLOCATION Dislocation of the TMJ occurs frequently and is caused by mandibular hypermobility. Subluxation is a displacement of the condyle, which is self reducing and generally requires no medical management. A more serious conditions occurs when the mandibular condyle translates anteriorly in front of the articular eminence and becomes locked in that position. It could be uni or bilateral, and may occur spontaneously after opening the mouth widely, such as when yawning, eating, or during the dental procedure. Dislocation should be reduced as soon as possible. Reduction is accomplished by applying downward pressure on the posterior teeth and upward pressure on the chin, accompanied by posterior displcement of the mandible. Ussually reduction is not difficult. However, muscular spasm may prevent simple reduction.In this cases anesthesia of the auricular temporal nerve and the muscles of mastication may be necessary. After reduction patient should be instructed to restict mabdibular opening for 2 to 4 weeks. ANKYLOSIS INTRACAPSULAR ANKYLOSIS: or fusion of the joint, leads to reduced mandibular opening that ranges from partial reduction in function to complete immobility of the jaw. The most common causes of A. involves macrotrauma, most frequently associated with condylar fractures. Other: previous surgical treatment that resulted in scarring, and in rare cases infections. Evaluations of the patient reveals severe restriction of maximal opening, deviation to the affected side, and decreased lateral excursion to the contralateral side. Rtg evaluation: irregular articular surfaces of the condyle and fossa, with varying degrees of calcified conection between these articulating surfaces. ANKYLOSIS EXTRACAPSULAR ANKYLOSIS: Usually involves the coronoid process and temporalis muscle. Frequent causes are coronoid process enlargement, or hyperlasia , trauma to the zygomatic arch area, and infection around temporomandibular muscle.Complete restriction of opening is rare, and limited lateral and protrusive movements can usually be performed. INFECTIONS Infection in the TMJ area are rare, even in this case of trauma and surgical intervention. In third world countries where antibiotic therapy of middle ear infections is not available TREATMENT REVERSIBLE TREATMENT PERMANENT OCCLUSION MODIFICATION TM JOINT SURGERY DISTRACTION OSTEOGENESIS REVERSIBLE TREATMENT In most cases including MPD, disc displacement disorders, and degenerative and systemic arthritis disorders- a nonsurgical reversible treatment phase may provide significant reduction in pain and improvement in function. Patient Education Medication Physical Therapy Splint Therapy Patient Education Patient should have awarenees of the factors associated with their pain and dysfunction. Myofascial pain often results from parafunctional habits or muscular hyperactivity resulting from stress and anxiety. Patients who are aware of this factors are often able to control their activity and thereby reduce discomfort and improve function. For example, the output from surface elecrodes over the masseter or temporalis muscle can be used to indicate clenching or grinding during the daytime and nocturnal activity. Patient Education

Other forms of stress control, such as physical exercise, reducing exposure to stressful situations can also be explored. Modification of diet combined with home exercise routines are also an imprtant of the patients educational process. Temporary alteration of the diet to a softer consistency may result in a significant reductions of symptoms. Aggravating factors including chewing of gum, fingernails,or ice should be rewieved, and cassation or limitation of these activities should be encouraged. Medication Pharmacologic therapy is an important aspest of nonsurgical management of TMJ. Medication typicaly used in treatment of TMDs include : 1)Non-steroidal anti-inflammatory drugs : propionic acid derivatives (ibuprofen, naproxen), salicylates (aspirin, diflunisal), and acetic acid compounds (indomethacin, sulindac) 2) occasionaly stronger analgesic (from acetaminophen to potent narcotics- no longer than 2 weeks!) 3) muscle relaxant (diazepam-Valium, carisoprodolSoma, cyclobenzaprine Flexeril, tiazanidyne-Zanaflex-max 2 weeks),4) antidepressants. Medication that must be administrated by injection may occasionaly be helpful (recently, the use of botulinum toxin A BOTOX- has show promise in decreasing masticatory muscle hyperactivity, and local anethetic combined with steroids). Physical Therapy The most common modalities used include range of motion exercises,relaxation training, ultrasound, spray and stretch, and pressure massage. Ranege of motion exercise- include gentle stretching exercise done within pain tolerance through passive opening or active exercise routines Physical Therapy Ultrasound is an effectiv way to produce tissue heating with ultrsonic waves, which alter blood flow and metabolic activity at deeper level. The effect of ultrasonic tissue heating is theoretically related to increase in tissue temperature, increase in circulation, increase in uptake of painful metabolic products, and disruption of collagen cross-linking, which may affect adhesion formation. All of these effect may result in more comfortable manipulation of muscle and wider range of motion Physical Therapy Massage involves the use of firm cutaneus pressure sufficient to produce a temporary degree of ischemia. This ischemia and the resultant hyperemia have been described as a method for inactivation of trigger points, which are areas responsible for pain referred to muscle in the head and neck area. Splint Therapy Splint therapy can be classified into two grups: Autorepositioning Splints Anterior Repositioning Splints Autorepositioning Splints

Autorepositioning splints are most frequently used to treat muscle problems or eliminate TMJ pain when no specific internal derangement or other obvious pathologic conditions can be identified. However, these splint may be used in some cases, such as anterior disk displacement or DJD, in an attempt to unload or reduce the force placed directly on TMJ area. These splints provide a flat surface with even contact in all areas of the occlusion. Wearing that splint allows full-arch dental contact with the condyles in a more posterior reduced position, which frequently result in reductionof muscle and join symptoms Anterior Repositionig Splints

Anterior repositioning splints are constructed so that the anterior ramping effect forces the mandible to function in a protruded position. This type of splint is most useful in providing temporary relief and, in rare cases, a long-term cure for anterior disc displacement with reduction. The anterior position is determined by protrusion of the mandibulae necessary to produce the proper disk and condyle relationship. The splint is usually worn 24 hours a day for several months. PERMANENT OCCLUSION MODIFICATION After completion of a course of reversible treatment, many patients may be candidates for permanent modificaton of the occlusion. This appears to most appropriate when patients have had significant improvement in masticatory function and reduction of pain as a result of temporary alteration of occlusal position with splint therapy.Permanent occlusion modification may include occlusal equilibration, prosthetic restoration, orthodontcs, and orthognatic surgery. TEMPOROMANDIBULAR JOINT SURGERY Arthrocentesis Atrthroscopy Disk-Repositioning Surgery Disk Repair or Removal Condylotomy Total Joint Replacement Arthrocentesis Arthrocentesis is minimally invasive technique that involves placing ports (needles or small cannulas) into the TMJ to levage the joint and to break up fine athesions.The most common method involves initially placing one needle into the superior joint space. A small amount of lactated Ringerss solution is injected to distend the joint space and release fine athesion that may be limiting disc mobility.With the joint insufflated, a second needle is placed into the superior joint space, allowing thorouhg lavage with large amounts of fluid. At the conclusion of the procedure, steroid, local anesthesia, or combination of bouth can be injected into the join space before the needle are withdrawn.The most common use appears to be in patients with anterior disk displacement without reduction Atrthroscopy Arhroscopic surgery has become one of the most popular and effectiv methods of diagnosis and treating TMJ disorders.The technique involves placement of a small cannula into the superior joint space, followed by insertion of an arthroscope to allow direct visualization of all aspect of the glenoid fossa, superior joint space, and superior aspect of the disk. Current surgical technique usually involve the placement of at least two cannulas into the superior joint space. One is used for visualization, whereas instruments are placed through the other cannula ( forceps, scissors, sutures, medication needle, cautery probes, and motorized instrumentation; laser fibers can also be used to eliminate adhesion and inflamed tissue and incise tissue within the joint. Atrthroscopy Athroscopy surgery has been advocated for treatment of a variety of TMJ disorders, including derangements, hypo or hypermobility. As with most TMJ surgical procedures, patients placed on some type of physical therapy and often continue splint therapy. Disk-Repositioning Surgery Disk plication and repositioning through an variety of open approaches has been a common surgical procedure performed to correct anterior disk displacement that has not responded to nonsurgical treatment. Although these disorders are often managed surgically with arthrocentesis or

arthroscopy, many surgeons still prefer this type of surgical correction. In this operation, the displaced disk is identified and repositioned into a more normal position by removing a wedge of tissue from the posterior attachement of the disk and suturing the disk back to correct anatomic position. Unfortunately, this surgery does not produced improvement in all patients, with 10% to 15% of patients describing no improvement or a worsening of the conditon. Disk Repair or Removal In some cases the disk is so severely danaged that remnants of disk tissue must be removed. With current technology, the distectomy procedure can be performed through arthroscopic techiques to minimize scat tissue formation and preserve lubrication provided by the synovium. In advanced internal pathologic conditions of the joint, the disc may be severely damaged and perforated but may have adequate remaining tissue so that a repair or patch procedure can be accomplished. Disk Repair or Removal Autogenous grafting techniques include the use of dermis, auricular cartilage, or temporalis fascia. Another alternative to the use of a free graft involves rotation of a temporalis muscle flap into the join to provide interpositional tissue between the condyle and fossa. Condylotomy The condylotomy is an osteotomy completed in a manner identicaly to the vertical ramus osteothomy. When used for treatment of TMJ problems, the osteotomy is completed, but no wire or screw fixation is placed, and the patient is placed into intermaxillary fixation for a period ranging from 2 to 6 weeks. The theory behind this operation is that muscles attached to the proximal segment will passively reposition the condyle, resulting in a more favorable relationship between the condyle, disk, and fossa. Total Joint Replacement In some cases, a pathologic condition of the joint results in destruction of joint structures and in loss of vertical dimension of the condyle and posterior ramus, malocclusion, limited opening, and severe pain. In these cases, reconstruction or replacement of condylar and fossa components of the TMJ may be necessary. Surgical techniques may involve replacement of the condyle or fossa but most commonly include both elements. One method of joint reconstruction involves grafting autogenous tissue using a costochondral bone graft. Acces to the joint and ramus are achieved through a preauricular and retromandibular incision, respectively. Removal of the diseased condyle is completed. The joint fossa and condylar prosthesis are placed after the occlusion has been established with maxillomandibular fixation. DISTRACTION OSTEOGENESIS The loss of vertical ramus height is a consequence of a condylar pathologic condition and may result in asymmetry and malocclusion, as well as dysfunction and pain.Sever alteration of condylar anatomy may result from a variety of conditions such as hemifacial microsomia, growth disturbances, trauma or pathologic condition. Distraction osteogenesis of the mandibular condyle involves exposing the mandibular ramus, usually through an extraoral approach. The distractor is temporary stabilized on a lateral surface of the mandible, an osteotomy of the posterior ramus is completed, and the distraction appliance is attached to the osteotomised segment and to the stable portion of the ramus. Following an initial latency period of 5 to 7 days, the distraction appliance is activated, producing approximately 1 mm of the bone movement per a day.

SEMINAR V

Sinusitis

Anatomy The paranasal sinuses are hollow cavities within the bones of the face and base scull. Anatomy Frontal are posterior to the superciliary arch between the outer and inner tables of the frontal bone. Anatomy Maxillary are pyramidal cavities in the bodies of the maxillae. Its base is formed by the lateral wall of the nasal cavity, and its apex extends into the zygomatic process. Its roof or orbital wall is frequently ridged by the infra-orbital Anatomy Ethmoidal consist of thin-walled cavities in the ethmoid labyrinth. They vary in number and size from 3 large to 18 small sinuses. Their openings into nasal cavity are highly variable. Anatomy Sphenoid- are sited posterior to the upper part of the nasal cavity contained within the body of the sphenoid bone Anatomy The sinuses are lined by respiratory epithelium The mucosal coat can be subdivided into

Superficial viscous layer

Deeper serous layer. Mucous secreted by the sinus mucosa traps bacteria and is naturally extruded through normal ostia. Then it is expectorated or swallowed. The cilia expel the sinus secretions towards the natural ostia by beating in the serous layer. Epidemiology Acute sinusitis affects 3 in 1000 people. Chronic sinusitis affects 1 in 1000 people. There in no significant race preponderance. The rate in women is 20,3% The rate in man is 11,5% Sinusitis is more common in children and young adults. Etiology the most important factors: Acute sinusitis - bacterial Acute sinusitis viral Chronic sinusitis fungal Classification

Acute bacterial sinusitis: Predisposing Conditions Viral infection Allergic/nonallergic rhinitis Anatomic variations Abnormality of the ostiomeatal complex Septal deviation Concha bullosa Hypertrophic middle turbinates Haller cells - are ethmoid sinus air cells that extend out under the orbit (eye). They may cause blockage or obstruction of the natural opening of the maxillary sinus, Topical nasal medications Cigarette smoking Diabetes mellitus Dental infections and procedures

Cocaine abuse Acute bacterial sinusitis: Probability of sinusitis if finding is: Cystic fibrosis Mechanical ventilation Head injuries Use of nasal tubes Samter's triad Sarcoidosis Wegener's granulomatosis Immune deficiency Iatrogenic Acquired immunodeficiency syndrome Immotile cilia syndrome Kartagener syndrom Acute sinusitis Clinical symptoms:

Pain over cheek and radiating to frontal region or teeth The pain increases with straining Redness of nose, cheeks or eyelids Tenderness to pressure over the floor of the frontal sinus immediately above the inner canthus

Referred pain to the vertex, temple or occiput Postnasal discharge A blocked nose Persistent coughing Facial pain

hyposmia Chronic sinusitis Clinical symptoms:

nasal obstruction postnasal drainage facial pain & headache rhinorrhea hyposmia / anosmia

Radiography Generaly plain radiography is said to be obsolete but it may be useful to confirm air-fluid levels and evaluate size and integrity of the paranasal sinuses. CT scanning and MR imaging are not wide available so plain radiograms are often taken as the only image. In general WATERS CALDWELL LATERAL views are obtained

Occipitomental or Waters view: This view shows the maxillary antra clearly. The frontal sinus is projected obliquely. The ethmoid air cells are obscured, but a few may be seen along the medial walls of the orbit and within the nose. The sphenoid sinus is seen through the open mouth.

Occipitofrontal or Caldwell view: The frontal sinuses are well seen. The floors of the maxillary sinuses are visible. The nasal septum and the middle and inferior nasal turbinate can be seen. The anterior ethmoid air cells are also seen. However, the sphenoid sinus is obscured.

Lateral view: The sphenoid sinus and frontal sinus are visualized. The rest of the sinuses are superimposed. The nasopharyngeal soft tissue and the adenoids are also well visualized.

A modified basilar view - a submental vertex view May be a useful adjunct when dealing with sphenoid sinus disease Common radiologic abnormalities:

Acute sinusitis This plane radiogram in Waters projection visualize acute process concerning right maxillary sinus. The air-fluid level is well seen. The left maxillary and frontal sinuses are not involved. Acute sinusitis On this x-ray an opacification of the right maxillary sinus is well seen. The sinus is filed with inflammatory fluid and mucous secreted by respiratory cells. The second maxillary sinus as well as both frontal are pneumatized Acute sinusitis CT-scan Acute Sinusitis MR imaging Acute Sinusitis MR Imaging Acute sinusitis

The aim of the therapy is: to eradicate infection to decrease severity and duration of symptoms to prevent complications The goals of management are: Provision of adequate drainage Appropriate systemic treatment of the likely bacterial pathogens

DRAINAGE can be achived: Medically Vasoconstrictors systemic oral adrenergetic

Pseudoephedrine Phenylpropanolamine

Phenylephrine for 10-14 days Topical vasoconstrictors

Oxymetazoline used for maximum 3-5 days because of high risk of:

Rebound congestion Vasodilatation Rhinitis medicamentosa

DRAINAGE can be achived: Surgically The aim of the surgical drainage is to enhance mucocillary flow and provide material for culture and sensitivity. Sinus puncture can be achived using: In children - general anasthesia In adults - local anasthesia Optimal drainage sites are : The inferior meatus Canine fossae

Antibiotic therapy The course of treatment usually lasts 14 days. First line therapy is AMOXICILLIN or MACROLIDE in patients allergic to penicillin. Second line therapy is usually required in patients who: Lives in communities with high incidence of resistant organisms Fails to respond within 40-72 hours of commencement of therapy Whose symptoms persist beyond 10-14 days Antibiotic therapy second line

Amoxicilin clavulate Second or third generation cephalosporins Macrolides Fluoroquinolones Clindamycin

Metronidazole is required in patients with dental causes of sinusitis or with foul-smelling discharge Chronic sinusitis Medical therapy is the first line of treatment of chronic sinusitis. It consists of: 3-6 weeks course of oral antybiotics: fluoroquinolone macrolides broad spectrum penicillins with beta lactamase inhibitor 7-28 days course of oral steroids in case of significant intranasal edema Short course of decongestant in case of significant nasal congestion

Sialine irigations Chronic sinusitis Surgical therapy is reserved for patients who have not responded to medical therapy. The main surgical options are: FESS Functional Endoscopic Sinus Surgery Caldwell-Luc procedure Inferior antrostomy naso-antral window Caldwell-Luc Procedure: history Caldwell-Luc is the fenestration of the anterior wall of the maxillary sinus and the surgical drainage of this sinus into the nose via an antrostomy. This procedure was first described by George Caldwell in 1893 of New York, Four years later Henri Luc of Paris described the same operation, and the procedure is now referred to as a Caldwell-Luc. Over the subsequent eighty years, this procedure became the work horse of much of sinus surgery .With the introduction of endoscopic sinus surgery, Caldwell-Luc is much more selectively employed as intranasal approaches often permit excellent access to the maxillary sinus.

