logging in or signing up CHRONIC PERIODONTITIS vyomika Download Post to : URL : Related Presentations : Share Add to Flag Embed Email Send to Blogs and Networks Add to Channel Uploaded from authorPOINT lite Insert YouTube videos in PowerPont slides with aS Desktop Copy embed code: Embed: Flash iPad Dynamic Copy Does not support media & animations Automatically changes to Flash or non-Flash embed WordPress Embed Customize Embed URL: Copy Thumbnail: Copy The presentation is successfully added In Your Favorites. Views: 2531 Category: Education License: All Rights Reserved Like it (0) Dislike it (0) Added: February 17, 2011 This Presentation is Public Favorites: 2 Presentation Description No description available. Comments Posting comment... Premium member Presentation Transcript Slide 1: CHAPTER 26 CHRONIC PERIODONTITIS Formerly known as “ ADULT PERIODONTITIS “ or “ CHRONIC ADULT PERIODONTITIS “ Slowly progressing disease . 2. Progress aggressively in patients having diabetes, smoking, stress and thyroid conditions. Can also occur in children and adolescents in response to plaque and calculus, this is the reason it is no more termed as adult periodontitis. Recently, defined as “ an infectious disease “ , resulting : In inflammation within the supporting tissues of the teeth. b) Progressive attachment loss. c) Bone loss. d) Presence of periodontal pocket of varying depths.Slide 2: CLINICAL FEATURES Accumulation of supragingival and subgingival plaque and calculus. Gingival inflammation. Pocket formation. Loss of attachment and bone. Presence of inflammatory swelling. Color ranging from pale red to magenta (purplish red). 7. Loss of stippling. 8. Blunted or rolled gingival margin. 9. Blunt or flattened interdental papilla. 10. All the signs of inflammation may not always be present. 11. Only sign may be bleeding on probing the pocket.Slide 3: Increase gingival fluid exudation. Purulent exudate may be present. Signs of inflammation may be masked because of the fibrotic changes. Horizontal and vertical bone loss. Progressive increase in the mobility of the teeth involved. Can be clinically diagnosed by: Presence of deepened gingival sulcus (pocket). Vertical zone of inflammatory changes from the marginal gingiva to the extent of attached gingiva involved. Loss of clinical attachment: Diagnosed radiographically. Evidence of bone loss.Slide 4: Differential diagnosis is based on : Age of the patient. Rate of disease progression. Familial nature of aggressive disease. Can be correlated with the amount of plaque and calculus present. DISEASE DISTRIBUTION Chronic periodontitis is : Site specific. Present only at the sites where there is plaque and calculus. Present only on the surfaces which show plaque and calculus accumulation. Can be localized or generalizedSlide 5: LOCALIZED PERIODONTITIS : When < 30 % of teeth show attachment loss . GENERALIZED PERIODONTITIS : When > 30 % of teeth show attachment loss . The pattern of bone loss observed in chronic periodontitis are : Vertical . Horizontal . VERTICAL BONE LOSS : When loss of attachment and bone loss is more in one tooth surface than the adjacent surfaces. Associated with angular bony defects and intrabony pocket formation . Seen in advanced periodontitis .Slide 6: HORIZONTAL BONE LOSS : When attachment loss proceeds at a uniform rate on all the tooth surfaces. Associated with suprabony pockets. Bone loss is usually horizontal . DISEASE SEVERITY : Described as being : Slight ( mild ) . Moderate . Severe. These terms describe the disease severity of : The entire mouth . A part of the mouth, such quadrant or sextant . The disease status of an individual tooth .Slide 7: Slight (mild ) periodontitis : 1 - 2 mm of clinical attachment loss . Moderate periodontitis : 3 – 4 mm of clinical attachment loss . Severe periodontitis : 5 mm or more clinical attachment loss. SYMPTOMS : Usually painless . Sometimes localized dull pain, radiating deep into the jaw . Sensitivity to hot and cold or both due to root exposure . Areas of food impaction cause discomfort . Itchiness in gingiva .Slide 8: DISEASE PROGRESSION Slow rate but may be modified by systemic and / or environmental and behavioral factors . Onset can occur any time in the presence of plaque and calculus . Usually becomes more evident in the mid - 30s therefore has accumulative effect . Does not progress at an equal rate in all affected sites . Some areas may remain static . More rapid progress in interdental areas . PREVALENCE Increase in prevalence and severity with age . Affects both sexes equally . Age associated disease , not age related and occurs depending on disease duration .Slide 9: RISK FACTORS FOR DISEASE Prior history of periodontitis : Not a true risk factor but rather a disease predictor . 2. Prior history of periodontitis would suggest that patient to be vulnerable to the disease . 3. Patient has to take more care for maintenance of oral hygiene and regular scalings . 4. Proper monitoring required . The risk factors that contribute to patient susceptibility are : Local Factors . Systemic Factors . Environment and Behavioral Factors . 4. Genetic Factors .Slide 10: 1. LOCAL FACTORS : Plaque accumulation on tooth and gingival surfaces is considered primary etiologic agent . Increase in the proportion of gram – ve organisms in the subgingival plaque biofilm like Bacteroides gingivalis, Bacteroides forsythus, and Treponema denticola . These microorganisms are associated with attachment and bone loss in chronic periodontitis and known as RED COMPLEX . These bacteria impart a local effect on : The cells of inflammatory response. Cells and tissues of the host . Results in a local site specific disease process . PLAQUE RETENTIVE FACTORS : Important in the development and progression of periodontitis . They retain plaque microorganisms in close proximity to the periodontal tissues . Provide an ecologic niche for plaque growth and maturation . Calculus is the most important plaque retentive factor because of its ability to retain and harbor plaque of chronic bacteria on its rough surface .Slide 11: Other factors that retain plaque or prevent its removal are : Subgingival and / or overhanging margins of restorations . Furcations exposed by loss of attachment and bone . Crowded or malaligned teeth . Root grooves and concavities . SYSTEMIC FACTORS : The rate of periodontal destruction is increased in patient suffering from systemic disease . Diabetes is a systemic condition that increase the severity and extent of periodontal disease in an affected patient . Type 1 or Insulin dependent diabetes mellitus ( IDDM ) is observed in children, teenagers, and young adults may lead to increased periodontal destruction when it is uncontrolled . ENVIRONMENT AND BEHAVIORAL FACTORS : Smoking increase the severity and extent of periodontal disease . b) Smokers with chronic periodontitis have : More attachment and bone loss . More furcation involvements . Deeper pockets .Slide 12: Smokers form more supragingival and less subgingival calculus . They demonstrate less bleeding on probing than nonsmokers . 4. GENETIC FACTORS : Periodontal destruction seen among family members and across different generations within family. Recent studies demonstrate a familial aggregation of localized and generalized aggressive periodontitis. Studies of monozygotic twins suggest a genetic component to chronic periodontitis . More aggressive periodontal breakdown in response to plaque and calculus accumulation may exist . Recent data indicates a genetic variation or polymorphism in the genes encoding interleukin 1 - alpha and interleukin 1- beta . These are associated with an increased susceptibility to a more aggressive form of chronic periodontitis. Smokers demonstrating the composite IL – 1 genotype are at greater risk for severe diseases. Heavy smokers and IL- 1 genotype increase risk of tooth loss by 2.9 times . The combined effect of IL- 1genotype and smoking increased the risk of tooth loss by 7.7 times . You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.