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Chronic Periodontitis PowerPoint Presentation

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Description : Check out this medical PowerPoint presentation titled "Chronic Periodontitis”.

This medical PowerPoint presentation is about chronic periodontitis, a type of periodontal disease, which is characterized by the inflammation and destruction of the gums, periodontal ligament, and the bone surrounding the teeth. It is a slowly progressing disease that can lead to tooth loss if left untreated.

The primary cause of chronic periodontitis is the accumulation of dental plaque, a sticky film of bacteria that forms on the teeth and gums. Plaque can harden into tartar or calculus, which cannot be removed by brushing or flossing alone and requires professional dental cleaning.

Symptoms of chronic periodontitis include swollen, red, or bleeding gums, persistent bad breath, and a receding gum line. As the disease progresses, teeth may become loose or shift out of place.

Treatment for chronic periodontitis usually involves a combination of professional cleaning, scaling and root planing, medication, and in some cases, surgery. It is also important to practice good oral hygiene habits, such as brushing twice a day, flossing daily, and using an antiseptic mouthwash to prevent the buildup of plaque and bacteria. Regular dental checkups and cleanings are also essential for maintaining healthy teeth and gums.

Tags : Chronic Periodontitis, periodontal disease, dental plaque, Dentistry, dental medicine, oral medicine, dental medicine PowerPoint presentation

Published on : Jun 20, 2023 | Views : 1195 | Downloads : 1

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Slide 1-

Chronic Periodontitis 1 This presentation will probably involve audience discussion, which will create action items. Use PowerPoint to keep track of these action items during your presentation In Slide Show, click on the right mouse button Select “Meeting Minder” Select the “Action Items” tab Type in action items as they come up Click OK to dismiss this box This will automatically create an Action Item slide at the end of your presentation with your points entered.
Slide 2-

Definition Chronic Periodontitis can be defined as “an infectious disease resulting in inflammation within the supporting tissues of the teeth, progressive attachment loss, and bone loss.” - Previously known as adult periodontitis or slowly progressive periodontitis. - Occur as a result of extension of inflammation from the gingiva into deeper periodontal tissue. 2
Slide 3-

Common Characteristics Onset - any age; most common in adults Plaque initiates condition Subgingival calculus common finding Slow-mod progression; periods of rapid progression possible Modified by local factors/systemic factors/stress/smoking 3
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Extent & Severity Extent: Localized: <30% of sites affected Generalized: > 30% of sites affected Severity: entire dentition or individual teeth/site Slight = 1-2 mm CAL Moderate = 3-4 mm CAL Severe =  5 mm CAL 4
Slide 5-

Clinical Characteristics Gingiva moderately swollen Deep red to bluish-red tissues Blunted and rolled gingival margin Cratered papilla Bleeding and/or suppuration 5
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Clinical Characteristics Plaque/calculus deposits Variable pocket depths Loss of periodontal attachment Horizontal/vertical bone loss Tooth mobility 6
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CLASSIFICATION 7 A) Based on Disease Distribution: Localized: Periodontitis is considered localized when <30% of the sites assessed in mouth demonstrate attachment loss and bone loss. Generalized: Periodontitis is considered generalized when >30% of the sites assessed demonstrate attachment loss and bone loss. The pattern of bone loss in chronic periodontitis can be vertical or horizontal.
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Sub classification of Chronic Periodontitis 8
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DISEASE DISTRIBUTION : It is a site-specific disease CLINICAL SIGNS - - Inflammation ,pocket formation ,attacment loss ,bone loss - All caused by site specific effects of a sub-gingival plaque accumulation - That is why the effect are on one side only –other surface may maintain normal attachment level. - Eg.-proximal surface with plaque may have C.A.L. - And plaque free surface –FACIALsurface of same tooth may be without disease.
Slide 10-

SYMPTOMS Patient notices-- gum bleed space appear between teeth due to tooth movement May be painless (sleeping disease )goes unnoticed Some time pain due to caries , root hypersensitivity To cold /hot or both PAIN-may be-- dull—deep radiating in the jaw Area of food impaction can cause more discomfort May be gingival tenderness or itchiness found
Slide 11-

Periodontal Pathogens Gram negative organism dominate P.g., P.i., A.a. may infiltrate: - Intercellular spaces of the epithelium - Between deeper epithelial cells - Basement lamina 11
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Periodontal Pathogens Contn. Pathogens include: Nonmotile rods: Facultative: Actinobacillus a. E.c. Anaerobic: P. g., P. i., B.f., F.n. Motile rods: Facultative: C.r. Spirochetes: Anaerobic, motile: Treponema denticola 12
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Pathogenesis – Pocket Formation Bacterial challenge initiates initial lesion of gingivitis With disease progression & change in microorganisms  development of periodontitis 13
Slide 14-

Pocket Formation Cellular & fluid inflammatory exudate  degenerates CT Gingival fibers destroyed Collagen fibers apical to JE destroyed  infiltration of inflammatory cells & edema Apical migration of junctional epithelium along root Coronal portion of JE detaches 14
Slide 15-

Pocket Formation Continued extension of JE requires healthy epithelial cells! Necrotic JE slows down pocket formation Pocket base degeneration less severe than lateral 15
Slide 16-

Pocket Formation Continue inflammation: Coronal extension of gingival margin JE migrates apically & separates from root Lateral pocket wall proliferates & extends into CT Leukocytes & edema Infiltrate lining epithelium Varying degrees of degeneration & necrosis 16
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Development of Periodontal Pocket 17
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Continuous Cycle! Plaque  gingival inflammation  pocket formation  more plaque 18
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Classification of Pockets Gingival: Coronal migration of gingival margin Periodontal: Apical migration of epithelial attachment Suprabony: Base of pocket coronal to height of alveolar crest Infrabony: Base of pocket apical to height of alveolar crest Characterized by angular bony defects 19
Slide 20-