Caldwell-Luc Procedure:

Indications In the past Caldwell-Luc was used for

treatment of chronic sinusitis, removal of polyps, cysts or foreign bodies, reduction of facial fractures, closure of dental fistulas into the maxillary sinus as a route to the ethmoid and sphenoid sinuses. visualization of the orbital floor for decompression, various forms of tumor surgery access to the pterygomaxillary fossa (the space behind the maxillary sinus

Caldwell-Luc Procedure:

Indications Current indications for Caldwell-Luc include: Exposure and removal of tumors within or adjacent to the maxillary sinus Removal of odontic tumors or cysts Occasionally the more conventional indications prior to endoscopic sinus surgery as

judged by the surgeon and their experience with the various approaches.

Anesthesia Caldwell-Luc may be performed under local or general anesthesia depending on the patients preference, the surgeons experience, the health and age of the patient, and the complexity of the proposed procedure. Local anesthetic with epinephrine should be injected into the soft tissue over the maxillary sinus and the common wall of this sinus and the nose. Several minutes should be allowed to lapse before beginning surgery to permit good anesthesia and vasoconstriction of blood vessels.

Caldwell-Luc Procedure: Operative Technique

Caldwell Luc begins with retraction of the upper lip and incising the mucous membrane above the teeth. There are several variations of the placement of this incision relative to the teeth The soft tissue over the maxillary sinus is elevated to visualize the anterior wall of the sinus. Then the maxillary sinus is opened. In making such a fenestration, the surgeon must be careful to avoid the roots of the maxillary teeth because the teeth may be devitalized if their blood supply or nerves are injured by the fenestration. A second potential complication is injury to the infraorbital nerve. This nerve is within the roof of the maxillary sinus to give sensation to mid face region and teeth. During fenestration the nerve may be directly injured or stretched leaving the patient with temporary or permanent numbness. After completing procedure which requires a Caldwell-Luc, an opening into the nose is routinely performed. This antrostomy is intended to either temporarily drain the maxillary sinus of post-operative blood or to provide a long term communication into the nose. Traditionally this opening into the nose is placed below the inferior turbinate or the area known as the inferior meatus. However, the maxillary sinus normally drains to the middle meatus or below the middle turbinate. Increasingly, a middle meatus antrostomy is being utilized as a more physiologic antrostomy. Following all of the surgical procedures, the soft tissue over the maxillary sinus is re-approximated with sutures. Complications of sinusitis Acute distant sequelae- TSS Acute orbital:

Proptosis Chemosis Ophtalmoplegia Orbital cellulitis Subperiosteal abscess Orbital abscess

Acute cranial:

Meningitis Encephalitis Cavernous or sagittal sinus thrombosis Extradural abscess Subdural abscess Intracerebral acces

SEMINAR VI

Trigeminal Neuralgia
TN is neurophatic disorder characterized by episodes of sudden intense, sharp, severe pain in the face and is often described as the most terrible pain known to man. TN is also called tic douloreux because there is a characteristic muscle spasm that accompanies the pain attack. The intermittent pain interferes with common daily activities such as eating, sleeping, patients live in fear of unpredictable pain attacs which leads to sleep deprivation and undereating. The condition leads to severe anxiety, depression and life-threating malnutrition. Suicide in this case is not uncommon. It is estimated that 1 in 15000 people suffer from TN In a majority of cases TN symptoms begin appearing after the age of 50 ant it is more common in females. The disorder is characterized by episodes of intense, severe, stabbing pain, electrical shock sensation, pressure or crushing sensation which last from a few seconds to several minutes or hours. The pain is generated most often spontaneously without apparent stimulation. But there are some cases thet the wind, touch to the affected area, loud noises, chewing, talking, eating, shaving can also caused the pain. Individual attack usually affect one side of the face (they are unilateral) The pain tends to occur in cycles with remission lasting weeks, months or even years. TN most often affects the maxillary branch or the mandibular branch of the trigeminal nerve. Some patient complain of pain in both maxillar and mandibular branches. Usually the pain occurs during the day (almost never at night during the sleep) In most cases the TN is intractable desease. The trigger zones are the small area that, when stimulated, triggers a tipical burst of pain. The pain is most commonly felt in the cheek bone, most of the nose, upper lip and upper teeth and spreading pain to the lower lip, teeth and chin. The trigger area on the face are so sensitive that touching or even air currents caused the pain episodes. There are several theories exist to explain the possible causes of the pain syndrome: enlargen blood vessel(possibly superior cerebellar artery) compress or throb the V nerv.Such a compression can injure the nervs protective myelin and cause erratic and hyperactive functioning of the nerve.This can lead the pain attacks at the slightest stimulation. Traumatic compression of the nerve by tumor Infectious agents (eg due to human herpes simplex virus) Demyeliating conditions due to sclerosis multiplex

Hypersensitivity of trigeminal ganglion cells Traumatic compression of the nerve by intracranial scars or osteal exostosis.

TYPES classical (idiopatic) TN symptomatic TN where the patogenesis is known. Pain could results in dentogenic infections, temporomandibular joint defects, sinus inflammations or othere otorhynolaryngologic diseases, bone diseases DIAGNOSIS 1. we must rule out a variety causes of facial pain besides Tn 2. we should perform a precise phisical examination, neurological examination, CT, MR Farmacological treatment (medication): 1. anticonvulsant are a common treatment strategy for TN 2. clonazepam and lidocaine may be also effective as well as low doses of antidepressants 3. farmacological treatment very often is not enough and doesn't bring a relief to patient Surgery treatment: Surgery may be recommended either to relieve the pressure on the nerve or to selectively damage the nerv. 1. the microvascullar decompression (MVD) in this procedure the surgeon enters the scull through the 25mm hole behind the ear. The nerve is then explored (for an offending blood) vessel and the nerve and the vessel are separated or decompressed with a small Teflon pad. 2. glycerol injections this liquid is corrosive to nerve fibres and injure the nerv 3. radiofrequency rhizotomy the surgeon uses an electrode to heat a selected division of the nerve 4. stereotactic radiation therapy 5. ballon compression Treatment with combine anaesthetic alcohol blocks. We carry out five to ten injections single injection once a week. In most cases it reduce or eliminate the pain for long period of time. Addictionally our patients appy antiepileptic drugs. The blocks anaesthetise, denaturate and distroy the nerv fibres. The complication which could appear in this method is necrosis of the surrounding soft tissues. Anathomy of trigeminal nerve.

SEMINAR VII

Diagnostic in face fractures

CT or plain X-Ray BEST MODALITY :high resolution CT plain film facial series -the facial trauma is very focal -CT is unavailable - focal small trauma Standard radiographic projections Waters view PA view Lateral view Ortopanthomogram Submentovertex view Oblique views Radiographic signs of facial fractures 1. Direct Signs -Nonanatomic linear lucencies -Cortical defect or diastatic suture -Bone fragments overlapping causing a double-density 2. Indirect Signs -Soft tissue swelling -Periorbital air (SCE, SE,Sub Q air) or intracranial air -Fluid in a paranasal sinus Important factors Anatomy Typical patterns of face traumas Cause of the trauma Medial face fractures Prevalance of Fracture Type Zygomaticomaxillary complex (tripod fracture) 40 % LeFortI 15 % Le FortII 10 % Le FortIII 10 % Zygomatic arch 10 % Alveolar process of maxilla 5 %

Smash fractures 5 % Other 5 % Main rules: ALWAYS ANALIZE RADIOGRAPHS AFTER PATIENTS CLINICAL EXAMINATON !!!!! Look at the orbits carefully Look for indirect signs of fracture Bilateral symmetry can be very helpful. Normal radiopacities are usually bilateral, while abnormal ones are usually unilateral. Know the most common patterns of facial fractures and look for them. Carefully trace along the lines of Dolan (elephant profile) when examining the Waters view in a facial series. Tear drop symptom- hernation of orbital soft tissue!!! Mandibular Fractures One of the most common Clinical findings : facial distortion, malocclusion of the teeth, abnormal mobility of portions of the mandible "ring bone rule"! Most often mistakes in mandibulae fracture reading One projection in condylar fracture Anatomical structures -air in oropharynx at the angle of the mandibule -calcification of stylohyoid ligament projecting over ascending ramus -hyoid bone shown over the posterior part of the ramus -the intervertebral spaces Superimpositions of other structures -medial part of mandible Wise sayings about mandibular fractures Remember the ring bone rule. Symphyseal fractures can be diabolically hard to see, even on a well-exposed AP film Look carefully along the cortical margin of the whole mandible for discontinuities. This may be the only sign of a fracture that you will see. Also carefully examine the mandibular canal for discontinuities. A fracture line entering the root of a tooth is considered an open fracture by definition. Pathologic fractures can occur in the mandible. Look carefully for evidence of a periapical abscess or a mandibular tumor, especially if there doesn't seem to be enough trauma to match the injury.

SEMINAR VIII

Midface fractures-symptoms,diagnosis ,classification and surgical treatment.

NEUROSURGICAL PROBLEMS OF MIDDLEFACE FRACTURES.CLINICAL SYMPTOMS OF INTRACRANIAL HAEMATOMAS.
Facial injuries have accompanied human beings since the earliest times,however the development of civilization vastly increased their occurance. Craniofacial injures are dangerous not only due to damages of integument and sceleton but they also result in severe and varied esthetic and functional complications. The most frequent reasons of facio-cranial injures according Polish and foreign authors(sources) are road accidents,assaults,sport, industrial injuries and falls. The head sceleton consists of two major parts:neurocranion and splanchnocranium.All bones are connected by osteosutures.Splanchnocranium consists of 14 bones,which are:mandible and vomer and symetrical maxilla,zygoma,lacrimal bones,nasal bones,palatal bones and conche nasal inferior. The facial part of cranium maybe devided horizontally into 3 levels:upper,middle and lower. The face is the area of splenchnocranium below the eyebrow line and it is divided into lower and upper face massif. MAXILLARY FRACTURES Maxillary fractures constitute(account) for approximatelly 15% of all facial fractures. In 1901 French military doctor Rene LeFort presentet a classification of maxillary fractures which has since been used by clinicist.He defined 3 major types of fractures which are called LeFortI,II,III.This division reflects 3 main fracture lines. LeFortI fractures(basal,horizontal) In typical LFI f. the main fracture line causes detachment and dislocation of palatal plate with alveolar processus(we call it floating palate) from upper facial massive(bridge). This f. most frequently results from a force of injury directed on upper lib and maxillary alveolar rim. The f.line begins at the lateral bone edge of nose and extends horizontally above the teeth apices towards the maxillar tuber.This f. is often(frequently)accompanied by the Volter f.which is the f.of medial line(along the palatal suture). The clinical symptoms are: -idiopatic and palpatic pains in the affected area, -nasal-mental section extension(colapse of facial bone), -mobility of bone fragments(we can feel the bone steps within zygomato-alveolar crists) -malocclusion, -oedema,ecchymosis, -subcutaneous emphysema(often located in the area of upper lip and cheek) X-rays are recommanded to be taken in 3 projectons: In case of doubts CT is recommanded LeFortII fractures(piramid shaped fracture)

The fracture line is multidirectional. It starts at nasal bridge at or below the nasofrontal suture,through the frontal process of the maxilla.Then it extends inferiolaterally through the lacrimal bones to inferior orbital floor and rim(near or through the inferior orbital foramen).Then it runs inferiorly through the anterior wall of the maxillary sinus to the zygomatoalveolar crist.Further its course is similar to LFI fracture line. CLINICAL SYMPTOMS The damage of soft and bone tissues in this type of fracture is extensive and is accompanied by serious functional and anatomical disfunctions. -extension of nasal fragment -oedema,ecchymosis,gross blood,hematoma -epistaxis, -malocclusion(usually open anterior bite deformity), -mobility of bone fragments(we can feel bone steps within bridge of the nose,inferior orbital rim,zygomatoalveolar crist) -exophtalmus(not always) -nasal cerebrospinal fluid rhinorrhea(it results from the cranial basis fracture within fossa cranial anterior) -pneumatosis subcutanea -paraesthesis LeFort III fracture(transverse) The avulsion of maxillo-orbital-zygomatical massive from the cranial base occurs.This fracture is frequently accompanied by the fracture of cranial base. The course of fracture line extends from nasal bridge,through(via)medial wall of the orbit,lacrimal and ethmoid bones,near or through inferior orbital fissure and than it passes to lateral orbital wall through zygomaticofrontal junction and the zygomatic arch. CLINICAL MANIFESTATIONS Are similar to those of type II however they are more evident and more frequently they pertain to vision and smell. The bone steps are observed at the nasal bridge,lateral orbital wall,and less clearly in the area of zygomatic arches. This fracture is often accompanied by basocranial fracture within anterior cranial fossa,therefore you must draw particular attention to possible leak of cerebrospinal liquid to nose and throat. The most serious ophtalmological complications which may result from this fracture are as follows; -superior orbital fissura syndrom which is characterised by:diplopia,exophtalmus ptosis,pupillary dilation and deep orbital pain.This syndrom occurs when the fracture line runs along the upper orbital wall,passes by optic canal and covers superior orbital fissura and damages its content(III,IV,VI,V1 nerves) -orbital apex syndrom-the damages include superior orbital fissura and optic canal.Blindness maybe an addictonal symptom of this syndrom.

In reality the LeFort classification is an oversimplification of maxillary fractures.In most instances,maxillary fractures are a combination of a various LeFort types.Fracture lines often diverge from the described pathways and may result in mixed-type fr,unilateral fr, comminute(multiple) maxilla fracture. Besides(instead) the afore mentioned fractures an isolated fracture of maxillar alveolar (processus)ridge,Volter fracture can occurs(may be observed).

TREATEMENT Although the principle of a prompt reposition and immobilazing bone fragments is valid also in the event of maxillary fractures,in some cases treatment must be postponed for about 3 weeks.This cases are life threatening states that is:extensive basocranial fracture with growing brain oedema,intracranial hematoma and many other co-existing extensive injures.In these cases a temporary treatment is required in order to prevent a further dislocation of bone fragments. Many years of experience point to the fact that conservativ-ortopedic methods are very efective. CONSERVATIV TREATMENT In this case we use:arch bars,intermaxillary rubber band fixation,submental band. In the case of toothlessness we use Gunning-Port unit and submental band SURGICAL TREATMENT The most popular sur.tr.is dressing wounds as well as extraction of teeth. Repositioning is most frequently used in this case.Repositioning is performed by means of: Hayton-Williams,Rowe forceps.When using force we are able to break even very strong accretions. Rigid miniplate fixation is usually carried out(performed) within lateral orbital rim(LFIII),inferior orbital rim and zygomaticoalveolar crist. THE FRACTURES OF ZYGOMATICOMAXILLARY COMPLEX Zygomaticomaxillary complex which constitutes the midface part of the scull generally called buccal(zygomatic bone) due to its anatomical location which builts not only the lateral facial shape but also is a part of valid structures as orbitals,maxillary sinuses. This bone due to its lateral position is especially effected by injuries.The fracture of the complex most often occur in the area which is least resistant to external force ie.lateral and inferior orbital rim,zygomatic arch and zygomaticoalveolar crist. German surgeons Bitter and associates suggested an interesting classification: -isolated zygomatic bone fracture -comminute zygomatic bone fracture -isolated orbital floor fracture -the fracture of zygomatic bone and orbital floor -isolated zygomatic arch fracture According to the latest sources zygomaticomaxillary fracture account for approximatelly 20% of all facial fractures. These injures caused varid symptoms such as: -malvision-often occurs diplopia resulting from displacements of eyeballs with relation to horizontal plane,limitations or lack of function of motioneye muscles by dislocated bone fragments of the orbital.Diplopia may be also caused by swelling of soft tissues of the orbital,intraorbital hematoma which is eliminated idiopatically.(spontaneous,essential) -disfunction of jaw opening caused by mechanical block of coronoid processus by the zygomatic bone -pseudoptosis -facial asymetry which is revealed by flattened cheek bone -parasthesia or anesthesia within second branch of trigeminal nerve distribution -eyelid,periorbital,subcutaneus ecchymosis,subconjunctival hemorrhages,zygomatic and periorbital oedema,pneumatosis subcutanea -epistaxis -distortion of facial expresion by a mechanical damage of facial muscles or postinjuries paresis of facial nerve branches.

