BY DR. M.S.

MOORE

OUTLINE
y INTRODUCTION y AETIOLOGY AND EPIDEMIOLOGY y CLINICAL SIGNS AND SYMPTOMS y TREATMENT y REFERENCES

INTRODUCTION
y Alveolar Osteitis (AO) is a well-known complication

after extraction or surgical removal of tooth.

y Commonly known as dry socket this condition

remains a common postoperative problem that results in severe pain and repeated practice/hospital visits.

y The increase in recovery period translates into

increased cost to the surgeon as 45% of patients who develop AO typically require multiple postoperative visits in order to manage this condition

INTRODUCTION

TERMINOLOGY
y Authors do not agree on terminology for this y

y y y y y

complication. Dry socket was first described in the literature in 1896 by Crawford . Since then, other terms have been used to refer to this complications, such as alveolar osteitis, alveolitis, localized osteitis, alveolitis sicca dolorosa, localized alveolar osteitis,

TERMINOLOGY
fibrinolytic alveolitis septic socket, necrotic socket, and alveolalgia, among others Birn, whose series of articles provided a better understanding of the pathophysiology, labeled the condition fibrinolytic alveolitis. Although most authors have accepted Birn s theories, the term fibrinolytic osteitis is the least used in the literature. y Dry socket , which is the generic term, and alveolar osteitis are more commonly used terms.
y y y y y

DEFINITION
y Eighteen definitions of AO have been reported. y The most recent defines AO as postoperative pain

inside and around the extraction site, which increases in severity at any time between the first and third day after the extraction, accompanied by a partial or total disintegrated blood clot within the alveolar socket with or without halitosis I.R BLUM

DEFINITION
y Literature is replete with varying descriptive

definitions for AO, usually owing to an inconsistency in diagnostic criteria . y This range from Vedtofte et al. (1974) defining OA as Complete or partial loss of the blood clot with denuded bone in the alveolus and severe irradiating pain, to y Akota et al. (1998) defining OA as The presence of a disintegrated blood clot, and/or increased pain in the socket region, and/or foul odour, and/or exudate or pus in the socket.

AETIOLOGY
y Aetiology y Myriad aetiological and precipitating factors for AO

have been suggested in the literature. Although AO is generally believed to be of multifactorial origin, the following have been implicated most commonly as aetiological, aggravating and precipitating factors:. y Oral micro-organisms y Difficulty and trauma during surgery

AETIOLOGY
y Roots or bone fragments remaining in the wound y Excessive irrigation or curettage of the alveolus after y y y y

extraction Physical dislodgement of the clot Local blood perfusion, anaesthesia Oral contraceptives Smoking

AETIOLOGY
Risk factors associated with true AO y Previous experience of AO y Deeply impacted mandibular third molar (risk factor is directly proportional to increasing severity of impaction) y Poor oral hygiene of patient y Active or recent history of acute ulcerative gingivitis or pericoronitis associated with the tooth to be extracted y Smoking (especially >20 cigarettes per day) y Use of oral contraceptives y Immunocompromised individuals

AETIOLOGY
Other risk factors y Gender: more in females y Smoking y Menstruation y Inadequate blood supply y Previous irradiation y Oral steroid drugs

AETIOLOGY
y According to a study by Younis et al,alveolar osteitis was found to be more common in smokers than in non smokers, y however this same study stated that there is no statistical difference between the persons age, sex and education y The study also suggests that it is also more common on surgical extractions than in non surgical extractions y In contrast, Parthasarathi did a study suggesting that there is no significant effect of smoking, oral contraceptive pills, surgical technique on the development of alveolar osteitis. osteitis.

EPIDEMIOLOGY
y It is the most common post operative complication of

extraction, occurring in about 80% of cases of complaints of post operative complications. y Most of the studies have given the incidence of dry socket in all extractions as ranging from 2% to 4.4% and as high as 12.5% whereas third molar extraction has been associated with an incidence of 0.5% to 15%. y This great variability in the reported incidence of dry socket is largely due to differences in diagnostic criteria and in the methods of assessment

EPIDEMIOLOGY
y It occurs more in females (female:male - 3:1) (female:male

Humagain et all y Occurs more in the mandible than the maxilla y Occurs in 3-4% of routine dental extractions 3y 1-45% after extraction of mandibular 3rd molars

PATHOGENESIS
y Dry socket is not characterized by y redness, swelling, fever, or pus formation y Microscopically, dry socket is characterized by the

presence of inflammatory cellular infiltrate, including numerous phagocytes and giant cells in the remaining blood clot, associated with the presence of bacteria and necrosis of the lamina dura.

