1. GINGIVAL DISEASESDental Plaque-Induced Gingival DiseasesGingivitis that is associated with dental plaque formation isthe most common form of gingival disease characterized bythe presence of clinical signs of inflammation that areconfined to the gingiva and associated with teeth showing noattachment loss
2. Gingivitis associated with Dental Plaque Only: is the result of an interaction between the microorganisms found in the dental plaque biofilm and the tissues and inflammatory cells of the host. The plaque-host interaction can be altered by the effects of*Local factors *Systemic Factors *Medications *Malnutrition
6. Gingival Diseases Modified by Malnutrition bright red, swollen, and bleeding gingiva associated with severe ascorbic acid (vitamin C) deficiency or scurvy.Nutritional deficiencies areknown to affect immune functionand may have an impact on thehosts ability to protect itselfagainst some of the detrimentaleffects of cellular products suchas oxygen radicals.
7. Non-Plaque-Induced Gingival LesionsThey are observed in lower socioeconomic groups, developingcountries, and immunocompromised individuals
8. Gingival Diseases of Specific Bacterial Origin: Streptococcal gingivitis or gingivostomatitis is a rare condition that may present as an acute condition with fever, malaise, and pain associated with acutely inflamed, diffuse, red, and swollen gingiva with increased bleeding and occasional gingival abscess formation.preceded by tonsillitis and have been associated with groupA hemolytic streptococcal infections.
9. Gingival Diseases of Viral Origin: the most common being the herpes viruses-Primary herpetic gingivostomatitis Clinically appear as: Multiple tiny vesicles that progress to form painful ulcers. Painful erythematous swollen gingival. Fever, malaise, cervical lymphadenopathy.
10. Gingival Diseases of Fungal Origin: under prosthetic devices in individuals using topical steroidsin individuals with decreased salivary flow increased salivary glucose decreased salivary pH.
11. A generalized candidal infection may manifest as white patches onthe gingiva, tongue or oral mucous membrane that can beremoved with gauze, leaving a red, bleeding surface.In HIV-infected individuals,candidal infection may presentas erythema of the attachedgingiva and has been referredto as linear gingival erythemaor HIV-associated gingivitisDiagnosis of candidal infection can be made by culture, smear.
12. Gingival Diseases of Genetic Origin:hereditary gingival fibromatosisthat exhibits autosomaldominant or (rarely) autosomalrecessive modes of inheritance.The gingival enlargement maycompletely cover the teeth,delay eruption, and present asan isolated finding or beassociated with several moregeneralized syndromes.
13. Traumatic Lesions: factitial iatrogenic accidentalas in the case of as in the case of as in the case oftooth brush trauma preventive or damage to theresulting in gingival restorative care gingiva throughulceration, that may lead to minor burns from hotrecession both; traumatic injury foods and drinks. of the gingiva
14. Foreign Body Reactions: Foreign body reactions lead to localized inflammatoryconditions of the gingiva and are caused by the introduction offoreign material into the gingival connective tissues throughbreaks in the epithelium. Common examples are theintroduction of amalgam into the gingiva during the placementof a restoration or extraction of a tooth, leaving an amalgamtattoo, or the introduction of abrasives during polishingprocedures.
15. PERIODONTITIS Periodontitis is defined as "an inflammatory disease of thesupporting tissues of the teeth caused by specificmicroorganisms or groups of specific microorganisms,resulting in progressive destruction of the periodontalligament and alveolar bone with pocket formation, recession,or both." The clinical feature that distinguishes periodontitisfrom gingivitis is the presence of clinically detectableattachment loss.
16. Chronic PeriodontitisChronic periodontitis is the most common form of periodontitisChronic periodontitis is most prevalent in adults but can beobserved in children therefore the age range of >35 yearspreviously designated for the classification of this disease hasbeen discarded. Chronic periodontitis is associated with theaccumulation of plaque and calculus and generally has a slow tomoderate rate of disease progression
17. Local factors may influence plaque accumulation systemic diseasessuch as diabetes mellitus and HIV infection may influence the hostdefenses; environmental factors such as cigarette smoking and stressalso may influence the response of the host to plaque accumulation Chronic periodontitis may occur as alocalized disease wherein <30% ofevaluated sites demonstrateattachment and bone loss, or as amore generalized disease wherein>30% of sites are affected. The diseasealso may be described by the severityof disease as slight, moderate, orsevere based on the amount of clinicalattachment loss.