- in clinical investigation we can observed steps bone Diagnosis(evaluation) Classical radiological diagnosis is still the standard while evaluating fracture of zygomaticomaxillary complex.The following projections are rutinelly recommended: -scan aimed at the orbitals -scan aimed at nasal sinuses(Waters projection) In the event of serious injuries when the damage of CNS or vision may occur it is adviced to perform CT or MR(at best 3D technology) Treatement Conservativ treatement is recommended when the fr is not accompanied by bone fragments displacement.In that case we recommended a diet,relaxed life style and antiinflammatory medications. The surgery threat should be performed within 24H following the injury.If the patient suffers from extensive swelling the operation should be postponed for 5-7 days.Standard surgical procedures are as follows: 1)Elevation with a hook-repositioning zygomatic bone by means of single tooth hook called Wassmund hook and placing it in supraposition in order to stabilized the fracture. 2)rigid internal miniplate fixation(rarely intraosseus wiring) This procedure is frequently combined with exploration of the orbital floor and its possible reconstruction using auto or allogenic materials. ISOLATED ORBITAL FLOOR FRACTURE Bone damages are usually not very serious and they are located within fragile,paperlike floor of the orbital(less frequently within the medial orbital wall) which breaks as a result of blunt injury of the eyeball and increased pressure within the orbital. This fracture result in: -falling of the orbital haernia to maxillary sinus -entrapped extraocular muscle and periorbital tissue The displacement and entrapment of soft orbital tissue lead to ocular motility disturbances which caused diplopia.Diplopia is accompanied by enophtalmus and hypesthesia in theV2 distribution.Addicionally we can observe a falling drop image in the Xray.

CRANIOCEREBRAL TRAUMA CCT is one of the three main reasons of death in Poland,the other two being cancer and circulatory system diseases. This injures are caused by road-accidents.The characteristic clinical picture occurs after facial injures:the force of injury causes
apparently serious external injures.

The symptoms which can occur after CCT: a)commotio cerebri-the main sign of CC is uncousciousnes usually lasting no longer than 1H. This is frequently accompanied by retrograde amnesia as well as vegetativ signs such as nausea,vomiting,tachycardia,vertigo.Clinical symptoms of CC retract(disappear) after a few days. b)contusio cerebri-in CC surface areas of the brain tissues are affected. c)epidural haematomas-result from damage of brain vessels d)posttraumatic oedema cerebri-is the most serious complication CCT.It is always accompanied by elevated ICP,usually resulting(caused) from swelling,epidural hematomas or hydromas.The physiological ICP is 4-12mmHg. Treatment-it is believed that when ICP is above 20mmHg conservativ treatement should be

applied(introduced)-this includes elevating the patients head,administering osmotic activ medicaments such as mannitol.Dehidrating treatment maybe applied using furosemid however the level of electrolytes should be monitored. Complications following the fracture of cranial base and not the fractures themselves require treatment.This complication are: -liquorrhea(rhinorrhea,otorrhea), -intracranial pneumatocele, -intracranial hematomas, -carotid-carvenosus fistula, -meningitis Liquorrhea Occurs as a result of damage of duramatral.If the fracture occurs within anterior cranial fossa cc liquid usually flows from the nose,but it also runs into the throat or gets into facial integument causing substantial swelling..When the fracture line occurs within medial cranial fossa cc liquid usually flows from the ear. Diagnosis of liquorrea is usually difficult.If in laboratory analisis 50-80mg% glucose is discovered in the liquid sampled from the nose(or ear) then this points to the fact that we have rhinorrhea(or otorrhea). 90% of liquorrhea disappeared idiopaticly.In the event of of acute posttraumatic injures any operation may be performed 2-3 weeks following the injury. Fistula causing liquorrhea is closed by using fibrogenic glue,neuropatch(it is artifical duramatral),temporal fascia. Intracranial hematomas IH results from blood accumulation between the cranial bones and meninges(epidural and subdural hematomas).EH is the most frequently occuring hematoma.70% of epidural hematomas are caused by damage of arteria meningea media. The clasical neurological signs of EH are:pupillary dilation on the side of the hematoma and hemiparesis on the oposite side from the H and bradycardia.Increasing H causes stronger headaches,the general state of the patient deteriorates and is followed by uncousciousnes and increased ICP.CT and immediate neurosurgical treatment is nessesary.

SEMINAR IX

Madibular Fractures
The mandible is the second most commonly fractured part of the maxillofacial skeleton because of its position and prominence. The location of the fractures are detrmined by the mechanism of injury, direction and intensity of the vector of the force, patients age, the presence of teeth. In the management of any bone fracures , the goals of treatment are to restore proper function, restore any contour defects, and to prevent infection at the fracture side. Restoration of mandibular function must include the ability to masticate properly, to speak normally, to allow for articular movements as ample as before the trauma. Classification of the mandibular fratures:

Anatomic location: Dentoalveolar fracture- it is limited to the tooth-bearing area of the mandible without disruption of continuity of the underlying osseous structurae Symphysis fracture Parasymphysis fracture- occurs in the region between the mental foramen Body fracture- between the mental foramen and distal portion of the second molar Angle fracture Ascending ramus fracture- line extends horizontally through both the anterior and posterior borders of the ramus, or that runs vertically from the sigmoid notch to the inferior border of the mandible Condylar process fracture Classification of the mandibular fractures: 2. Pattern of fracture

Simple fracture single fracture line that does not communicate with the exterior (ramus or conyle or fracture in a edentulous portion with no tears in the periosteum. Compound fracture- communication with external environment, usually by the periodontal ligament of tooth Greenstick fracture- frequently occurs in children and involves incomplete loss of continuity of the bone- without mobility betwen before the proximal and distal fragments Comminuted fracture- exhibit multiple fragmentation of the bone at one fracture site. Complex or complicated fracture implies damage to structures adjacent to the

bone such as major vessels, nerves, or joint structures (f.i.: inferior alveolar artery, vein, and nerve in mandibular fracures proximal to the mental foramen and distal to the mandibular foramen Classification of the mandibular fractures:

Indirect fracture- arise at a point distant from the side of the fracturing force (an example subcondylar fracture occuring in combination with a symphisis fracture. Direct fracture Pathologic fracture- occure when a fracture results from normal function or minimal in a bone weakened by pathology (cyst or metastatic tumor, or as part of generalized skeletal disorder, such as osteopetrosis. Dislocated fracture Nondisplaced fracture Depending on contact with surrounding tissues we divide: -Closed fracture ( fractura occlusa ) -Open fracture ( fractura aperta ) Due to fracture line we divide: -Incomplete fracture ( fractura incompleta without periosteum damage ) -With periosteum damage ( fractura completa ) -Transverse fracture ( fractura conversa ) -Spiral fracture ( fractura spiralis ) -Impacted fracture ( fractura impacta) Incidence of fractures of the various anatomic part of the mandible Evaluation of Mandibular Fractures Local examination of the face and jaws should be conducted in a logical sequence. The first objective is to obtain an accurate history from the patient, or relative if the patient cannot cooperate. Patients often complain of the following: Pain or tenderness is often present Difficulty chewing- pain could be limiting mandibular function or there may be malocclusion or mobility at the fracture side Malocclusion Numbness in the distribution of the inferior alveolar nerve (nondisplaced fracture often does not give rise to numbness in the distribution of the inferior alveolar nerve. Clinical Examination The clinical examination should consist of inspection and palpation. The skin around the face should be inspected for sweling, hematomas, and laceration.A comon site for a laceration is under the chin, and this should alert the clinician to the possibillty of an associated subcondylar or symphysis fracture.

The clinician should palpate the movement of the condyle both over the lateral aspect of the joint and through the external acoustic meatus and observe the movement of the mandible itself. Any significant deviation on opening may be indicative of subcondylar fracture on the side to which the mandible deviates. In unilateral fracture, there is deviation of the occlusion toward the fractured side, with premature occlusal contact in the posterior region on tha side. If bilateral condylar fractures are present, the occlusion may not be deviated. The midlines are often concident, andpremature contact is present bilaterally on the posterior dentition with the anterior open bite. We can also observe limited range of motion caused by pain. Occasionally a fracture of the condylar process will produce a tear in the epithelial lining of the anterior wall of the canal, which produces bleeding from the acoustic meatus. It is important to determine that this bleeding is not coming from behind a ruptured tympanic membrane, which may signify a basilar skull fracture. A detailed intraoral examination should be undertaken. The most intraoral findings are:malocclusion, fracture of the dentition, and decrease interincisal opening. Than the soft tissue should be undertaken. The gingival tissue should be inspected for tears or lacerations. With the aid of tongue the floor of the mouth is examined- sublingual ecchymosis is almost pathognomic of fracture of the mandible. Next the dentition are examinated for evidence of broken teeth and for steps or irregularities in the dental arch. The patient is asked to lightly bite the teeth together and to say whether the bite feels different from norma, following which the occlusion is inspedcted. Premature occlusal contact are note. If the patient is edentulous and has intact dentures with him, these can be replaced in the mouth and the occlusion inspected. The mandible should then be grasped on each side of any suspected fracture and gently manipulated to assess mobility. If no fracture can be found but clinical suspicion remains high, the mandible can be compressed by appluing pressure over the both angles. This nearly always gives rise to pain at a fracture site. Fracture of the body ( fractura corporis mandibulae ) The most common location of the fracture line is : -Canine area -Bicuspids area Symptoms: -Pain and tenderness at the site of impact -Swelling -Speach, swallow and masticating disorders -Bleeding

-Numbness in the distribution of the inferior alveolar nerve -Malocclusion -Wound of mucous membrane -Change of the face shape Fracture of the ramus (fractura rami mandibulae): transverse or longitudinal Symptoms : -Speach, swallow and masticating disorders -Pain or tenderness at the site of impact -Deviation in fracture direction -Swelling -Numbness in the distribution of the inferior alveolar nerve -Malocclusion -Change of the face shape Fracture of the condyle ( fractura processus condylaris mandibulae ) -Fracture of the head ( fractura condylaris ) -Fracture of the neck ( fractura condylaris superior ) -Subcondylar fracture ( fractura condylaris inferior ) Symptoms: -Unilateral fracture-cross bite and mandible deviation -Bilateral fractures-open bite -Swelling -Pain -Limited mandible mobility -Limited mandible protrusion -Limited mouth opening and closing Fracture of the coronoid (fractura processus coronoidei mandibulae Symptoms: -Pain -Limited mouth opening and closing Fracture of the alvelous proccess (fractura processus alveolaris mandibulae) Symptoms: -Pain or tenderness at the site of impact -Wound of the mucous membrane (gingival laceration) -Hematoma formation -Malocclusion -Complete or incomplete dislocation of teeth Radiographic Evaluation To adequatly screen for the presence of the mandibular fracture, at least two views are necessary:

-panoramic radiograph -lateral oblique view -posteroanterior mandibular view -CT Treatment of mandibular fractures -Debridement -Reduction (open or closed) -Fixation -Immobilization: 3 to 6 weeks -Functional rehabilitation Treatment of mandibular fractures Closed reduction(conservative treatment)- involves the blind manipulation of the fracture without directly exposing the fracture site and using the teeth (or dentures) and occllusion as guides to proper positioning (restoration of the dental occlusion by ligature wire splinting and intermaxillary rigid or elastic fixation The indication for closed reduction may simply be stated as all cases in which an open red. is either not indicated or is contraindicated Treatment of mandibular fractures- Closed reduction Several condition deserve specific mention:

Grossly comminuted fractures because using o.r. techniques would jeopardize the blood supply to the small bone fragments and lead to increased likelihood of infection (gunshot wound) Fractures in the severely atrophic edentulous mandible represent a difficult clinical situation In situation where there is a lack of soft tissue overlying the fracture site, soft tissue flaps have to be transported to cover the fracture site. The presence of bone plates, screws, and wires may increased the likelihood of infection under these circumstances Fractures in children involving the developing denition are difficult to menage by open r. because of possibility of damage to the tooth buds or partialy erupted teeth. The lenght of intermaxillary fixation for adult mandibular fractures is 6 to 8 weeks, for condylar fractures up to 3 weeks using hypomochlion and elastics(non-rigid fixation) Inermaxillary techniques in Dentate patients include application of arch bars, direct wiring, Ivy loop wiring, continous wire loop technique, cast cap splints and IMF screws. Closed reduction in Edentulous patients is achieved with Gunnings splints or splints made from the patients own dentures. Gunnings splint

Old modality Edentulous patient Rigid fixation is not possible To establish the occlusion

Treatment of mandibular fractures- Open reduction In open reduction, the fracture site is surgically exposed to allow direct inspection of fracture reduction and alignment. O.R. has developed to become more frequent treatment options for the management of mandibular fractures.

Open reduction and semi-rigid fixation (using inter-ossous wirings) Open reduction and rigid fixation (using bone palates osteosynthesis)

The major indication for open reduction of a fractured mandible are:

Unfavorable or Unstable Fracture Prolonged Delay in Treatment of the Fracture with Interpositional Soft Tissue Complex Facial Fractures

Medically Compromised Patients ( patients with special medical conditions like with decreased pulmonary function,gastrointestinal disorders, with psychiatric and neurologic problems) Concurrent Condylar Fracture Associated with Fractures Elsewhere in the Mandible Management of teeth retained in fracture line Good quality intra-oral periapical radiograph Insinuation of appropriate systemic antibiotic therapy Splinting of tooth if mobile Endodontic therapy if pulp is exposed Immediate extraction if fracture becomes infected Follow up for 1 year and endodontic therapy if there is a loss of vitality Removal of teeth in fracture line Absolute indications

Longitudinal fracture Dislocation or subluxation from socket Presence of periapical infection Infected fracture line

Acute pericoronitis

Relative indications Functional tooth that would be removed Advanced caries or periodontal diseases Doubtful tooth which would be added to existing denture

Tooth in untreated fracture presenting more than 3 days after injury Edentulous Fractures The loss of teeth result in resorption of alveolar bone, which weakems the mandible. The loss of bone also means that there is less crosssectional area of bone in contact in fracture patients and less periosteum and endosteum to supply the osteogenic cells for fracture healing. Because of the aging process the majority of the bllod supply to the endontulous mandible is from periosteum rather than the inferior alveolar artery. A larger percentage of fractures in the endontulous patients are not compound because of the lack of teeth. Edentulous Fractures Minor displacement of the bones can be easily accommodated in the construction of new dentures. The edontulous population also tends have more health problems resulting from conditions such as osteoporosis, diabetes, mellitus, and steroid therapy , which may directly affect bone healing. If the location of the fracture is posterior to the denture-bearing area, then either additional fixation (eg external pin fixation), or open reduction and fixation may be necessary to control the proximal fragment. The bilateral body fracture deserves special mention because the pull of the suprahyoid muscles tends to displace this fracture inferiorly. These usually occur in the pencil-thin atrophic mandible. The bilateral body fracture deserves special mention because the pull of the suprahyoid muscles tends to displace this fracture inferiorly. These usually occur in the pencil-thin atrophic mandible. A variety of treatment modalities have been suggested to treat these difficult fractures including open reduction with rigit internal fixation, closed reduction with and without bone grafts, end external pin or plate fixation. When the edentulous mandible is comminuted again because of the poor blood supply to the bone fragments, those fragment are best managed by closed reduction. Fracture mandible in children Their management is complicated by the presence of deciduous teeth, which may be mobile during the mixed dentition stage and whose shape has little in the way of undercut areas, which means that they do not retain wire as well as adult teeth. The presence of tooth buds reduced the area available for interosseal fixation, and there exist a greater potential for ankylosis and growth disturbances in the younger

population. Also children do not tend to tolerate IMF as well as adult. On the other hand, fractures tend to heal quiker in chldren and slight malocclusion problems can be compensated for growth of the patient. Fracture mandible in children These fractures are rare in chldren under 5 years of age because of greater elascity of the bone and lighter weight of children, which lowers the forces of impact during falls. Mandibular fractures in children can often be successfully managed by acrylic splint therapy of the mandible only or with eyelet wires and IMF. A shortened period of IMF 2 to 3 weeks, is all that is required. When an open reduction is required, it has been successfully acommplished by the extraoral route using inferior border wiring in order to avoit the tooth buds. If adequate bone height is available below the area where the tooth buds are located, the use of resorbable plates offers a great advantage to fixate these fractures Complications Delayed Union and Nonunion Infection (antibitics!!) Malunion Nerve Injury Growth Alteration Temporomandibular Join Dysfunction

SEMINAR X

UPPER FACE FRACTURES

Principles Of Craniomaxillofacial Fracture Managemtent Precise anatomic diagnosis Direct fracture exposure Reduction / rigid internal fixation Mandible fracture stabilization Reconstruction of horizontal and vertical facial buttresses Primary bone grafting Periosteal and soft-tissue suspension and repair Naso-Orbital-Ethmoidal (NOE) Fractures; Anatomy Interorbital Space two ethmoidal labyrinths superior and middle turbinates perpendicular plate of ethmoid Medial Orbital Wall anteriorly - lacrimal bone and lamina papyracea posteriorly - body of sphenoid NOE Fractures: pathophisiology Interorbital space displaced backwards Medial Canthal Tendon and Lacrimal Apparatus frequently injured May extend into: cribiform plate and anterior cranial fossa optic foramen Associated Orbit and Midface Fractures Common NOE Fractures: Symptoms Flat nose Swollen medial canthal area Telecanthus (12-20%) Lack of skeletal support on palpation of nose CSF leak

Positive eyelid traction test NOE Fractures - Telecanthus Normal intercanthal distance (Stranc) Males: Males: Females: 33-34mm 32-33mm

Consider >35mm abnormal (Manson)-TELECANTHUS NOE Fractures: Classification (Markowitz) Type I - Single central segment Type II - Comminuted central segment Type III - Avulsed medial canthal tendon NOE Fractures: Management Early open reduction! Four Objectives: correct epicanthal folds restore bony contour reestablish lacrimal system continuity medial canthoplasty / canthopexy Aprouches: Wide Exposure! coronal incision open sky - transverse across root of nose vertical midline nasal subciliary extend existing lacerations Surgical goals: Correct nasofrontal separation Elevate nasal bones Reduce comminuted nasal bones Bone graft where needed Explore septum Stabilize nasomaxillary buttresses Medial Canthus Repair Transnasal Wireing: Through central fragment, posterior and superior to lacrimal apparatus.