PATHOGENESIS
y In 1973, Birn reported that the inflammatory process can extend

to the medullar spaces and sometimes the periosteum, resulting in connective tissue inflammation of the contiguous mucosa, with microscopic features typical of osteomyelitis. y Degradation of the blood clot in association with dissolution of erythrocytes and fibrinolysis, deposits of hemosiderin, and the absence of organized granulation tissue have also been described in histopathologic investigation of dry socket y Many denominations, classifications, and descriptions of dry socket have been reported. However, despite the controversies, in general, dry socket has been characterized as an inflammation in the alveolus of recently extracted teeth, for which pain and the period of onset are specific clinical signs indicative of proper diagnosis.

PATHOGENESIS
y Real dry socket is characterized by the partial or total premature loss of the blood clot that forms in the interior of the alveolus after extraction. This must be distinguished from other conditions, such as hypovascularizationof the alveolar bone, caused by vascular and hematologic impairment; osteonecrosis induced by radiotherapy; osteopetrosis; Paget s disease; cement-osseous dysplasia, and so forth, in which the clot forms in the interior of the alveolus y Clinical and experimental studies have described an increased local fibrinolytic activity as a principal factor for the etiology of dry socket.

PATHOGENESIS
y Birn observed an increase in fibrinolytic activity in the

alveolus with dry socket compared with a regular alveolus. He reinforced that the partial or total lyse and destruction of the clot is caused by mediators released during inflammation by direct or indirect activation of plasminogen into the blood y When mediators are released by the cells of the alveolar bone after trauma, the plasminogen is converted into plasmin, causing clot rupture by disintegration of fibrin.

PATHOGENESIS
y This conversion occurs in the presence of cellular or plasmatic proactivators and other activators. y Those activators have recently been classified as direct (physiologic) and indirect (nonphysiologic) and have also been subclassified according to their origins as intrinsic or extrinsic activators. y The intrinsic activators originate from the components of plasma, such as activator factor XII-dependent or factor Hageman-dependent and urokinase. In contrast, direct extrinsic activators originate outside the plasma and include activators of tissue and endothelial plasminogen.

PATHOGENESIS
y The activators of tissue plasminogen are found in most

mammalian tissues, including the alveolar bone. The indirect activators include streptokinase and staphylokinase, substances produced by bacteria that interact with plasminogen and form an activator complex that converts plasminogen into plasmin. y The characteristic pain associated with dry socket has been attributed to the formation of kinins in the alveolus.

PATHOGENESIS
y The kinins activate the primary afferent nerve

terminations, which could have been sensitized previously by other inflammatory mediators and other allogeneic substances, which in concentrations of 1 ng/mL cause intense pain. y Plasmin is also involved in the conversion of kallikrein into kinins in the osseous alveolar marrow. Thus, the presence of plasmin might be a possible explanation for both significant aspects of dry socket (ie, neuralgic pain and clot disintegration).

PATHOGENESIS

CLINICAL SIGNS AND SYMPTOMS

SYMPTOMS y Pain which can spread to any part of the head, usually the ear, described as dull, throbbing by the patient y Halitosis y Bad taste in the mouth SIGNS y Tenderness around the tooth socket y Halitosis y Necrotic slough of the base y Denuded bone wall

CLINICAL SIGNS AND SYMPTOMS

Onset and duration y Early and recent studies have reported that AO onsets 1 3 days after tooth extraction y It is highly unlikely for AO to occur before the first postoperative day, because the blood clot contains antianti-plasmin that must be consumed by plasmin before clot disintegration can take place.

