THE MEMBERS

Poor Oral Hygiene Plaque Accumulation

DM

Weakened Immune System Oral Microflora Increased (Gram + and -) Antibody Deficiency

Hypersensitivity

Dental Plaque

Plaque On Gingiva Sulcus (Junctional Epithelium)

Focal Infection

Initiate Caries Chronic Gingivitis Profunda Perforating Caries Infection cause Pulpitis

Oral Infection Periodontitis Marginalis

Bacteraemia

Pocket Periodontal

Inflammation and Destruction in Attachment Apparatus of Teeth

Migration to Junctional Epithelium Immune System cant control Microflora(Bacteria) invasion SIRS

Get Progressive Worse and Untreated

Oral Sepsis

Sepsis to Related Tissue

 In

this case, a woman with 34 years old came to the dentist with pain on the tooth 27. After checking, the dentist found that there is a hole and the gingiva surrounding the tooth is swollen. She experience bleeding especially after brushing her teeth. The tooth 27 before this was treated by a dentist but still the wound was not healed. She undergoes fever, headache, flu, difficulty in breathing, frequent urination and easily feels thirsty.

 Periodontal

disease, is the most common disease in the world and the leading cause of tooth loss in adults is a chronic infection that slowly attacks and destroys the gums and bone that support the teeth.

 In

America, one-third of children ages 6-11 and two-thirds of adolescents have some form of periodontal disease

 Periodontal

disease is caused by more than 200 species of bacteria. These bacteria form masses of sticky film called plaque, which is able to adhere to the surface of teeth and gums. When left untreated, the bacteria begin to spread to areas that are hard to reach with normal brushing and flossing; for instance, areas below the gum line, thus causing periodontal disease (periodontal).

 Here

as a dentist we should know what is periodontal disease and how we can responsible about that.

 Bacteremia

is usually defined as the presence of viable bacteria in the blood stream, as evidenced by blood cultures (Young,2000). Bacteremia is usually classified according to the microbial agent and an eventual coexisting focus of infection, assessed on the basis of microbiological and clinical findings

 In

this thesis we focused on communityacquired bacteremia, as our aim was to investigate diabetes as a risk factor for bacteremia in the general population, not among patients already hospitalized.

 Pulpitis

is the process of inflammation in dental pulp tissue, which in general is a continuation of the caries process. Pulp tissue located within the dental hard tissues so that when experiencing inflammation.

 Based

on the duration and severity

Acute pulpitis Sub acute pulpitis Chronic pulpitis

Based

on the presence or absence of symptoms

Symptomatic pulpitis Asymptomatic pulpitis

Based

On Histo pathologic And Clinical Diagnosis

Reversible Pulpitis Irreversible Pulpitis.

 Irreversible

pulpitis is an inflammatory condition of persistent pulp, can be symptomatic or asymptomatic due to a stimulus / lesion, where the defense can not tackle pulp inflammation that occurs, and the pulp can not return to its original or normal.

 On

the pulpitis irreversible humoral immune response seen increased IgG and IgM high, but IgA decreased considerably indicating that low mukosalnya resistance. The high IgG and IgM showed high pulp tissue resistance to microorganisms.

 This

is due to the wet zone products: Drain of carious lesions The product is absorbed by the venous circulation or lymphatic spread to adjacent tissue combination of the above ways that do not increase blood pressure vessel changes of irreversible symptomatic pulpitis (acute) that are dormant.

 The

bone of the alveolar crest shows resorption as demonstrated by the presence of Hownships lacunae sometimes still containing multinucleated osteoclasts. Caries may add to the damage caused by periodontitis by attacking the cementum covering the exposed root surface.

 Chronic

gingivitis is asymptomatic, low grade inflammation of the gingivae. The latter become red and slightly swollen with oedema. Pressure on the gingival margins causes bleeding, and sometimes pus can be expressed from round the necks of the teeth.

 Gingivitis

is an inflammatory response to plaque bacteria. By definition, inflammation is restricted to the gingival margins and does not affect the periodontal ligament or bone. It must be appreciated that these stages are artificially distinguished, being largely based on animal studies. (DeBowes LJ. 2002)

 Pregnancy

gingivitis Down's syndrome Diabetes mellitus

 Clinical

features :Chronic periodontitis (the 'advanced lesion') is the chief cause of tooth loss in later adult life, but symptoms are typically minimal. Many patients remain unaware of the disease until teeth become loose. (Cawson, 2002)

 Radiography

:Bone resorption usually progresses in a regular manner and its level remains the same along a row of teeth.Complex patterns of bone loss may also be seen, but where alveolar bone is thicker, partial destruction gives rise to vertical or angular bone defects. (Cawson, 2002)

 Plaque

:Bacterial plaque, a dense mat of bacteria, extends from the gingival margins into pockets. (Cawson, 2002) Subgingival calculus :Extension and calcification of plaque leads to formation of subgingival calculus within periodontal pockets. Chronic inflammation :Dense masses of these cells accumulate, especially under the epithelium in the connective tissue apposed to plaque and calculus. (Cawson, 2002)

 Pocketing

:Patients suffering from gingivitis will have a pocket depth of 3mm; a normal patient will have a pocket depth of less than 3mm (Hafernick). The second stage of periodontal disease is periodontitis II; this is characterized by puffy, bleeding gums with a pocket depth of up to 5mm and the early stages of bone loss (Hafernick).