Three sets of wire: bone reduction medial canthus reattachment reapproximate skin to nasal skeleton Naso-Orbital-Ethmoidal FracturesLacrimal System Injury Incidence <20% Routine exploration not justified Persistent dacryocystitis sighn of obstruction. Treatment :Dacryocystorhinostomy Naso-Orbital-Ethmoidal FracturesComplications Telecanthus (related to inadequate / delayed treatment) Lacrimal system obstruction / infection Meningitis

Frontal Sinus Fractures: Anatomy Begin to Develop At 2 Years of Age Extension of the Ethmoid Air Cells Radiographically Evident At ~ 8 Years Do Not Reach Adult Size Until 12 or Older 10% - Unilateral Development 4% - Absent All Together Drain Into Middle Meatus 3 Usually Small, 5 cm in adults Anterior Wall Thicker Than Posterior Close To Other Structures Posteriorly (cribiform plate, dura mater, frontal lobes) Inferiorly (orbit, nasofrontal duct) Frontal Sinus Fractures: Signs And Symptoms Forehead Laceration CSF Rhinorrhea Supraorbital Nerve Anesthesia

Depressed Frontal Region Subconjunctival Ecchymosis Frontal SinusFractures: Diagnosis X-Ray (Air Fluid Levels) CT Scan (Axial and Coronal Images) Frontal Sinus Fractures: indication to surgery Anterior Table Displacement With Contour Change Nasofrontal Duct Involvement Displaced Posterior Table Nasofrontal Duct Injury: treatment procedure Remove mucosa, burr inner cortex, occlusion of duct, sinus obliteration Frontal Sinus fractures:Treatment Anterior table: close reduction. Posterior Table: Cranialization Bicoronal Approach Preserve Pericranial Flap Dural Repair Remove Sinus Mucosa Obliterate Nasofrontal Duct Remove Intersinus Septum And Posterior Wall Pericranial Flap To Floor Of Sinus Frontal Sinus Fractures: Complications Early (within 6 months) Frontal Sinusitis Meningitis Late Mucocele Mucopyocele Brain Abcess

Osteomyelitis Late complications complications Meningitis Mucopyocele With Osteomyelitis Of Frontal Bone Orbital Fractures :Anatomy The bony orbit refers to the shell of bone which surrounds and protects the eye. (Zygoma,Maxilla,Lacrimal,Ethmoid,Palantine,Sphenoid,Frontal) The bony orbit is a pyramidal cavity with an elliptical base presenting anteriorly and the apex posteriorly at 22 degrees lateral from the visual axis. Orbital Fractures : etiology Sporting /recreations events (football, baseball, painball, trampoline, etc) MVAa Work accidents Orbital Fractures: Clasiffication 1. Orbital Blowout Fracture PURE - orbital rim intact IMPURE associated with orbital rim fracture 2. Orbital Fracture without Blowout mechanizm: -Comminuted Fr.- Le Fort II, III+ Herniation of orbital contents into Maxillary Sinus -Linear Fractures: Malar, Le Fort II,III Maxillary -Displaced Fr.- Fronto-Zygomatic separation, Naso-orbito-etmoidal fracture( NOE complex fracture), Cranio-orbital fractures Orbital Fractures: Mechanizm of injury : 2 theories 1.Hydraulic theory More energy Larger fracture involving entire floor and medial wall Should suspect more extensive orbit involvement with associated injuries (globe rupture) 2.Bone conduction theory buckling Less energy Small fractures limited anterior floor Orbital Fractures: Clinical aaperances IMPORTANT: History, time and mechanism of injury

Change in appearance of eye State of vision immediately after injury Immediate loss of vision severe damage to retina Loss of light perception - vascular occlusion or optic nerve compression Initial good vision compression optic neuropathy Symptoms Enophthalmos ( rarely exophtalmos) Anesthesia Epistaxis Diplopia, blurry vision Infraorbital step-off deformity Subcutaneous emphysema Limitation of movement of the eyeball Nusea and vomitting, Aschers reflex Penetrating Injuries Occult globe penetration Eyelid lacerations Orbital Fissure Syndrome Blindness Ptosis of upper eyelids Extraocular motor palsies Malocclusion Enophthalmos Inferior and Posterior Displacement of Globe and Intraorbital Soft Tissue Etiology of Enophtalmos Enlargement of the Bony Orbital Cavity Escape of Orbital Fat or Fat Necrosis Muscle Entrapment in Fracture Line Soft Tissue Scarring and Contracture Orbital Fractures: clinical examination Full Head and Neck exam Bimanual Palpation Facial asymmetry

V2 exam - numbness cheek Cardiac exam (Bradycardia, low BP) Periorbital and Orbital Exam: Look for exophthalmos or enophthalmos (Hurtel exophthalmometry) Pupillary exam (pupil shape etc) Visual acuity, Hyphema, fundus exam retinal exam Entrapment signs: EOM eham: active mobility test. Intraoperatively follow with Passive Passive mobility test- forced duction test DIFFERENTIATE: Raccoon sign =panda eyes VERSUS Black eye = periorbital echymosis Do not hesitate to obtain an ophthalmologic consultation Medial orbital wall fractures common orbital wall fracture, one of the weakest area of the orbit Very commonly asymptomatic Can have entrapment of medial rectus Can get orbital emphysema with nose blowing Approach through Lynch or Transcaruncular/Medial fornix incision Orbital Fractures:imaging Plain Films of limited use (Waters,Caldwell) MRI if retinal, optic nerve, or intracranial concerns CT Facial bones (most useful) Orbital Fractures:Treatment Concervative treatment Minimal diplopia Not in primary or downgaze Good ocular mobility No significant enophthalmos No significant hypoglobus Surgical treatment Diplopia that persists beyond 7 to 10 days Obvious signs of entrapment Relative enophthalmos greater than 2mm Fracture that involves greater than 50% of the orbital floor (most of these will lead to significant

enophthalmos when the edema resolves) Entrapment that causes an oculocardiac reflex with resultant bradycardia and cardiovascular instability Progressive V2 numbness Orbital Fractures: Approuches Transconjunctival, Subciliary, Subtarsal Approaches Marerials for reconstruction Autogenous tissues: Calvarial bone, iliac crest, rib, septal or auricular cartilage Avoid risk of infected implant Additional operative time, donor site morbidity, graft absorption Alloplastic implants: Decreased operative time, easily available, no donor site morbidity, can provide stable support Risk of infection 0.4-7% Gelfilm, polygalactin film, silastic, marlex mesh, teflon, prolene, polyethylene, titanium Orbital Fractures: Complications Infection Implant problems Persistent Diplopia (2-50%) Persistent Enophthalmos (15- 22%) Ectropion (1%) Blindness Superior Orbital Fissure Syndrome extension of fracture into SOF ophthalmoplegia with injury to III, IV or VI anesthesia in V1 plus loss of corneal reflex Ptosis +proptosis (egzophtalmus) parasympathetic block fixed, dilated pupil Orbital Apex Syndrome same as superior orbital fissure syndrome plus blindness

SEMINAR XI

Infections of the oro-facial and neck region

ANATOMY OF CERVICAL FASCIA 1) Superficial cervical fascia 2) Deep cervical fascia SUPERFICIAL CERVICAL FASCIA Encircle H&N and attached to clavicle and zygomatic arch Contain plastysma m. and external jugular v. Marginal mandibular br. of facial n. lies just deep to superficial cervical fascia Superior attachment zygomatic process Inferior attachment thorax, axilla. Similar to subcutaneous tissue Ensheathes platysma and muscles of facial expression DEEP CERVICAL FASCIAL(DCF) superficial layer of DCF(enveloping,investing,anterior) Completely surrounds the neck. Arises from spinous processes. Superior border nuchal line, skull base, zygoma, mandible. Inferior border chest and axilla Splits at mandible and covers the masseter laterally and the medial surface of the medial middle layer of DCF(cervical layer,pretracheal layer) Superior border Anterior hyoid and thyroid cartilage Posterior skull base Inferior border continuous with fibrous pericardium in the upper mediastinum. Name for portion that covers the pharyngeal constrictors and buccinator. Envelopes:thyroid gland, trachea,esophagus,pharynx,larynx deep layer of DCF Cover vertebral body and paraspinous m. Devided into

1. Alar division from base of skull to T2 level 2.Prevertebral division from base of skull to diaphram CAROTID SHEATH Extend from skull base to clavicle Made up of 3 layer of deep cervical fascia Contain carotid a., internal jugular v., vagus n. and sympathetic chain Avenues for spread of infection from neck to mediastinum DEEP NECK SPACES: CLASSIFICATION 1.Space Involving Entire Length Of Neck Superficial space Retropharyngeal Danger Prevertebral Vascular visceral 2.Space Limited To Above The Hyoid Bone Suprahyoid Submandibular Pharyngomaxillary (Parapharyngeal) Parotid Peritonsillar Temporal Masticator 3.Space limited To Below The Hyoid Bone Infrahyoid Anterior visceral DEEP NECK SPACES : DISCUSSION ETIOPATHOGENESIS Before the widespread use of antibiotics, 70% of deep neck space infections were caused by spread from tonsillar and pharyngeal infections. Today, tonsillitis remains the most common etiology of deep neck space infections in children, whereas odontogenic origin is the most common etiology in adults. CAUSES OF DENTOGEROUS INFECTIONS

dentogenous cystes, apical granuloma,suppurative inflammation of pulp, pulp gangrene, periodontal diseases, dentitio difficilis,post-traumatic wounds,conduction anaesthesia SOURCES OF NON-DENTOGEROUS INFECTIONS salivary glands inflammations, purulent skin diseases, tonsillar and peritonsillar infection, trauma of upper aerodigestive tract, retropharyngeal lymphadenitis, necrosis and suppuration of a malignant cervical lymph node or mass... As many as 5-20% of deep neck infections have no identifiable source. Other important considerations include patients who are immunosuppressed because of human immunodeficiency virus (HIV) infection, chemotherapy, or immunosuppressant drugs for transplantation. These patients may have increased frequency of deep neck infections and atypical organisms, and they may have more frequent complications. FACTORS ASSOCIATED WITHIMMUNE SYSTEM COMPROMISE Diabetes Steroid therapy Organ transplants Malignancy Chemotherapy Chronic renal disease Malnutrition Alcoholism End-stage AIDS ETIOPATHOGENESIS mixed bacterial flora Streptoccocus constalatus,intermedius, anginosus, mitis, sanquis, salivarius, hemoliticus, pyogenes Staphylococcus epidermalis, aureus Fusobacterium Actinomyces bovis, israeli, naeslundi Enterococcus faecalis Esherichia coli, Klebsiella pneumoniae, Pseudomonas aeruginosa, protus vulgaris ANTIBIOTIC THERAPY

Clindamycin Ampicillin + metronidazole Ampicillin + sulbactam Penicillin allergy: Clindamycin Third-generation cephalosporin IV (only if the penicillin allergy was not the anaphylactoid type; use caution) Moxifloxacin (especially for Eikenella corrodens) Metronidazole alone (if neither clindamycin nor cephalosporins can be tolerated) *Empiric antibiotic therapy is used before culture and sensitivity reports are available. MANAGEMENT AND TREATMENT ANAMNESIS+CLINICAL TRIAL +IMAGING= DIAGNOSIS!+ TREATMENT! (SURGICAL+PHARMACOLOGICAL) CLINICAL FEATURES (and other important statements) Mass effect of inflamed tissue or abscess cavity on surrounding structures. Direct involvement of surrounding structures with the infectious process. The microbiology of deep neck infections usually reveals mixed aerobic and anaerobic organisms, often with a predominance of oral flora. Both gram-positive and gram-negative organisms may be cultured. Asymmetry of the neck and associated neck masses or lymphadenopathy. Medial displacement of the lateral pharyngeal wall and tonsil caused by parapharyngeal space involvement Trismus caused by inflammation of the pterygoid muscles Torticollis and decreased range of motion of the neck caused by inflammation of the paraspinal muscles Fluctuance that may not be palpable because of the deep location and the extensive overlying soft tissue and muscles (e.g., sternocleidomastoid muscle) Possible neural deficits, particularly of the cranial nerves (eg, hoarseness from true vocal cord paralysis with carotid sheath and vagal involvement), and Horner syndrome from involvement of the cervical sympathetic chain Regularly spiking fevers (may suggest internal jugular vein thrombophlebitis and septic embolization)

Tachypnea and shortness of breath (may suggest pulmonary complications and warn of impending airway obstruction) CLINICAL STAGES Inoculation Cellulitis 03 days 37 days Mild Severe(g) Small Large Diffuse Diffuse Soft, doughy Hard, tender Normal Reddened Normal Thickened Slightly heated Minimal or none Edema Mixed

Characteristic Duration Pain Size Localization Palpation Appearance Skin quality Surface temp. Loss of function Tissue fluid

Predominant bacteria Aerobic

Abscess 5 days severe (l) LARGE Circumscribed Fluctuant, tender Peripherally red Centrally undermined and shiny Hot Moderately heated Severe Moderately severe Serosanguin. Pus flecks of pus Anaerobic

STAGES OF DENTOGEROUS ABSCESS FORMATION periapical intraosseous subperiosteal soft tissues abscess *************************************************************** RETROPHARYNGEAL SPACE Between visceral division of middle layer and alar division of deep layer Extend from skull base to T2 level Midline raphae More commom in children due to presence of retropharyngeal node DANGER SPACE Between alar division and prevetebral division of deep layer (locate posterior to retropharyngeal space)

Extend from skull base to diaphram No midline raphae Infection spread from neck to posterior mediastinum easilZ

PARAPHARYNGEAL SPACE(LATERAL PHRYNGEAL SPACE) (PHARYNGOMAXILLALY SPACE) Superiorly : Skull base Inferiorly Laterally Medially : Hyoid bone : Medial pterygoid m. :Buccopharyngeal fascia

Anteriorly : Submandibular space Posteromedialy : Prevertebral fascia and retrophryngeal space Most common cause : Peritonsillar infection, often dental infections (eg 3d molar) Typical finding 1.Trismus 2. Angle mandible swelling 3. Medial displacement of lateral pharyngeal wall Others : fever, limit neck motion,neurologic deficit (C.N 9,10,12,Horners s.) Treatment Evaluate and maintain airway & fluid hydration Parenteral antibiotic high dose S urgical drainage Dental origin ! Surgical drainage Intraoral approch (for peritonillar abscess only) External approach -transverse submandibular -T. shape incision (Mosher) incision

SUBMANDIBULAR SPACE Divided into 2 spaces by mylohyoid m. Sublingual space (above mylohyoid m.) Submandibular space (below mylohyiod m.) These 2 spaces can communicate each other by mylohyoid cleft Most common cause : DENTAL