TREATMENT
Management
y A. Prophylactic management

Noni.Non-pharmacological ii.Pharmacological ii.

y B. Symptomatic management

TREATMENT
Prophylactic management In an era of evidence-based care, few areas of clinical controversy pose evidenceas substantial a dilemma to clinicians, as the topic of the alleged factors that are targets for the various preventive regiments, and the topic of what prophylactic medicaments and materials, if any, should be placed in an alveolar socket following exodontia. exodontia. Non Pharmacologic management Besides the possible elimination of risk factors, it is imperative for active nonpharmacological preventive measures to be implemented. A summary of non-pharmacological measures to prevent AO nony Use of good quality current preoperative radiographs y Careful planning of the surgery y Use of good surgical principles

TREATMENT
Non Pharmacologic management contd. y Extractions should be performed with minimum amount of trauma and maximum amount of care y Confirm presence of blood clot subsequent to extraction (if absent, scrape alveolar walls gently) y _ Wherever possible preoperative oral hygiene measures to reduce plaque levels to a minimum should be instituted y _ Encourage the patient (again) to stop or limit smoking in the immediate postoperative period

TREATMENT
Nonpharmacologic Mgt. Contd. y _ Advise patient to avoid vigorous mouth rinsing for the first 24 h post extraction and to use gentle toothbrushing in the immediate postoperative period y _ For patients taking oral contraceptives extractions should ideally be performed during days 23 through 28 of the menstrual cycle y _ Comprehensive pre- and postoperative verbal preinstructions should be supplemented with written advice to ensure maximum compliance

TREATMENT
Pharmacological Mgt. Mgt. y These pharmacological prophylactic interventions are related to one or more of the following groups: y 1. Antibacterial agents:penicillins, clindamycin,erythromycin, and metronidazole. y 2. Antiseptic agents and lavage: chlorhexidine y 3. Antifibrinolytic agents e.g. para-hydroxybenzoic acid (PHBA) y 4. Steroid anti-inflammatory agents: hydrocortisone and oxytetracycline mixture y 5. Obtundent dressings: eugenol containing dressing y 6. Clot support agents: polylactic acid (PLA)

TREATMENT
Symptomatic management y management of AO can be divided into non-dressing nonand dressing interventions. y Summary of non-dressing interventions to manage AO nony Remove any sutures to allow adequate exposure of the extraction site. As the socket may be exquisitely tender local anaesthesia may be required

TREATMENT
Symptomatic management contd.
y Irrigate the socket gently with warm sterile isotonic saline or local anaesthetic solution, which is followed by careful suctioning of all excess irrigation solution y Curette the socket under L.A y Prescription of potent oral analgesics y The patient is given a plastic syringe with a curved tip for home irrigation with chlorhexidine solution or saline and instructed to keep the socket clean. Once the socket no longer collects any debris, home irrigation can be discontinued.

TREATMENT
y However, common treatment modalities are: y the gold standard is irrigation and curettage 1. Irrigation and curettage alone 2. Irrigation and curettage followed by primary

suturing 3. Irrigation and curettage followed by Alvogyl TM 4. Irrigation and curettage followed by Salicept PatchTM 5. irrigation and curettage followed by low level laser therapy

TREATMENT
y A study by Kaya et al comparing alvogyl, salicept patch and low level laser therapy shows statistically significant differences between low level therapy as compared with alvogyl and salicept patch. y In that same study there were no statistically significant differences between alvogyl and salicept patch suggesting that salicept patch is a plausible alternative. y It should be noted however that all three treatment modalities show statistically significant differences when compared with irrigation and curettage alone in alleviation of pain and promotion of healing.

TREATMENT

ALVOGYL

LOW LEVEL LASER THERAPY

ALVOGYL

TREATMENT

TREATMENT

REFERENCES
y
Blum: Contemporary views on dry socket (alveolar osteitis): a clinical appraisal of standardization, aetiopathogenesis and management: a critical review. Int. J. Oral Maxillofac. Surg. 2002; 31: 309 317.

y T. P. Osborn, G. Frederickson Jr., I. A. Small, and T. S. Torgerson, A prospective study of y y y y y

complications related to mandibular third molar surgery, Journal of Oral and Maxillofacial Surgery, vol. 43, no. 10, pp. 767 769, 1985. P. E. Larsen, Alveolar osteitis after surgical removal of impacted mandibular third molars: identification of the patient at risk, Oral Surgery Oral Medicine and Oral Pathology, vol. 73, no. 4, pp. 393 397, 1992. J. Y. Crawford, Dry socket, Dental Cosmos, vol. 38, pp. 929 931, 1896. I. R. Blum, Contemporary views on dry socket (alveolar osteitis): a clinical appraisal of standardization, aetiopathogenesis and management: a critical review, International Journal of Oral and Maxillofacial Surgery, vol. 31, no. 3, pp. 309 317, 2002. D. Torres-Lagares, M. A. Serrera-Figallo, M. M. Romero-Ruz, P. Infante-Cosso, M. Garca-Caldern, and J. L. Gutirrez-Prez, Update on dry socket: a review of the literature, Medicina Oral, Patologia Oral y Cirugia Bucal, vol. 10, no. 1, pp. 77 85, 2005. R. E. Alexander, Dental extraction wound management: a case against medicating postextraction sockets, Journal of