18. Aggressive Periodontitis Aggressive periodontitis differs from the chronic form primarily by the rapid rate of disease progression seen in an otherwise healthy individual, an absence of large accumulations of plaque and calculus, and a family history of aggressive disease suggestive of a genetic trait.early onset periodontitisusually affect young individuals ator after puberty and may beobserved during the second andthird decade of life (i.e., 10 to 30years of age). The disease may belocalized (LJP) or generalized(GJP)
19. NECROTIZING PERIODONTAL DISEASESNecrotizing Ulcerative Gingivitis Clinical features of necrotizing periodontal disease mayinclude necrosis and/or punched out ulceration of theinterdental papillae ("punched-out papillae") or gingivalmargin, pseudomembranous formation painful, bright redmarginal gingiva that bleed upon gentle manipulation,halitosis
20. Treatment*irrigation*and debridement of necrotic areasoral hygiene instruction and the •uses of mouth rinses* pain medication. •* As these diseases are often •associated with systemic medicalissues, proper management ofthe systemic disorders isappropriate
21. Necrotizing Ulcerative PeriodontitisNUP" differs from NUG in that loss of clinical attachment andalveolar bone is a consistent feature.Several case reports havedescribed extensive destructionleading to exfoliation of teethwithin 3-6 months of onset, withsequestration of necrotic alveolarbone and necrotic involvement ofthe adjacent mandible andmaxilla. Patients may presentwith concomitant malnutritionresulting from inability to takefood by mouth.
22. Treatment*Removal of plaque and debris from the site ofinfection and inflammation* Debridement of necrotic hard and soft tissues*Chlorhexidine gluconate rinse (0.12%) twice daily afterbrushing and flossing*Antibiotic therapy Metronidazole is the drug of choice,500 mg for 7-10 days.
23. PERIODONTITIS ASSOCIATED WITH ENDODONTICLESIONSEndodontic-Periodontal LesionsIn endodontic-periodontal lesions, pulpal necrosis precedesperiodontal changes. A periapical lesion originating frompulpal infection and necrosis may drain to the oral cavitythrough the periodontal ligament, resulting in destruction ofthe periodontal ligament and adjacen alveolar bone. Thismay present clinically as a localized deep, periodontal pocketextending to the apex of the tooth. Pulpal infection also maydrain through accessory canals, especially in the area of thefurcation, and may lead to furcal involvement through loss ofclinical attachment and alveolar bone.
24. Periodontal-Endodontic Lesions In periodontal-endodontic lesions, bacterial infection from aperiodontal pocket associated with loss of attachment and rootexposure may spread through accessory canals to the pulp,resulting in pulpal necrosis. In the case of advanced periodontaldisease, the infection may reach the pulp through the apicalforamen.Scaling and root planing removes cementum and underlyingdentin and may lead to chronic pulpitis through bacterialpenetration of dentinal tubules.
25. Combined Lesions Combined lesions occur when pulpal necrosis and aperiapical lesion occur on a tooth that also is periodontallyinvolved. A radiographically evident infrabony defect is seenwhen infection of pulpal origin merges with infection ofperiodontal origin
26. Diagnostic Methods*Initially a detailed medical and dental history must be obtainedfrom the patient.*The clinical examination should include inspection of thegingival and mucosal tissues, palpation, mobility testing,percussion*Periodontal probing is essential to identify and determine thedepth of periodontal pockets and the degree of loss ofattachment.*Pulp testing should be carried out with both carbon dioxide (dryice) and an electric pulp tester*Radiographs are an essential tool to the diagnosis of anyendodontic or periodontal condition.
27. Treatment periodontal disease *scaling *root planing *oral hygiene instructions follow-up maintenance therapy, including surgery in some cases.Diseased pulp tissue or infected root canals*cleaning* shaping* medicating* filling of the root canal system
28. DEVELOPMENTAL OR ACQUIRED DEFORMITIES ANDCONDITIONS Tooth Anatomic Factors Anatomic factors such as * cervical enamel projections and enamel pearls have been associated with clinical attachment loss, especially in furcation areas. *Palatogingival grooves, found primarily on maxillary incisors * Proximal root grooves on incisors and maxillary premolars Cervical enamel projectionEnamel pearl
29. Dental Restorations or Appliances Dental restorations or appliances are frequently associatedwith the development of gingival inflammation, especiallywhen they are located subgingivally. This may apply tosubgingivally placed onlays, crowns, fillings and orthodonticbands.
30. Root FracturesRoot fractures caused by traumatic forces or restorative orendodontic procedures may lead to periodontal involvementCervical Root Resorption and Cemental Tears Cervical root resorption andcemental tears may lead toperiodontal destruction when thelesion communicates with the oralcavity and allows bacteria tomigrate subgingivally