Anterior teeth & first molar : infection enter sublingual space Second & third molar : infection enter submaxillary space Infection in both spaces mentioned above, bilaterally developed is named oral phlegmone or Ludwig phlegmone or Ludwig angina. Clinical features : Start unilateral and progress bilaterally Induration of submandibular region and floor of mouth ( severe cellulitis) Tongue trusted posteriorly and superiorly (cause airway obstruction) Drolling, odynophagia, trismus, fever Treatment Early stage (unilateral,mild swelling and edema) -IV antibiotic, extration of infected tooth, incision and drainage Advance stage (bilateral swelling, dysphagia with drolling) -early airway intervention -surgical drainage (submandibular incision) MASTICATOR SPACEs ( Submasseter, pterygomandibular) Between masticator m. and superficial layer of deep cervical fascia (Masticator m. = massester m.,medial and lateral pterygoid m. and temporalis muscle) Locate anterior and lateral to parapharyngeal space Most common cause DENTAL

Clinical features Extream trismus with minimum facial swelling. Additionally depends on location: Massesteric space (lateral compartment) : edema at ramus of mandible - Ptrygomandibular space (medial compartment): edema at retromolar trigone Treatment 1. Intraoral drainage (medial compartment) along inner margin of mandibular ramus to the retromolar trigone trismus in most cases make it impossible: it is prefered external aproach as below - submandibular incision - preauricular incision or Gilles incision for temporal space abscess PAROTID SPACE Between parotid gl. and superficial layer of deep cervical fascia Infection can spread easily to parapharyngeal space due to incompleted encircle at upper inner surface of parotid gland. Most common cause : Bacterial retrograde from oral cavity through Stenson duct. Rarely dental Clinical feature high fever, weakness, mark swelling and tenderness of parotid gland, fluctuation, pus at stensens duct N.VII paralysis: iv antibiotics Surgical drainage indicated for -fluctuation -medical failure after 24-48 hr. or progression of disease

External approch (lateral compartment)

PHLEGMON acute suppurative diffuse inflammation of conective tissue consider (spread) several fascal spacies CAUSES OF TREATMENT FAILURE Inadequate surgery Depressed host defenses Foreign body Antibiotic problems Patient noncompliance Drug not reaching site Drug dosage too low Wrong bacterial diagnosis Wrong antibiotic COMPLICATIONS OF DEEP NECK INFECTION Internal jugular vein thrombosis Cavernous sinus thrombosis Neurologic deficit Osteomyelitis of the mandible Osteomyelitis of the spine Mediastinitis Pulmonary edema Pericarditis Aspiration Sepsis

SEMINAR XII

Fungal Sinusitis
Clinical presentation, imaging features, and treatment differ based on type of fungal sinusitis Broadly categorized into invasive and noninvasive Invasive: Presence of fungal hyphae within the mucosa, submucosa, bone, or blood vessels of the paranasal sinuses Acute Invasive Fungal Sinusitis Chronic Invasive Fungal Sinusitis Chronic Granulomatous Invasive Fungal Sinusitis Noninvasive: Absence of fungal hyphae within the mucosa and other structures of the paranasal sinuses Allergic Fungal Sinusitis Fungus Ball (fungus mycetoma) Classification: (Stammberger 2008 AAO-HNS) Invasive: Acute Fulminant Invasive Fungal Sinusitis (AFIFS) Chronic Invasive Fungal Sinusitis (CIFS) Granulomatous Invasive Fungal Sinusitis (GIFS Non-invasive: Saprophytic Fungal Infestation (SFI) Sinus Fungus Ball (SFB) Eosinophil Mediated Forms Allergic Fungal Sinusitis ( AFS ) Eosinophilic Fungal Rhino-sinusitis (EFRS) Transitional. ACUTE FUNGAL SINUSITIS Most lethal form of fungal sinusitis mortality 50-80%, rare in immunocompetent patients.Two clinical populations Poorly controlled Diabetics ususally caused by fungi of order Zymocycetes (Rhizopus, Rhizomucor, Absidia, and Mucor) Immunocompromised with severe neutropenia (chemotheraphy patients, BMT, organ transplants, AIDS) Aspergillus accounts for 80% of infection in this group

Characteristic features necrotic nasal septum ulcer, sinusitis, rapid orbital and intracranial spread resulting in death Angioinvasion and hematogenous dissemination common Present with fever, facial pain, nasal congestion, epistaxis progressing to proptosis, visual disturbance, headache, mental status changes, seizures as spread occurs 73% of patients with intracranial spread die Imaging in acute fingal sinusitis Noncontrast CT: Severe unilateral nasal cavity soft tissue thickening is most consistent (but nonspecific) early CT finding Hypoattenuating mucosal thickening within lumen of paranasal sinus with rapid aggressive bone destruction of sinus walls occurs as disease progresses Often unilateral involvement of ethmoids, sphenoids Intracranial extension can result in cavernous sinus thrombosis, carotid artery invasion, occlusion, or pseudoaneurysm MRI: better for evaluating intracranial and intraorbital extension Evaluate for inflammatory change in orbital fat and extraocular muscles Obliteration of periantral fat is a subtle sign of extension Leptomeningeal enhancement progressing to cerebritis and abscess Treatmment: URGENT!!! Aggressive surgical debridement and systemic antifungal therapy Reversal of underlying cause of immunosuppression if possible Recovery from neutropenia is most predictive of survival Intracranial spread is most predictive of mortality CHRONIC INVASIVE FUNGAL SINUSITIS Inhaled fungal organisms deposited in nasal passageways and paranasal sinuses Progression over months to years with fungal organisms invading mucosa, submucosa, blood vessels, and bony walls Usually immunocompetent patients

History of chronic rhinosinusitis Usually persistent and recurrent disease Clinical signs: Maxillofacial soft tissue swelling, orbital invasion with proptosis, cranial neuropathies, decreased vision, can invade cribiform plate causing headaches, seizures, decreased mental status Imaging in chronic invasive fungal sinusitis: Noncontrast CT Hyperattenuating soft tissue mass withing one or more of paranasal sinuses, bone involvement often gives mottled appearance with or without sclerosis May mimic malignancy with masslike appearance and extension beyond sinus confines MRI decreased signal on T1, markedly decreased signal on T2 weighted images Treatment in chronic fungal sinusitis: AGRESSIVE!!! Surgical exenteneration of affected tissues and systemic antifungal Sample collections! Surgical handling of specimen very important mucus versus tissue:allergic or chronic invasive All surgical procedures should be performed without a power microdebrider or the use of suction devices until sample collection is complete. Mucus should be manually removed, together with inflamed tissue, and placed on a saline-moistened sheet of sterile used x-ray film (approx. 10 x 10 cm) to prevent absorption of the mucus. It should not be placed on a surgical towel or gauze. Each specimen is then fixed in 10% formalin and embedded in paraffin. Multiple serial sections of different specimens from each patient should be stained with H & E and with GMS. ALLERGIC FUNGAL SINUSITIS Most common form of fungal sinusitis Common in warm, humid climates Hypersensitivity reaction to inhaled fungal organisms resulting in chronic noninfectious inflammatory reaction - IgE type I immediate hypersensitivity and type III hypersensitivity are involved Allergic mucin within affected sinus which is inspissated mucous the consistency of peanut butter with eosinophils on histology Statistics: Younger individuals, third decade, immunocompetent Often associated history of atopy with allergic rhinitis or asthma Clinical symptoms:

Chronic headaches, nasal congestion, and chronic sinusitis for years Usually bilateral with multiple sinuses involved if not pansinus involement Often has a nasal component Imaging: Noncontrast CT high attenuation allergic mucin within lumen of sinuses can mimic a mucocele with expansion of the sinus MRI variable T1 appearance, low T2 signal (attributed to high concentration of iron, magnesium, and manganese concentrated by fungal organisms and also due to a high protein, low free water content of allergic mucin Treatment of allergic fungus sinusitis: Surgical removal of allergic mucin with restoration of normal sinus drainage is goal Longterm use of topical nasal steroids helps suppress the immune response and minimize recurrence Topical or systemic antifungals are not indicated FUNGUS BALL Mass within the lumen of paranasal sinus and is usually limited to one sinus Noncontrast CT hyperattenuating mass often with punctate calcifications MRI variable T1 and hypointense T2 due to absence of free water, calcifications and paramagnetic metals also generate decreased T2 signal no central enhancement to differentiate from neoplasm The most characteristic feature of fungus ball: METAL-LIKE CONCRETIONS IN SINUS LUMEN ( looking like amalgam particles) Treatment: Surgical removal with restoration of drainage of the sinus Antifungal medications usually unnecessary Recurrence is rare Surgical removal and establishment of sinus aeration resolves this condition without further treatment in most individuals. Conclusions: The same spectrum of Aspergillus disease in the lung is found in the sinuses Bony erosion is consistent with all invasive forms The rapidity of the disease is a good guide to the severity Histology of mucosa and mucous is a key to determining disease classification and management Metal like X-ray enhancement is a specific sign of fungus ball

SEMINAR XIII

Odontogenic cysts
Intra-bony cysts are most common in the jaws,becouse the mandible and maxilla are the only bonem with epithelial components Residual cyst-when cyst is persisting even after extraction of offending tooth Paradental cyst-appear in relation to crown or root of partially erupted molar toothoften developed in the distal region of third molar Radicular cyst (periapical cyst) is caused by pulpa necrosis secondary to dental caries or trauma. The pulpal necrosis causes release of toxins at the apex of the tooth leading to periapical inflammation-this inflammation leads to formation of reactive inflammatory tissue called periapical granuloma.The necrosis and damage of granuloma stimulates the Malassez epithelial rests resulting the formation of cyst (there is proliferation of epithelial rests in periapical area involved by granuloma-the basal layer cells of epithelial mass fail to obtain sufficient nutrition,they eventually degenerate become necrotic and liqify-and this create an epithelium lined cavity filled with fluid). These lesions can grow into large lesions because they apply pressure over the bone causing resorption-osmotic pressure of cystic fluid on cysts walls caused resorption of bone and enlargement of cyst. The toxins released by the breakdown of granulation tissue is also one of the common causes of bone resorbtion. So OC is defined as a inflammatory origin, that is preceded by a chronic periapical granuloma and stimulation of cell rests of Mallasez present in the periodontal ligament. Clinical Presentation Usually the periapical cyst is asymptomatic,but a secondary infection can cause pain. Larger lesions show slowly enlarging swelling-at the biginning the covering bone is hard but later when the cyst increase in size bone becomes very thin. On rare occasion there may be occurance of parasthesia or there may be a pathological fracture. If a radicular cyst is large the displacement of adjacent roots can occur-the resorbtion of the teeth roots is uncommon. The cyst may invaginate the antrum but there is almost always evidence of a cortical boundary between cyst and maxillary sinus. Cyst may also displace the mandibular alveolar nerce canal in interior direction.

TREATMENT The necrotic pulp should be removed (by endodontic treatment)or extraction of the offended tooth,and the cyst should be enuclated. Enucleation-the cyst is carefully separated from its bony wall,the entire cyst should be removed intact. Marsupialisation-the cyst is opened essentially and epithelial lining is sutured to mucous membrane at margines of opening.The aim is to produce a self-cleansing cavity.This cavity is initially packed with gibbon garze and after margines are healed a plug or extension of denture is made to clone the openings.The main purpose is for temporary decompression of exeptionally large cyst when fracture of jaw is a risk factor-when enough New bone is form we can curry out enucleation. DENTIGEROUS CYST Occurs in association with an unerupted tooth,most commonly mandibular third molar but also maxillary third molars,maxillary canines and mandibular second molars. DC are usually asymptomatic lesions that are discovered by chance on routine radiographs although some may grow to considerable size causing bone resorption and secondary infection can occur. TREATEMENT-most DC are treated with enucleation of cyst and removal of the associated tooth DC obligatory should be sent to histopathologic examination for differential diagnosis to avoid occasional formation of-odontogenic keratocyst,unicystic ameloblastoma,squamosus cell carcinoma,mucoepidermoid carcinoma ODONTOGENIC KERATOCYST Its a developmental cyst with agressive clinical behavior. It is derivedfrom remnants of the dental lamina.

SEMINAR XIV

Management of oro-antral fistulas.

Maxillary sinus The largest part of upper jaw is taken up by the maxillary sinus, which is described as a large pneumatic space It is also know as Highmores Antrum- from the name of the English anatomist Nathaniel Highmore who the first described the sinus as a space in bone and called it the antrum in the17th century At birth the maxillary sinus is present as a small cavity, and its growth begins in the in the third month of foetal life, and ends between the 18th and 20th year of life. The volume of the maxillary sinus is the result of functional development of the maxilla and its pneumatisation, and it therefore increases at the same rate as the growth of the jaws and eruption of permanent teeth. In adults volume of the sinus amounts to 20-25 ml. Because of the smaller volume of the sinus the risk of the occurence of oroantral communication in children and adolescents is less. Oroantral fistula Oroantral fistula is abnormal communication between the maxillary sinus and the oral cavity and may be the result of several different pathologic processes. Most comonly, it occurs after dental extraction, however other causes include infection, inflamatory conditions, neoplasm, Pagets disease, iatrogenic injury, and trauma The term of oroantral fistula is understood as the fistular canal covered with epithelia which may or may not be filled with granulation tissue. Most frequently communication between the oral cavity and the maxillary sinus occurs as result of extraction of upper lateral teeth The fistula may spontaneously close by swelling of the gingiva (secialy when no inflamation is present), although the chances of this occuring are not great. With the presence of the fistula the sinus is permanently open, which enables the passage of microflora from the oral cavity into the maxillary sinus and the occurence of inflamation with all possible consequeces. In 1991 Lin reported that maxillary sinus is more developed in woman and that there is therefore greater possibility of the occurence of oroantral communication and fistula in women. Floor of the sinus The floor of the sinus is often uneven and deepened, which can be determinated by determining the position of the lowest part of the sinus to the floor of the nasal cavity. The floor of the sinus can have three basic positions: beneath the level of the floor of the nasal cavity, on its level or above its level. The relations is particulary important in which the floor of the maxillary sinus is beneath the level of the floor of the nasal cavity, because its floor can extend to the tops of the dental roots, or go even deeper between the Floor of the sinus Such roots are separated from the sinus by a thin bony lamela and its mucous membrane, or very rarely only by the mucous membrane of the sinus. The thickness of the bone wall varies and is on average 0,2-16 mm. Symptoms The symptoms which occur during the occurence of an oroantral fistula are similar to the symptoms of oroantral communication: A purulent discharge may drip trough the fistula When the patient drinks he feels as though part of the liquid enters the nose from that side of the jaw and ocasionally runs out of the nostril on the same side

When the nostrils are closed with the fingers and the patient is asked to blow through the nose, air hisses from the fistula into the mouth In some cases the test of blowing through the nose or mouth does not necessarily give a positive answer- when the fistular canal is filled with inflammatorily changed sinal mucous membrane. However, the test with a blunt probe will confirm the existence of fistular canal