REFERENCES
y Oral and Maxillofacial Surgery, vol. 58, no. 5, pp. 538 551, 2000. y H. Birn, Etiology and pathogenesis of fibrinolytic alveolitis ('dry y y y y y

socket'), International Journal of Oral Surgery, vol. 2, no. 5, pp. 211 263, 1973. H. Birn, Fibrinolytic activity of alveolar bone in "dry socket", Acta Odontologica Scandinavica, vol. 30, no. 1, pp. 23 32, 1972. H. Birn, Bacteria and fibrinolytic activity in "dry socket", Acta Odontologica Scandinavica, vol. 28, no. 6, pp. 773 783, 1970. G. E. Lilly, D. B. Osbon, E. M. Rael, H. S. Samuels, and J. C. Jones, Alveolar osteitis associated with mandibular third molar extractions, Journal of the American Dental Association, vol. 88, no. 4, pp. 802 806, 1974. E. A. Field, J. A. Speechley, E. Rotter, and J. Scott, Dry socket incidence compared after a 12 year interval, British Journal of Oral and Maxillofacial Surgery, vol. 23, no. 6, pp. 419 427, 1985. A. J. MacGregor, Aetiology of dry socket: a clinical investigation, British Journal of Oral Surgery, vol. 6, no. 1, pp. 49 58, 1968.

REFERENCES
y A. E. Swanson, Prevention of dry socket: an overview, Oral Surgery Oral y y y y y y y

Medicine and Oral Pathology, vol. 70, no. 2, pp. 131 136, 1990. K. L. Fridrich and R. A. J. Olson, Alveolar osteitis following surgical removal of mandibular third molars, Anesthesia Progress, vol. 37, no. 1, pp. 32 41, 1990. P. J. Vezeau, Dental extraction wound management: medicating postextraction sockets, Journal of Oral and Maxillofacial Surgery, vol. 58, no. 5, pp. 531 537, 2000. W. E. Shafer, M. K. Hine, and B. M. Levy, Textbook of Oral Pathology, Saunders, Philadelphia, Pa, USA, 4th edition, 1993. M. O. Hindle and A. Gibbs, The incidence of dry socket following the use of an occlusive dressing, Journal of Dentistry, vol. 5, no. 4, pp. 288 293, 1977. K. H. Thoma, Oral Surgery, CV Mosby, Saint Louis, Mo, USA, 5th edition, 1969. M. Ritzau and K. Swangsilpa, The prophylactic use of propylic ester of p hydrobenzoic acid on alveolitis sicca dolorosa. A preliminary report, Oral Surgery Oral Medicine and Oral Pathology, vol. 43, no. 1, pp. 32 37, 1977. J. B. Sweet and D. P. Butler, Predisposing and operative factors: effect on the incidence of localized osteitis in mandibular third-molar

REFERENCES
y J. H. Brekke, M. Bresner, and M. J. Reitman, Effect of surgical trauma and y y y y

polylactate cubes and granules on the incidence of alveolar osteitis in mandibular third molar extraction wounds, Journal of the Canadian Dental Association, vol. 52, no. 4, pp. 315 319, 1986. P. A. Heasman and D. J. Jacobs, A clinical investigation into the incidence of dry socket, British Journal of Oral and Maxillofacial Surgery, vol. 22, no. 2, pp. 115 122, 1984. W. S. Johnson and E. E. Blanton, An evaluation of 9-aminoacridine/Gelfoam to reduce dry socked formation, Oral Surgery Oral Medicine and Oral Pathology, vol. 66, no. 2, pp. 167 170, 1988. J. K. Barclay, Metronidazole and dry socket: prophylactic use in mandibular third molar removal complicated by non-acute pericoronitis, New Zealand Dental Journal, vol. 83, no. 373, pp. 71 75, 1987. P. E. Larsen, The effect of a chlorhexidine rinse on the incidence of alveolar osteitis following the surgical removal of impacted mandibular third molars, Journal of Oral and Maxillofacial Surgery, vol. 49, no. 9, pp. 932 937, 1991.

TH NK THANK

ATTENTI N