 Smokers

have greater susceptibility to periodontitis but paradoxically less gingivitis. The reasons for this are not understood but smoking is known to interfere with inflammatory and immune reactions probably by activating endothelial and inflammatory cells inappropriately in the lungs and circulation, and by inducing them to secrete cytokines and other compounds.

 The

first response triggered by bacterial infection is the innate immune response. Bacteria are taken up by macrophages, causing the macrophage to release cytokines. The cytokines cause the inflammation associated with periodontal disease. Interleukin-8 (IL-8) is a chemoattractant for neutrophils, therefore it is logical that increased levels of IL-8 are found in gingival cells.

 Chronic

periodontitis, once established, is self-perpetuating. Pockets cannot drain effectively and favour proliferation of bacteria. The epithelial lining, plaque and subgingival calculus effectively obstruct healing.

 Control

of bacterial plaque Establishment of healthy gingiva accessible to plaque control Minimisation of periodontal tissue loss Use of antibiotics in selected cases Mucogingival surgery in selected cases

Subgingival scaling or root planing will not remove subgingival plaque entirely and may force pocket bacteria into the tissues. However, competent performance of these procedures reduces bacterial bulk, changes the composition of the flora and frequently produces clinical improvement. (Cawson, 2002)

 In

1992, the American College of Chest Physicians (ACCP) and the Society of Critical Care Medicine (SCCM) introduced definitions for systemic inflammatory response syndrome (SIRS), sepsis, sepsis induced hypotension, septic shock, and multiple organ dysfunction syndrome (MODS).

 SIRS

is defined as 2 or more of the following variables: - Fever of more than 38C or less than 36C - Heart rate of more than 90 beats per minute - Respiratory rate of more than 20 breaths per minute or a PaCO2 level less than 32 mm Hg - Abnormal white blood cell count (>12,000/@L or <4,000/@L or >10% bands) (Abrahamson, 1993)

 The

most common causes of SIRS related to infectious disease are as follows: bacterial infection, wound infection (burns, surgical wounds, diabetic foot and other infectious complications), cholecystitis, cholangoitis, other abdominal infections, pneumonia both nosocomial or community acquired, urogenital infections, meningitis and other less frequent conditions Noninfectious

 1.

Fever 2. Hypotension 3.Tachykardia 4. Increase oxygen tissue supply increased breathing rate and hypocapnia 5.Changes of the leucocytes (WBC) count

 Sepsis

describes a complex clinical syndrome that results from a harmful or damaging host response to infection. As a result of a concerted effort to understand the underlying pathogenetic mechanisms, there have been significant advances that have illuminated not just the process of sepsis, but also fundamental principles governing bacterialhost interactions.

 Determining

the structural components of bacteria that are responsible for initiating the septic process has been important not only in understanding the underlying mechanisms, but also in identifying potential therapeutic targets.

 Diabetes

mellitus is one of the oldest diseases in humans. By the definition,the definition of medical diabetes extends to a collection of symptomps that arise in a person that is caused by the presence of elevated levels of blood glucose resulting from insulin deficiency is either absolute or relative nature.

 Type

1 diabetes (b-cell destruction, usually leading to absolute insulin deciency) Type 2 diabetes (ranging from predominantly insulin resistance with relative insulin deciency to predominantly an insulin secretory defect with insulin resistance)

 Vascular

disease (diabetic angiopathy), atherosclerosis, heart conditions and stroke: These cardiovascular disorders are the leading cause of death in people with diabetes. Kidney disease (diabetic nephropathy): Diabetes is the chief cause of end-stage renal disease, which requires treatment with dialysis or a kidney transplant. Eye diseases: These include diabetic retinopathy, glaucoma and cataracts.

 Genetics

and family history Family medical history Weight and body type Sex Level of physical activity Diet

 Here

we have found one of the main reasons for this to happen is poor oral hygiene. The poor oral hygiene will cause continual accumulation of minerals from saliva on plaque on the teeth. It is rough surface provides an ideal medium for further plaque formation, threatening the health of the gingiva (gums). Once the plaque formed, it is too hard and firmly attached to be removed with a toothbrush.

 The

condition of too much plaque on the teeth can be the reason of oral micro flora increased. Oral micro flora is a colony of bacteria in the mouth which can be aerobe or anaerobe. The example is lactobacilli, staphylococci, corynebacteria, streptococcus mutans and various anaerobes in particular bacteroides.

 Another

effect of increased bacteria is plaque on gingiva sulcus (junctional epithelium). This long time condition can cause chronic gingivitis. Gingivitis (inflammation of the gum tissue) is a non - destructive periodontal disease. The most common form of gingivitis, and the most common form of periodontal disease overall, is in response to bacterial biofilms adherent to tooth surfaces, termed plaque-induced gingivitis.

 Tooth

decay disease is caused by specific types of bacteria that produce acid in the presence of fermentable carbohydrates such as sucrose,fructose, and glucose. Another effect of increased bacteria is plaque on gingiva sulcus (junctional epithelium). This long time condition can cause chronic gingivitis. Chronic gingivitis makes a dental pocket. Thus, chronic gingivitis and junctional epithelium destruction together lead a pocket periodontal that cause periodontitis.

ANY QUESTION?