Operative techniques Numerous surgical methods have been described for teatment of oroantral fistulas, although only a few have been accepted in daily practice. Operative techniques In 1936 Rehrmann first published a method for closing an oroantral fistula , method of the buccal flap. The method of a buccal flap starts with an incision around the opening of the communication, at distance of 3 to 4 mm. The communication can be closed with one layer, if the tissue around the opening is cut and removed, and the vestibular flap is the only layer, or it can be closed with two layers, if after partial elliptic incision the soft tissue from the vestibular and pallatinal side is turned and carried over the fistular opening and resorptive sutures made above it. In vestibular flap two vertical incision are made from each side towards the buccal sulcus. The base of the flap is always wider to enable a better supply of blood to the flap. If the flap cannot be brought over the opening of the comunications, a horisontal counter incision is made in base through the periosteum The adventage of the buccal method is that it can be used in cases when the alveolar ridge is very low and when it is impossible to apply the method of interseptal alveotomy. A disadvantage of the method is that the buccal flap significant lowering the vestibulum and cheek oedema may occur In 1939 Ashley first described a method of using a palatinal flap of full thickness to close the oroantral fistula. The method of palatinal flap enable the closure of fistular opening with the mucous membrane of the hard palate. A medial incision is slightly more lateral than the medial line of the palate, and a lateral incision follows the edge of gingiva or is about half a centimetre along the edge of the gingiva of the tooth on that side of the jaw. A convex incision is made towards the front, which joins the medial and lateral incision. The flap is bent to a right angle and its front edge is sutured with edges of vestibular mucous membrane. A palatinal flap contains blood vessels, which enable a satisfactory blood supply, and with its thickness and width covers the site of the fistula better and safer. 3. An adventage of this method compared to the buccal flap, is that no lowering of the vestibulum occurs and the flap is firmer and more resistant to a trauma and infection 4. A disadventages of this method may be considered the denudation of the the palatal surface, pain, and later appearance of roughness and deepening of this area as a result of secondary epithalization over two to three months. The most unpleasant possible complication is necrosis of palatinal flap. Takahashi and Henderson and than James modified the operational method of the palatinal flap by the aplication of mucosal palatinal island flap so that in the anterior of the flap only the

mucous membrane was separated from the palate, but submucosal layer and periosteum remains on the site of the defect in the palatal surface. In this way the area of the palatal surface is more protected. The technique of interseptal interradicular alveotomy is one of the possibilities for treatment of oroantral fistula ( described by Hori at al.) Operative techniques The gingivoperiostal flap is separated 2-3 mm from the buccal and palatinal sides, in order to enable to removal of the alveolar bone and avoidance of soft tissue damage. The interradicular septum is removed until resistance is felt by the floor of the maxillary sinus, and the palatinal and buccal cortices remain intact.Vertical osteotomy follows by means of a fine chisel, with which the buccal and the palatinal wall of the alveolar ridge is broken.Their closeness facilitates suturing by individual sutures. This method cannot be applied when there is space of less than 1 cm between the neighboring teeth, and when the alveolar ridge is extremaly low. In 1995 Hanazawa et al. closed an oroantral communication by applying a BFPpediced buccal fad pad graft. After removal of the mucosus membrane of an oroantral fistula 3mm up to healthy tissue, a divergent incision is made from each side in the vestibulum, with which a buccal mucoperiostal flap of trapezoid form is obtained. This is followed by a vertical inision 10 mm through the periosteum from the internal side of the released flap and preparation in the soft tissue so that fatty tissue is obtained from the cheek. The preparation is carried to the zygomatic ridge and cheek, and through the opening obtained the buccal flap of fatty tissue is pulled up to the opening of the oroantral fistula and sutured to the edge of the palatinal mucous membrane. The mucoperiostal flap only partially covers the flat of fatty tissue up to the edge of the vestibular alveoli where it is sutured.It is used in patients with a fistula of 8 to 20 mm in diameter. Over a period of three weeks the fatty tissue converts into granulation tissue and epithelises. An advantage is smaller retraction in the area of the vestibulum. In case of unsuccessful closure of an oroantral fistula by multiple surgical procedures or long-term persisting fistulas, hyperplasia of the mucous membrane of the sinus occurs, which should be solved surgically. An opening is made on the anterior wall of the maxillary sinus in the area of the fossa canine. The tickened hyperplastic mucous membrane in the sinus is removed. Finally the sinus is tamponaded with iodineform gauze, which is pulled through the lower nasal passage and throuhg the nostril and fixed with an adhesive bandage to the nose. An antibiotic is applied postoperatively for a period of seventh days after the operation.

SEMINAR XV

Management of patients: after radio- and chemiotherapy, with cardiovascular disorders and diabetes.
The diabetic patient
We should remember that long-standing diabetics frequently have compromise in one or more organ system.Commonly associated diseases include: atherosclerosis,coronary arthery disease,cardiomyopathia,renal insufficiency, hypertension. We should have actual,complex laboratory values include blood glucose,blood urea nitrogen,creatinine and haemoglobin levels. Many factors are present that determine the glycemic response including insulin secretion,insulin sensitivity,overall metabolism and nutritional intake in addition to stress and length of the procedure. Surgical stress and some general anaestetics agents themselves are associated with increases hormones such as epinephrine,norepinephrine,glucagons and other.Patient receiving pharmacologic therapy to control their diabetes may also be susceptible to hypoglycemia. Management of diabetes patient should be coordinated with the individual daily protocol. The patient with DM are treated with: proper diet,oral hypoglycemic agents,short acting insuline,intermidient acting I,rapid acting I,long acting I. We should all the time control the level of glucose to avoid the hypoglycemia specially postoperatively.The signs; confusion,irritability,fatigue,headache.Prolonged hypoglycemia can caused even coma and death.500ml 5% glucose should be administered intravenously,before or after surgery-it increase glucose on the blood about 100mg/Dl

(<40 mg/Dl-hupoglicemia)
Diabetes is a chronic disorder of carbohydrates , fat, and protein metabolism whereby a defective or deficient insulin secretory respons leads to impaired glucose use. Diabetes creates a physiologic predisposition for developing microvascular, macrovascular, neuropathic complications. Normal blood glucose level 60 -130 mg/dl. Excess glucose is converted to glycogen, which is stored in liver and muscles. The role of insulin Insulin is released in a rapid surge during thr first 10 30 min after a meal. This is followed by a second phase of a slower, sustained release of insulin. There are two insulin receptors in the cell membrane. Insulin binds to alpha, which causes the aforementiond change in beta subunit. This promotes the activity of tyrosine kinaze, which is essential to bring glucose into the cell. There are four types of diabetes 1. Type 1 usually associated with young people. Patient requires insulin. Destruction of beta cells in the pancreas 2. Type 2 patients cells have lost their sensivity to insulin secondary to environmental and genetic factors. Their muscles and adipose cells cannot transport glucose.

3. Gestational diabetes usually developes secondary to pregnancy. Up to 40% women with gestational diabetes will develope type 2 diabetes within 10 years of developing gestational diabetes 4. Secondary diabetes related to a specific cause, such as removal of the pancreas Symptoms type 1 poliuria polidypsia polifagia diabetic patients break down protein from muscle to make glucose. Proteins are required for antibody production, white blood cell production and healing of wounds. Deficiency of these proteins leads to susceptibility of infections and poor wound healing. Insulin deficiency leads to lipolysis of triglycerides into FFAs, which yields acetyl coenzyme A. Symptoms of hypoglycemia mild 60-70 mg/dl tachycardia, palpitations, pallor, shakiness, irritability modrate - 50-60 mg/dl impaired CNS function: confusion, inability to concentrate, slurred speech, blurred vision severe 40-50 mg/dl loss of consciousness, difficulty awakening, seizures Acute complications assotiated with type 1 diabetic ketoacidosis - glucose levels > 250 mg/dl, ketons in the urine and serum. pH < 7,2 and plasma bicarbonate < 15 mEq/L. Nausea, vomiting, Kussmaul respirations to reduce CO2 levels in blood. Treatment 0,9% NaCl iv. Regular insulin, reversing the acidosis and treating K+ deficiency.mately, ketone bodies are formed, which can lead to metabolic acidosis. Acute complications assotiated with type 2 hyperosmolar nonketotic coma usually age 65 or older, May go unrecognized for weeks, severely hyperglycemic > 600 mg/dl. Untreated become dehydrated and progress into comatose state. Treatment increased insulin and slow fluid replacement to prevent cerebral edema because of the sorbitol accumulation in the brain Treatment of mild to moderate hypoglycemia initially treat with 10-15 g of carbohydrates give cup of orange juice or 3-5 hard candies, 1 cup of milk, 3 glucose tablets or 2 tbsp of raisins. Glucose level control as soon as possible. If symptoms do not improve in 15 min. Treat with an additional 10-15 g of carbohydrate source. Treatment of severe hypoglycemia if possible injection of glucagon (adult 1 mg, children < 5 years 0,5 mg, < 1 year 0,25 mg) If patient can swallow without risk of aspiration 15-50 g of carbohydrate source on the inside of the cheek, 1-4 tbsp of honey (except infants), syrup or jelly. When the patient is more alert, follow with a liquid such as orange juice. The patients with mild diabetes or well-controlled severe diabetes can be treated as reasonably normal patients. Only when the desease process becomes uncontrolled should the patient not have

dental surgery procedures in a routine manner. As a dentists you have to remember: Because of impared leukocyte function, inability to make antibodies against the bacteria and vascular insufficiency diabetic patients have enhanced susceptibility to infections of the skin, tuberculosis, pneumonia and pyelonephritis. Together these infections cause the death of about 5% of diabetics. Additionally they are very susceptible to fungal infections. Surgical stress related to trauma to the tissues during the procedure, pain that the patient experiences after the procedure, and anxiety before and after the surgery lead to surges of epinephrine which antagonize insulin and increase blood glucose. Also infections cause stress to the tissues. Stress from surgery and infections may override feedback mechanisms to result in cortisol surge and contribute to the effects of epinephrine on glucose. All minor surgical procedures as: tooth extractions, apex resections should be covered by antibiotics. In patients with oral hypoglicemic-controlled diabetes the advanced surgical procedures as cystectomy, oro-antral communications a.e. which are connected with oral intake limitations should be hospitalized and undergo insulin-controlled treatment.

Pregnant patient
Pregnancy lasts 275 days (ca 40 weeks) I trimester ( 0-14 weeks) II trimester (15-27 weeks) III trimester (28-40 weeks) 24 weeks low end of fetal survival 34 weeks lung maturatio; fetal survival increases mortality equal to 37 weeks The organogenesis take place in period from 3 14-th week and in this time is extremely sensitive to exogenous insult. The best time for surgery is in second trimester In third trimester there is the risk of inducing a preterm delivery The blood volume, cardiac output and heart rate increase in first trimester and minimal increase in the third. In the second and third trimesters the blood pressure can decrease when pregnant patient is in a supine position. This can lead to limitation in uteroplacental perfusion. Patient should be positioned in the left lateral decubitus position and 5-15% tilt during surgery. Acc. to FDA the NSAIDs should not be used. Connection between aorta and pulmonary artery begins to close at birth. Its remaining open after 32 weeks depends on fetal prostaglandins. Inhibiting these prostaglandins at this point may result in fetal death secondary to compromised fetal circulation. N2O in pregnant patient Potential teratogenic effects of N2O are related to its ability to inactivate methionine synthese. It is responsible for converting homocysteine and methyltetrahydrofolate to methionine and tetrahydrofolate, which are needed for synthesis of DNA. Folate supplementation preoperatively has been recommended. N2O is used heavily in European obstetrics. ----------------------------------------------------------------------------------------------------------------

Patients with coagulation problems

Causes of bleeding disorders liver disease anticoagulant therapy aspirin therapy DIC (disseminated intravascular coagulation) vit. K, vit.B 12 deficiency Aspirin and some of the NSAIDs affect the platelet phase of coagulation. They inhibit the activity of cyclooxygenase in platelets prolonging the bleeding. This effect has led to its accepted controlled use as a prophylactic measure against coronary and cerebral vessels thrombosis. For dental surgery it should be quit for 2 days before the operation. Warfarin (Coumadin) shoud be discontinued at least 3 days before the procedure. Its duration time is 3-5 days (half-life 1,5 2,5 days) Vit. K reverses the action of warfarin. Once vit. K is administered, the patient may be resistant to further anticoagulation with warfarin for a few days. Additionally, certain patient may have an underlying thrombotic tendency that puts them at risk for thrombosis and embolic complications should the effects of the anticoagulant be stopped abruptly. Therefore administering vit. K or abruptly stopping warfarin medication can be harmful to some patients. Heparin affects the intristic and common pathway of blood coagulation by preventing the formation of prothrombin activator and inhibits the action of thrombin on fibrinogen. Heparin increases the normal clotting time (4-6 min.) to 6-30 min. Duration of action is 3-4 hr. Its effect can be reversed by the use of protamine sulfate. Too rapid administration of protamine sulfate can result in hypertensive and anaphylactic reactions. In this cases we should perform a precise preoperative assessment (by taking history and physical examination),very often intraoperativelly monitoring (specially due to big maxillofacial procedures) and postoperatively care.

Cardiovascular diseases
Most oral and maxillofacial surgical procedures are considered to be intermediate CVD risk. The primary cardiac risk factor is the existence of one or more of the major clinical predictors of risk such as:recent Myocardiac Ischemia,unstable or severe angina,decompensated heart failure,significant dysarythmias,coronary blood vessels diseases (coronary arteries diseases with narrowing of the coronary vessels), hypertension (which often accompanies of all CVD) It is important to attempt to avoid the stress of surgery specially if patient is experiencing acute ischemia or has a history of recent infarction.Tradicionally a 6 month interval between the initial incidence of Myocardial Ischemia with Myocardial Infarction and noncardiac surgery has been advocated to avoid stress and risk of re-infarction. But the proper cardiological treatment by using: antihypertensive therapy,betablokers,thrombolytics or surgical procedures like coronary angioplasty with stent placement or revascularization after MI shorten this 6 month period and allow us to carry out our procedures without any hesitation and fear. In generally apart of avoiding the stress we have to also avoid katecholamins which increase in huge degree the blood tension. There are some symptoms and signs like : acute episode of spreading chest pain,shortness of breath,difficult ventilation with patient gasping for oxygen that can suggest M Infarction-

decompensated heart failure. Then immidiete intervention shoul be performed.we should administer : oxygen,nitroglycerin tablets,aspirin,relanium,carry out echocardiography.

Radiotherapy
Osteoradionecrosis Radiation therapy can be used alone or as adjunctive therapy in combination with chemiotherapy or most often surgery.Radiotherapy like every treatment has side effects for example mucositis and xerostomia.But most severe side effect is ORN. Many writers have shown that ORN represent a chronic nonhealing wound that is hypoxic,hypocellular and hypovascular.The modern radiation therapists use megavoltage which is felt to be kinder to bone and soft tissues than technict which were use in the past Like orthovoltage therapy).Thats why preoperatively dental evaluation and care are so important and could dramatically decrease occurance of ORN. Orn is generally caused by trauma to the radiated area usually by dental extraction but also it can occur spontaneously. The clinical picture of ORN is most commonly seen with pain and exposed bone in ,maxillofacial region.Orn more often occurs in the mandible than in maxilla. The dosage above 5000 to 6000 rads make the mandibule susceptible to Orn. On the orthopantomogram or CT scans we can see a conventional picture of osteomyelitis with area of ostheolysis and bony sequestrum.Often there is an appearance of moth-eaten bone.The treatment consist in removing a necrotic tissue and allowing the body to heal itself. We must always be aware that removed tissue we have to sent to pathology to rule out occulant or recurrent of malignant disease that is masquerading as a bony infection.Very often only debridments and conservational treatment are used. Current therapy consist in HBO-therapy is based on 100% oxygen delivered in a pressureized manner.Tissues treated with HBO have increased levels of oxygen which has a negative effects to bacteria and a positive effect to angiogenesis and increase blood flow to the area. HBO has been used effectively to treat ORN and as adjunctive treatment with dental extraction dental implants and jaws reconstruction In radiated patients. HBO consist of 20 or 30 -90 minutes treatment sessions before any surgical intervention is performed.HBO treatment are expensive and facilities are often scarce. Microvascular surgery with free flaps are more and more common treatment in ORN. Free flaps bring hard and soft tissues which have their own independent blood supply. The fibula,scapula,iliac crest and radius are all considered applicable donor sites.

The clinical advantage of microvascular surgery is that the surgeon doesnt have a lack of soft tissue which very often occur in ablative cancer surgery.