Histopathology Connective Tissue: Edematous Dense infiltrate: Plasma cells (80%) Lymphocytes, PMNs Blood vessels proliferate, dilate & are engorged. Varying degrees of degeneration in addition to newly formed capillaries, fibroblasts, collagen fibers in some areas. 20
Slide 21-

Histopathology Periodontal pocket: Lateral wall shows most severe degeneration Epithelial proliferation & degeneration Rete pegs protrude deep within CT Dense infiltrate of leukocytes & fluid found in rete pegs & epithelium Degeneration & necrosis of epithelium leads to ulceration of lateral wall, exposure of CT, suppuration 21
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Clinical & Histopathologic Features Clinical : Pocket wall bluish-red Smooth, shiny surface Pitting on pressure Histopathology: Vasodilation & vasostagnation Epithelial proliferation, edema Edema & degeneration of epithelium 22
Slide 23-

Clinical & Histopathologic FeaturesContn… Clinical: Pocket wall may be pink & firm Bleeding with probing Pain with instrumentation Histopathology: Fibrotic changes dominate  blood flow, degenerated, thin epithelium Ulceration of pocket epithelium 23
Slide 24-

Clinical & Histopathologic FeaturesContn… Clinical : Exudate Flaccid tissues Histopathology: Accumulation of inflammatory products Destruction of gingival fibers 24
Slide 25-

Stages of Periodontal Disease 25
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Root Surface Wall Periodontal disease affects root surface: Perpetuates disease Decay, sensitivity Complicates treatment Embedded collagen fibers degenerate  cementum exposed to environment Bacteria penetrate unprotected root 26
Slide 27-

Root Surface Wall Contn… Necrotic areas of cementum form; clinically soft Act as reservoir for bacteria Root planing may remove necrotic areas  firmer surface 27
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Inflammatory Pathway Stages I-III – inflammation degrades gingival fibers Spreads via blood vessels: Interproximal: Loose CT  transseptal fibers  marrow spaces of cancellous bone  periodontal ligament  suprabony pockets & horizontal bone loss transseptal fibers transverse horizontally 28
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Inflammatory Pathway Interproximal: Loose CT  periodontal ligament  bone  infrabony pockets & vertical bone loss  transseptal fibers transverse in oblique direction 29
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Inflammatory Pathway Facial & Lingual: Loose CT  along periosteum  marrow spaces of cancellous bone  supporting bone destroyed first  alvoelar bone proper  periodontal ligament  suprabony pocket & horizontal bone loss 30
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Inflammatory Pathway Facial & Lingual: Loose CT  periodontal ligament  destruction of periodontal ligament fibers  infrabony pockets & vertical or angular bone loss 31
Slide 32-

Periodontal Disease Activity Bursts of activity followed by periods of quiescence characterized by: Reduced inflammatory response Little to no bone loss & CT loss Accumulation of Gram negative organisms leads to: Bone & attachment loss Bleeding, exudates May last days, weeks, months 32
Slide 33-

Periodontal Disease Activity Period of activity followed by period of remission: Accumulation of Gram positive bacteria Condition somewhat stabilized Periodontal destruction is site specific PD affects few teeth at one time, or some surfaces of given teeth 33
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Prevalence: Chronic Periodontitis increases in prevalence & severity with age. Affect both the sexes equally. It is an age-associated, not age related disease.
Slide 35-

RISK FACTORS FOR DISEASE: 1) PRIOR HISTORY OF PERIODONTITIS—predictor-more risk for developing damage to periodontium. 2) LOCAL FACTORS: Plaque Accumulation Oral Hygiene Tooth Malposition Restoration Preserve & Quantity of certain bacteria Host defences Subgingival Restoration Environment Calculus, smoking Connective Tissue destruction Genetic influence Inflammation Periodontopathic bacteria Smoking, Calculus Loss of Attachment M O D I F Y I N G F A C T O R S
Slide 36-

3) SYSTEMIC FACTORS: Type II or Non – Insulin dependent Diabetes Mellitus (NIIDDM) 4) ENVIRONMENTAL & BEHAVIORAL FACTORS: Smoking Emotional Stress 5) GENETIC FACTORS: Frequent among family members and across different generations. GENERAL CONCEPT FOR ETIOLOGY OF CHRONIC PERIODONTITIS Plaque accumulation Maturation of Plaque Quality & Quantity of periodontopathic Plaque accumulation Maturation of Plaque Quality & Quantity of periodontopathic bacteria InflammationPlaque accumulation Maturation of Plaque Quality & Quantity of periodontopathic bacteria Inflammation Connective tissue destruction. Connective tissue destruction. bacteria Inflammation Connective tissue destruction. Host status and defences Plaque accumulation Maturation of Plaque Quality & Quantity of periodontopathic bacteria Inflammation connective tissue destruction.
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MANAGEMENT The treatment consists of – Non-surgical procedures Scaling Root planing Curettage Surgical procedure Pocket reduction surgery Resective Regenerative Correction of morphological / anatomic defects
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Overall Prognosis Dependent on: Client compliance Systemic involvement Severity of condition # of remaining teeth 38
Slide 39-

Prognosis of Individual Teeth Dependent on: Attachment levels, bone height Status of adjacent teeth Type of pockets: suprabony, infrabony Furcation involvement Root resorption 39