SEMINAR XVI

Tumor like lesions

Tumor-like lesions include: 6. SOLITARY BONE CYST - SBC 7. Solitary bone cyst is a radiolucent pseudocyst widely known as the traumatic bone cyst. Synonyms are: 8. Simple bone cyst 9. Haemorrhagic cyst 10. Idiopathic bone cavity 11. Progresive bone cavity Solitary unicameral bone cystSince 1992 SOLITARY BONE CYST is recommended in WHO international histologic classification of tumors Pathology: 4. Low grade infections 5. Intraosseous vascular abnormalities 6. Degeneration of bone tumors 7. Local alteration of bone metabolism 8. Trauma Although SBC is an intraosseous empty cavity, it is sometimes lined by a thin layer of fibrous connective tissue without epithelium. It can also contain 12. serosanguinous fluid 13. granulation tissue 14. erythrocytes 15. hemosiderin 16. osteoclasts Solitary bone cyst occurs in variety of shapes including cone oval round irregular It is usually seen in patients 10 to 20 years of age Males are affected more often than females (3:2 ratio). The lesions occasionally have been reported in the maxilla but are far more common in the mandible between canine and the third molar. The second most common site is the mandibular symphysis. Fewer cases are reported in the ramus and condyle. SYMPTOMS 17. Most SBCs are asymptomatic and found during routine radiographic examination. 18. Some patients present with: i. pain ii. swelling iii. tooth sensitivity and less commonly: fistula root resorption paresthesia pathologic fracture The teeth in the involved area are usually vital. Pathologic fractures asocciated with SBC presence

occur but are rare. SOLITARY BONE CYST - treatment 19. These lesions are usually surgically explored to establish a diagnosis. Since material for histologic examination may be scant or non-existent it is very difficult for definite histologic diagnosis to be achived 20. No further treatment is generally necessary because surgical manipulation causes the cavity to fill with blood. The scraping of bony cavity is the treatment of choice. 21. Soft tissues are closed, and the lesion tends to heal without further intervention. 22. Rapid healing follows surgical exploration but even without surgical intervention the cyst will resolve spontaneously with time. Aneurysmal bone cyst - ABC 23. It is a benign osseous lesion recognized by Jffe and Lichtenstein in 1942 24. The term aneurysmal is used to define the blow-out distension of part of the contour of affected bone that results in a striking radiographic appearance. 25. It causes local expansion of the affected bone leaving only a thin layer of overlying subperiosteal new bone. Aneurysmal bone cyst - ABC 26. `74 85% aneurysmal bone cysts of the jaws occurs in 10-20 years group 27. The molar region and ramus of the mandible are the commonest sites for this lesion to occur. RADIOLOGY 28. Aneurysmal bone cyst of the jaw appears as radiolucency. 29. well-circumscribe 30. usually unilocular with eccentric expansion In some cases it can be 31. honeycomb 32. or soap bubble 33. mixed 34. radiolucent radiopaque CT scans often reveals 35. a thin cortex of the bone, 36. expansile nature of the lesion 37. and fluid-fluid levels within the lesion. 38. Diagnosis: Similarity to other lesions: 39. Ameloblastoma 40. Giant cell tumor 41. Hyperprarathyroidism 42. Myxoma 43. Traumatic bone cyst 44. Odontogenic keratocyst 45. Diagnosis 46. Diagnostic aspiraton of blood from the lesion should give suspicion of 47. Vascular lesion Aneurysmal bone cyst absence of bruits

absence of thrill lack of pulse pressure Definitive diagnosis can be made only after incisional biopsy. Biopsy should be attempted only when vascular lesion has been ruled out. SURGERY is the treatment of choice for these lesions. FIBROUS DYSPLASIA Fibrous dysplasia is non-hereditary disease, caused by a mutation in a somatic cell in which abnormal differentiation of osteoblasts leads to replacement of normal marrow and cancellous bone by immature bone and fibrous stroma. Extent of lesions depends on the timing of the mutation. If the mutation occurs earlier, the disease will be more widespread throughout the body - an example is McCune Albright Syndrome Fibrous dysplasias can be divided into four forms: MONOSTOTIC FIBROUS DYSPLASIA Monostotic simply means involving one bone. Most often it occurs in ribs, femur and scull. POLYOSTOTIC FIBROUS DYSPLASIA POLYOSTOTIC - means occuring in more than one bone. Head and neck are involved in half of these patients Mc Cune - Albrights Syndrome almost exclusively found in females It only occurs in 3% of cases. It is characterized by: Polyostotic fibrous dysplasia Skin pigmentation -caf au lait spots Endocrinopathies early puberty in females Hyperthyroidism Craniofacial fibrous dysplasia Confined to bones of the craniofacial complex. The jaws are commonly associated with all forms of fibrous dysplasia. In the jaws the onset is usually during the first and second decades of life. It produces painless swelling of the involved bone. In this form the maxilla, zygoma, sphenoid and frontal bones are involved. growth hormone excess 48. Monostotic and polyostotic forms usually begins in the second decade of life. 49. Its expansion of the jaws is slow and painless. 50. Patients may complain of swelling or have no complaint. 51. Growth stops when bones stop growing at the end of puberty 52. Lesions may start to expand again during pregnancy. 53. Usually, fibrous dysplasia is not a fatal disease. 54. A small percentage of patients die when the bone lesion is complicated by malignant change. 55. Race 56. No specific racial predilection exists. 57. Sex

58. The incidence rates are equal in males and females. FIBROUS DYSPLASIA clinical symptoms 59. Fibrous dysplasia may cause few or no signs and symptoms, particularly if the condition is mild. Signs and symptoms may develop during childhood, adolescence or adulthood. The polyostotic form is more likely to develop signs and symptoms, usually by age 10. 60. More severe fibrous dysplasia may cause: 61. Bone pain 62. Difficulty walking 63. Bone deformities 64. Fractures Fibrous Dysplasia 65. Radiographic Features: 66. Shape and Borders are usually poorly defined, with the lesion gradually blending into the normal trabecular pattern. 67. Internal Architecture is highly variable, mixed lucent and opaque. 68. Early lesions may be more lucent, trabeculae are shorter, thinner, more numerous, and irregularly aligned. 69. Fibrous Dysplasia - radiographic features: 70. Terms used to describe the internal architecture include: 5. ground glass 6. orange peel 7. cotton wool 8. thumb whorl The lesion may contain a central lucent area that is analogous to a simple bone cyst. Fibrous Dysplasia- Radiographic Features Effects on adjacent structures 71. Small lesions are entirely contained in the bone 72. Expanded and thinned cortices. 73. Maxillary lesions may expand into the maxillary sinus 74. Teeth may be displaced. 75. Lamina dura may be replaced with the abnormal bone of the lesion. A pathognomonic feature of fibrous dysplasia may be the superior displacement of the mandibular canal. This is due to the epicenter of the lesion being below the canal. Differential Diagnosis While many other lesions present similar alterations in radiographic appearance, the patients age, unilateral, monostotic lesions, and painless bony expansion often lead to a diagnosis of fibrous dysplasia based on the radiographic appearance alone. It is usually confirmed by histopathological study. 76. Lesions to be considered include: 77. Periapical cemental dysplasia 78. Pagets disease of bone 79. Healed simple bone cyst 80. Osteomyelitis 81. Osteosarcoma 82. Cementoossifying fibroma Malignant degeneration 83. The estimated frequency is 0.4-1% in fewer than 50 reported cases. 84. The interval from the diagnosis of fibrous dysplasia to the development of malignancy varies and is usually years or decades.

85. Osteosarcoma and fibrosarcoma are the most common tumors. 86. Chondrosarcomas occur less frequently. Radiographic features suggestive of malignant degeneration include: 87. a rapid increase in the size of the lesion 88. change from a previously mineralized bony lesion to a lytic lesion 89. Clinical findings that suggest malignant change are: - increasing pain - enlarging soft-tissue mass.

Eosinophilic Granuloma 90. Eosinophilic granuloma (EG) is the benign form of the thre clinical variants of Langerhans cell histiocytosis, which include: - Letterer-Siwe disease - Hand-Schller-Christian disease - Eosinophilic granuloma 91. predominantly affects children, adolescents, and young adults. 92. Solitary lesions are more common than multiple lesions 93. Any bone can be involved; the more common sites include: skull

mandible spine ribs

long bones The age range of patients with EG is 2-30 years. The highest frequency occurs in patients aged 5-10 years. 75% of patients with EG are younger than 20 years The male-to-female ratio is 3:2 SYMPTOMS: Most patients have no symptoms. 94. Localized bone pain 95. focal tenderness 96. a pathologic fracture may occur as a result of bone erosion. 97. Swelling 98. Mass may be palpable at the site of osseous involvement. Rarely, children present with 99. Fever 100. leukocytosis Unifocal lesions occurring at certain sites may lead to complications. A lesion of the mastoid process may extend into the middle ear, destroy the ossicles, and lead to deafness A lesion in the mandible may lead to floating teeth and fractures. Mandibular involvement may present as gingival and continuous soft tissue swelling 101. Examination 102. The diagnosis is usually based on radiographic demonstration of a destructive bone lesion arising from the marrow cavity and on characteristic morphologic findings. - Plain radiography - is the mainstay in the diagnosis of EG

Bone biopsy - to confirm the diagnosis Radionuclide study CT , MRI, angiography

of EG

Differential Diagnoses include: 103. 104. 105. 106. 107. 108. Aneurysmal bone cyst Bone infarct Bone metastases Acute Pyogenic Osteomyelitis Chronic osteomyelitis Osteosarcoma

SEMINAR XVII

Benign tumors of the oral cavity

BENIGN TUMORS - the main features a new growth resembling the tissue of origin has an insiduous onset grows slowly has a smooth outline may displace adjacent structures such as teeth. is usually painless does not metastasize is not life threatening forms septae or compartments does not invade adjacent tissue - ameloblastoma the exception ODONTOGENIC BENIGN TUMORS OF THE JAWS

AMELOBLASTOMA Ameloblastoma is the most prevalent of all the odontogenic tumors. It is most clinically significant odontogenic tumor .

10% of all tumors in maxillomandibular region. Ameloblastoma histological view Ameloblastoma is a tumor in which the tumor cells form caricatures of the enamel organ and some of them resemble ameloblasts. However, they are incapable of making enamel matrix. Carcinogen converts a cell in one of the epithelial rests to become a tumor cell. As such, it starts to divide endlessly to form a tumor. AMELOBLASTOMA- Subtypes: Multicystic 86% Unicystic 13% Extraosseous - 1% They may occur in any part of both jaws but most are in the middle and posterior regions of the mandible.

AMELOBLASTOMA Clinical symptoms: Ameloblastoma occurs in patients between the ages of 30 to 60 years, predominantly in the fourth and fifth decades . It is a locally aggressive, slow-growing tumor. The tumor is painless and remains asymptomatic as it enlarges. The patient notices a gradual jaw expansion producing facial asymmetry. It is unencapsulated and infiltrates surrounding bone marrow. Even though they are locally infiltrative, they do not metastasize. Some are associated with unerupted teeth (usually mandibular third molars) and,

therefore, cannot be differentiated radiographically from dentigerous cysts. Can perforate lingual cortex and extend to adjacent soft tissues. Absorption of the apices of adjacent teeth (seen in about 40% of cases).

AMELOBLASTOMA Treatment: For unilocular cystic lesions in young patients, curettage or enucleation is effective treatment. Solid lesions show high recurrence rates (50%90%), necessitating tumor excision or partial resection of the jawbone. Although malignant transformation is rare, repeated recurrences increase the likelihood of malignancy. Odontogenic adenomatoid tumor (Adenoameloblastoma) benign, encapsulated, painless, epithelial odontogenic neoplasm grows by expansion usually associated with an unerupted tooth. the tumor is asymptomatic, small lesions are discovered incidentally on radiographic examination About 65% of the cases occur in the maxilla. The canine region is the most frequently involved area in both jaws. The mean age of patients is about 18 years. Females tend to be more commonly affected than males. males.

Calcifying epithelial odontogenic tumor (Pindborg tumor) 9. is a rare lesion which behaves very much like an ameloblastoma 10. has a definite predilection for the mandible and any site in the jaw may be affected but the premolar - molar areas are more susceptible 11. is mainly asymptomatic but may sometimes produce a painless swelling over the involved region 12. is locally aggressive, infiltrates the surrounding tissues like an ameloblastoma

I.

ODONTOMA (Hamartoma) Two types of odontoma occur: Compound composite odontoma It is a collection of small radiopaque masses, some or all of which may be tooth-like. the numbers vary from two to several dozen have a tendency to occur in the anterior segments of the jaws, with a somewhat greater incidence in the maxilla. Microscopic sections show multiple tooth-like structures complete with enamel matrix,

dentin and a central pulp chamber. The toothlets are so closely packed together that they appear to be one mass.

Complex composite odontoma is a mass of unorganized dental tissues. conglomerate calcified mass has no resemblance to a normal tooth.

tends to occur in the posterior segments of the jaws with a somewhat greater incidence in the mandible. whether the lesion arises from a normal tooth follicle or a supernumerary tooth follicle, there might not be a missing tooth

Cementoblastoma Benign neoplasm of cementum Rare and usually diagnosed by early 20's 50% lesions associated with apical 1st mandiblualr molar Most commonly asymptomatic Radiographically "sunburst" mass attached to apex Treatment consists of surgical extraction of tooth and lesion Recurrence is rare

ODONTOGENIC MYXOMA ( Odontogenic fibromyxoma Myxofibroma) 109. originates from the mesenchymal portions of the tooth bud 110. it is not found in bones outside the facial skeleton and occurs almost exclusively in the tooth-bearing regions of the jaws 111. is asymptomatic although some patients complain of pain 112. occurs in individuals between the ages of 10 and 30 years 113. some cases are associated with impacted teeth 114. the body and posterior portion of the mandible are the favored sites 115. is asymptomatic although some patients complain of pain 116. when it grows to a large size, it causes 117. cortical expansion rather than perforation of the cortical bone 118. although myxomas are benign, they are locally invasive NON-ODONTOGENIC BENIGN TUMORS OF THE JAWS Exostoses and Tori Osteoma Osteoid osteoma Central hemangioma Arteriovenous fistula Neurogenic tumors (neurilemmoma,neurofibroma) Traumatic neuroma Chondroma Calcifying peripheral fibroma Central / Peripheral giant cell tumor

EXOSTOSES Exostoses are developmental, localized overgrowths of bone. They are usually bilateral and multiple and often produce a nodular protuberance. When multiple, they may coalesce to form an irregular, linear, horizontal elevation. They are almost always limited to the buccal surface, posterior to the canines in the mandible. In the maxilla they may be seen posteriorly, palatally to the second or third molar teeth or buccally to all the molars.

TORUS PALATINUS Torus palatinus is an exostosis that arises at the margins of the palatal processes at the median suture of the palate. Both sides of the suture line are almost always involved and tend to divide it into right and left portions. The presence of a torus of appreciable size often presents a problem in making a satisfactory intraoral radiographic examination of the maxillary teeth. [ or a denture]. NOTE - this is a developmental anomaly

TORUS MANDIBULARIS OR LINGUAL TORUS Torus mandibularis occurs on the lingual surface of the mandible, in the premolar regions. It may occur singly; however, there is a marked tendency to multiple and bilateral occurrence. The lesion is not necessarily confined to the premolar region. These tori arise above the mylohyoid ridge. Their size varies, some reaching such size that tori from opposite sides come in contact with each other and occupy a large portion of the floor of the mouth.

OSTEOMAS Osteomas are benign tumors composed of bone. They vary greatly in size. May be attached by a pedicle; or may grow from a wide base. The pedenculated type occurs more frequently in the mandible. The skull is the most common site for the development of an osteoma, with the calvarium and frontal sinus areas being affected most frequently. Multiple osteomas are associated with Gardner syndrome

OSTEOID OSTEOMA Small, oval or roundish tumor-like nidus which is composed of osteoid and trabeculae of newly formed bone deposited within a substratum of highly vascularized osteogenic connective tissue. The long bones of the lower extremities and the vertebrae are most commonly affected. The skull and facial bones are involved exceptionally. Most patient with osteoid osteoma are: children, teenagers and young adolescents. The tumor occurs most frequently in the second decade, with a peak age in the early twenties and affects males twice as often as females. The classic presentation is that of focal bone pain at the site of the tumor. The pain worsens at night and increases with activity.

Pain may be relieved by aspirin or other nonsteroidal anti - inflammatory drugs. It disappears within 20 to 30 minutes of treatment with these medications. The four diagnostic features include a sharp round or oval lesion less than 2 cm in diameter, a homogeneous dense center a 1-2 mm peripheral radiolucent zone.

CHONDROMA A benign tumor composed of mainly of cartilage which is encapsulated with a lobular growing pattern. The chondroma may become partially ossified and is then called as osteo-chondroma. Theoretically, complete replacement of the cartilage by bone could occur - producing an osteoma. Any cartilaginous lesion of the jaws must be treated as potentially malignant. A chondrosarcoma may arise from pre-existing chrondromatous tumors

CALCIFIED PERIPHERAL FIBROMA A peripheral fibroma arising from the fibrous connective tissue of the periodontium may demonstrate the odontogenic potential of that tissue. It rarely reaches a diameter of more than 2 cm. Calcified substances form in many of these tumors and may be: bone, cementum, amorphous and nonspecific calcifications, or a combination of these. Clinically - seen on gingiva as a hard swelling, often between the teeth. Those in which extensive calcifications have taken place may become sufficiently radiopaque to permit visualization in the radiograph. CENTRAL GIANT CELL GRANULOMA CGCG Etiology Central giant cell granuloma is a non-neoplastic proliferative lesion of unknown etiology. Localization It occurs most commonly in the mandible than in the maxilla. Most mandibular lesions occur anterior to first molars and often cross the midline. Central giant cell granuloma also occurs in other bones of the facial skeleton and cranial vault. It rarely occurs outside the craniofacial bones Clinical symptoms It ranges from slow-growing, asymptomatic swelling to an aggressive lesion which manifests with pain. The most common presenting sign of CGCG is a painless swelling with noticeable facial asymmetry. CENTRAL GIANT CELL GRANULOMA -CGCG - may be noted as an incidental finding on routine radiographic screening. The radiological appearance of CGCG is variable and demonstrates two variations:

osteolytic, unilocular lesion in which the cortex may be partially destroyed. multiple osteolytic foci with bone trabeculations within the tumor (soapbubble appearance) It may be well-defined or ill-defined and shows variable expansion and destruction of the cortical plate.

CGCG usually presents as a painless solitary radiolucent expansion in most of the cases. The radiological appearance of the lesion is not pathognomonic . The final diagnosis rests on histopathology because the clinical and radiological features are not specific. Some lesions are more destructive with a marked tendency to recur. A more aggressive type of such lesion will require more radical treatment. The recurrence rate is reported to be 13-22%.

Papiloma evolves from epithelial tissue are usually stalked and have a cauliflower-like surface, but they can also have a broad base and a fairly smooth surface. grow slowly and almost invariably remain benign. are caused by local trauma, but cases exist where papilloma virus has been demonstrated

SEMINAR XVIII

Malignant tumors of oral cavity and maxillo-facial areaclassification, symptoms and clinical features, principles of tnm classification.
incidence rate number of affected patients per 100,000 population in a given year Morbidity rate - number of deaths in a given year Mortality rate relationship of morbidity to incidence of a disease The closer the value is to 1, the higher is the mortality rate. If mortality rate approaches the incidence level, then the tumor is more malignant Host factors include phenotypic characteristics, genetic syndromes, precursor lesions, immunologic factors Host factors associated with an increased risk of cancer (in whites) Advanced age Male sex Fair complexion Light eye color Red hair color Poor tanning ability Precancerous lesions Genetic syndromes The risk of NMSC is connected to race and ethnicity. Fair-skinned people of Celtic ancestry have the highest incidence rates. The risk of BCC is higher in an Australian born individual without southern European ancestry. This is associated with less pigmentation and greater sun sensitivity. Fair complexion, red hair, inability to tan, tendency to freckle, sunburn greatly predispose to the development of NMSC. Scandinavian people have fair complexions but have good tanning capacity, have a low BCC incidence, whereas the Irish, who tan poorly have a higher incidence. Dark-skinned people show the lowest incidence of NMSC but a higher mortality as compared to fair-skinned people. SCC is the most common NMSC that affects darkskinned people. Genetic syndromes associated with high risk of cancer Nevoid basal cell ca syndrome (Gorlins syndrome) Albinism (autosomal recessive) Xeroderma pigmentosum (autosomal recessive) Epidermodysplastic verruciformis (autosomal recessive, ca developing in sun-

exposed areas from flat warts commonly infected with HPV) Precursor lesions Keratosis actinica prevalence in fair-skinned older individuals, occurs after exposure to sunlight, ionizing radiation, arsenic and policyclic hydrocarbons 20% of actinic keratosis undergos transformation to SCC Bowens disease, SCC in situ exposed or unexposed areas of the skin or mucosa. Probable risk factors are: arsenium, radiotherapy, viral agents. 0.1%/ year develop SCC Immunologic factors Immunosuppression in patients after renal transplantation, SCC develops on sunexposed skin. Occurs in younger patients, have higher metastatic rates Leukemia, lymphoma, epidermolysis verruciformis, mycosis fungoides, psoriasis, rheumatoid arthritis, patients with aplastic anemia environmental factors UV radiation is responsible for 90% of NMSC desease of white people fair-skinned population on body areas directly exposed to sunlight in people with genetic disorders such as albinism pigment. Ionizing radiation in 1902 skin cancer in x-ray technician after atomic bomb uranium miners Chemicals polycyclic aromatic hydrocarbons exposure to arsenic 18-45 years after exposure Diet beta carotens, cruciferous vegetables, vit.C foods, fish are agents protective

or xeroderma

In USA The incidence of BCC is comparable for men and woman at early ages. The rates for men are higher after age 45 SCC more men are affected at all ages Men develop BCC and SCC 2 - 3 times more frequently than woman do The probability of developing a skin malignancy ranges from 1128% for BCC and 1.5 11% for SCC and varies with sex, cell type, geographic area of residence. Most frequent neoplasm of the facial region is BCC (75 -80% of all cases) SCC is most frequent neoplasm of the oral mucosa

lip cancer - > 1% malignant neoplasm in men, 0.3% in women cancer of the oropharynx approx. 1% of malignant neoplasms cancer of the tongue 0.6% of neoplasms in men. Constitutes 40% of neoplasms of the oral cavity cancer of the floor of the oral cavity 0.4% of all neoplasms. 5 times more often in men cancer of buccal mucosa - 10% of malignant tumors of the oral cavity retromolar area - 7% of malignant tumors of the oral cavity Prognosis lip cancer - 5-yr survival 93.5% ( without metastasis), 58.4% (with metastasis) oral cavity ca - 5-yr survival 35 65% cancer of the tongue and oropharynx have a worse prognosis 25% (with metastasis), 60% (without metastasis), retromolar area with T1 70% and in T3-4 20% Neoplasm Condition in which there arises uncontrolled growth of own, morphologically and functionally transformed cells, first in the area of the primary lesion, then infiltrating to surrounding tissues and finally migrating and proliferating transformed cells in distant localizations (metastasis) Development of Neoplasm Theory Genetic mutation in DNA causes change of cell phenotype Epigenetic a change beyond the genetic apparatus induces a change in DNA and the transformed genotype transfers the new cell characteristic to its progenyDevelopment of Neoplasm Theory Genetic mutation in DNA causes change of cell phenotype Epigenetic a change beyond the genetic apparatus induces a change in DNA and the transformed genotype transfers the new cell characteristic to its progeny The presence of a neoplasm is due to many factors. According to Schmhl, a neoplasm is a function of such factors as: predisposition, age and exposure to carcinogenic effects. C = f (P + E + A) C - carcinoma, P - predisposition, E - exposure, A - age Schmhl D. ( red .) : Combination effects in chemical carcinogenesis. VCH ,

Weinheim, Germany, 1988. The probability of developing a skin malignancy ranges from 1128% for BCC and 1.5 11% for SCC and varies with sex, cell type, geographic area of residence. The most important factors predisposing to the development of cancer of the mucous membrane of the oral cavity are: smoking and chewing tabacco, alcohol consumption (especially in high concentrations), poor oral hygiene and exposure to certain chemicals. HPV virus (human papillomavirus) or fungal infections may also have relevant significance. Almost half the cases develop from leukoplakia. Most often, in the oral cavity, it is localized in areas known as salivary pathways ", that is, in the floor of the oral cavity, in the recess of the pharynx and ventral tongue, places where saliva with food debris and dissolved products of tobacco smoke can be found. A provoking factor (carcinogen) changes the genetic code of a cell, which transfers this defect to the progeny cells. Fixed carcinogen Initiation phase cells increase their tendency to abnormal proliferation. Hyperplasia is present. It is accepted that this trait appears in one cell per one million. Besides the tendency to excessive division of the cell, it also takes on new morphological features, described as dysplasia. Promotion phase in which a cell undergoes a series of changes leading to a gaining of neoplastic cell (biochemical) traits. An organism can still destroy such a cell. Progression phase in the right conditions of weak homeostasis, the next stage of carcinogenisis begins. In this stage, the neoplasm is clinically recognizable. in the initiation and promotion phase reversible changes are possible Development of Neoplasm in the Epithelial Tissue Genetic mutation increases the tendency of a cell to proliferate. The transformed cell and its progeny still have correct features but they divide excessively hyperplasia. After years, one cell per million undergoes another mutation causing a weakening of growth control. Progeny of this cell changes its appearance - dysplasia The next mutation leads to even more incorrect growth of transformed phenotype cells ca in situ further genetic changes allow neoplastic cell invasion into deeper situated tissues through seepage into blood and lymph and forming metastasis Precancerous States in the Oral Cavity

These are clinically distinguishable changes presenting on the skin or mucosa, in which a malignant neoplasm (cancer) can develop. Precancerous states may undergo a malignant change but also may regress completely. For this reason, the diagnosis of clinical presentation must be confirmed by a histopathological examination. Keratosis actinica (sun), keratosis senilis (old age), cornu cutaneum Parchment-like and pigmented skin Postirradiated skin damage Bowens Disease Chemical keratosis (post arsenic, tar-like) Keratotic papilloma Hypertrophied scars White keratosis (leukoplakia) Hairy leukoplakia of the tongue Bowens Disease (Erythroplasia Queyrata) Keratotic papilloma Desquamative inflammation of lower lip salvilary glands (cheilitis glandularis) Plummer-Vinsons syndrome (achlorhydria) Chronic decubitus ulcer (bedsore) Chronic inflammatory states Tuberculous lupus lesions Melanoplakia White Keratosis ( leukoplakia ) White plaques of smooth or papillomous surface, localized on the mucous membrane of the oral cavity (vulva) I limited epithelial clouding/opacification II - limited white and white-gray maculae somewhat above the level of mucosa, visible mosaic-like fissures III discs and eruptions of a course surface, disruption and infiltration of interstitium, erosions IV - verrucous lesions, outgrowths and erosions with inflammatory reactions Grade III and IV are considered precancerous states Papillous/verrucous and ulcerative leukoplakia can be distinguished clinically Classification of Neoplasms in the Oral Cavity and the Maxillo-Facial Regions Present classification WHO is based on histogenesis, histoformation ability and some biological traits (esp. malignancy) of neoplasms Neoplasms from epithelial tissue Benign

Papilloma Malignant interepithelial pre-invasive cancer ( ca praeinvasivum ) papillous/verrucous cancer (ca verucosum ) Fusocellular cancer ( ca fusocellularae ) lymphoepithelioma ) planoepithelial cancer ( ca planoepitheliale ) Neoplasms from Glandular Tissue Benign adenoma Malignant adenocarcinoma/malignant adenoma Neoplasms of Soft Tissues Benign Fibroma Lipoma Leiomyoma Rhabdomyoma Chondroma Osteochondroma Haemangioma - from capillaries - cavernous - cystic Neurofibroma Neurilemmoma, schwannoma Malignant fibrosarcoma liposarcoma leiomyosarcoma rhabdomyosarcoma haemangiosarcoma lymphosarcoma schwannoma malignum Neoplasms of Pigmented Tissue Benign pigmented nevus Malignant

malignant melanoma Neoplasms of Mixed Genesis Benign myxoma myoblastoma granulocellulare epulis congenita Malignant tumor granulocellularis alveolar sarcoma Kaposis sarcoma Neoplasms associated with Bone Outgrowths from bone osteoma fibroma ossificans Sarcomas of the bone (from bone, cartilage, bone marrow) osteosarcoma chondrosarcoma Ewings tumor reticulosarcoma myeloma, plasmocytoma Non-neoplastic bone lesions fibrous dysplasia cherubism traumatic bone cyst aneurysmal bone cyst giant cell granuloma Epithelial cysts Developmental odontogenic - primordial - eruption - follicular non-odontogenic - incisive canal - globulomaxillary - medial palatal

Inflammatory radicular Neoplasms and Odontogenic Tumors Benign adamantinoma tu epithelii odontogenes calcifficans fibroma ameloblasticum adenoameloblastoma dentinoma fibrocementoma ameloblasticum ameloblastic odontoma odontoma mixtum odontoma compositum fibroma dentogenes myxoma cementoma - cementoma - fibrocementoma calcificans - cementoma gigantoformis melanotic neuroectodermal tumor of infancy melanoameloblasyoma infantum Malignant odontogenic cancers - ameloblastoma malignum - ca intraosseum primarium - cancer from epithelial odontogenic or odontogenic cysts. odontogenic sarcoma - ameloblastic fibrosarcoma - ameloblastic odontosarcoma Salivary glands tumors: Salivary gland enlargement is more often caused by inflammatory or nonneoplastic conditions than neoplasia. Salivary gland tumours accounts for around 3 % of all tumors in the head and neck region and around 85% of them occur in the parotid gland. In general, 80% of parotid gland tumors are benign, 50% of submandibular gland and 25% of minor salivary tumors are benign. Tumors arising from the sublingual gland are rare and most of them are malignant. The difficulties encountered with salivary gland tumors, especially the malignant neoplasms are the wide range of histological features with a spectrum of clinical behavior; the different types of classification and the number of patients encountered in individual centers are limited. Practical Classification:

Benign Neoplasms 1. Adenomas a. Pleomorphic adenoma (Mixed tumor) b. Monomorphic adenoma c. Adenolymphoma (Warthins tumor) 2. Oncocytoma 3. Haemangioma etc Tumor-like conditions 1. Benign lymphoepithelial lesions a. Mikuliczs syndrome b. Sjgrens syndrome 2. Chronic sialadenitis and sialolithiasis 3. Vascular/lymphatic malformation 4. Granulomatous disease Malignant Neoplasms 1. High malignant potential Adenoid cystic carcinoma, adenocarcinoma, squamous cell carcinoma, high grade mucoepidermoid carcinoma, carcinoma ex-pleomorphic adenoma and undifferentiated carcinoma. 2. Low malignant potential Acinic cell carcinoma, low and intermediate grade mucoepidermoid carcinoma 3. Lymphoma 4. Secondary tumors Malignant Epithelial Neoplasms Most commonly found skin cancers are: Basal cell carcinoma BCC Squamous cell carcinoma - SCC Odontogenic Carcinomas Odontogenic carcinoma ( primary intraosseous carcinoma ) arises from chronic, intraosseous residual odontogenic epithelium Ameloblastoma malignum ( embryonic ) primarily malignant or as the result of malignant transformation Malignant transformation in odontogenic cysts most commonly within stratified squamous keratotic epithelium Malignant forms of other odontogenic neoplasms Odontogenic Sarcoma

Fibrocementoma ameloblasticum Fibro-(pulp stone)denticlar-sarcoma ameloblasticum, fibro-odontoma-sarcoma ameloblasticum adenocystic carcinoma ( cylindroma ) ductal epithelium cells and myoepithelium cells. More often in palatal small salivary glands, buccal, sinus, nose. Infiltration of nerve ( paralysis of n.VII ). Persistently recurs. Mucoepidermoid carcinoma ( Stewarts ) squamous cell epithelium, secreting glandular mucus cells and intermediate cells. Large and small salivary glands. Often localized on the palate. Growth is slow but a rapid, aggressive growth form does exist, paralyzing n.VII and is metastatic ( bone, liver ). Prone to ulceration. Spreads by lymphatic and blood vessel pathways. Squamous cell carcinoma of the oral cavity develops in the epithelium covering the mucous membrane of the oral cavity Its advanced clinical stage can have the following forms: exophytic of a wide base, fungal, cauliflower-like extending above the surrounding mucousal membrane surface, endophytic infiltrating deep, erosive , mixed Diagnosing cancer is based on histopathologic examination of the tumor tissue specimen which is collected in many ways. The most significant is an exam of the excised section of a tumor, then material from biopsy or fine-needle aspiration. On the basis of microscopic examination, it is possible to differentiate the stages of malignancy of squamous cell carcinoma. G1 relates to histologically mature cancer, forming keratin pearls. Architecture of cell is somewhat distorted. Hyperchromatic nucleus of the cell may have an irregular shape and may be enlarged. Cell divisions are few. G2 cell divisions are frequent, but keratin pearl creation is rarely found. G3 cancer of low differentiation. Pleomorfism appears in cell nuclei. Keratinization and creation of intercellular briges are slightly noticable. Atypical mitotic figures appear. G4 relates to anaplastic cancer, a form very poorly differentiated Classification System of Tumors TNM Topografic Localization Buccal mucous membrane lip mucosa

buccal mucosa retromolar area oral vestibule Upper gingiva Lower gingiva Hard palate Tongue dorsal surface and lateral to the border of circumvallate papilla ventral surface Oral cavity floor TNM classification system T Primary Tumor Tx primary tumor cannot be assessed T0 no evidence of primary tumor Tis ca in situ T 1 tumor 2 cm or less in greatest dimension T 2 tu > 2 cm < 4 cm T 3 tu > 4 cm T 4 tumor invades adjacent structures, e.g., through cortical bone, into deep muscle of tongue, maxillary sius, skin. Superficial erosion alone of bone/tooth socket by gingival primary is not sufficient to classify a tumor as T 4 N Regional Lymph Nodes Nx regional nodes cannot be assessed N0 no regional l.n. metastases N1 meta in single ipsilateral l.n. < 3 cm N2a meta in single ipsilateral l.n. > 3 cm < 6 cm N2b meta in multiple ipsilateral l.n. < 6 cm N2c meta in bilateral or contralateral l.n. < 6 cm N3 meta in a l.n. > 6 cm Sobin L.H., Wittekind Ch.- TNM Classification of Malignant Tumors (UICC) Fifth Edition, NY, 1997 M (metastases) distant Mx cannot be assessed M0 no distant metastasis M1 positive distant metastasis Classification System of Tumors TNM Clinical Stages of Advancement TNM

Stage Grouping St 0 St I St II St III

Tis T1 T2 T3 T1 T2 T3 T4 T4 anyT

N0 N0 N0 N0 N1 N1 N1 N0 N1 N2 anyT anyT N3 anyN

M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M0 M1

St IVA St IVB StIVC

Sobin L.H., Wittekind Ch.- TNM Classification of Malignant Tumors (UICC) Fifth Edition, NY, 1997