This is a brief compilation of the how periodontal diseases come about. It explains the concept of the causative agent and all virulence factors used. it also outlines the host response to these irritating factors which has been known to be more responsible for the clinical outcome of periodontal diseases.

1. PATHOGENESIS OF PERIODONTAL DISEASES
By Patrick Bannerman-Agbesi

2. Outline
•Introduction
•Clinically healthy gingiva
•Different lesions in Gingivitis/Periodontitis
•Host Parasite Interaction
•Host Defense process
•Summary and Conclusion

3. INTRODUCTION
•Definition –Origination and development of a disease
•-Mechanism by which an etiologic factor causes disease
•Greek “pathos”-suffering “genesis”-creation
•Unique clinical entity due to its anatomy and defensive processes

4. INTRODUCTION
•Referred to as a “mixed bacterial infection”– commensal and pathogenic interplay
•Sub gingival biofilm and host-immune- inflammatory events leads to breakdown of periodontal fibers-----Clinical attachment loss and bone resorption.
•The qualityand quantityof the micro-organisms should be noted

5. CLINICALLY HEALTHY GINGIVA
•Oral epithelium-keratinized
•Junctional epithelium (JE)— intrinsically “leaky”-reduced desmosome
•CT-collagen types I and III.
•Fiber arrangements-

6. CLINICALLY HEALTHYGINGIVA
•Pink in colour, scalloped margins, knife edge volume, firm consistency,
•Page and Shroeder (1976)--- polymorphonuclear neutrophils ( PMN) in the gingival crevice
•Gingival crevicular fluid (GCF)
•harbour of Chemo-attractant and chemotactic factors
•SUBCLINICAL GINGIVITIS ?

7. CLINICALLY HEALTHY GINGIVA
•Kept in check by the following-
•Intact barrier of JE
•Regular shedding of cells into the oral cavity
•Mechanical wash from the fluid into the crevice /dilution and FLUSH
•Antibodies, neutrophils, macrophages in sulcus
•Complement action
•When these responses are overwhelmed---periodontal disease presents
•NB---GINGIVITIS DOES NOT ALWAYS PROGRESS TO PERIODONTITIS

8. GINGIVAL INFLAMMATION
•CLINICAL FINDINGS
•EDEMATOUS
•ERYTHEMATOUS
•BLEEDS EASILY ON GENTLE PROBING
•ROLLED
•SOFT

9. GINGIVAL INFLAMMATION
•HISTOPATHOLOGICAL FINDINGS
•VASCULAR NETWORK CHANGES
•DISRUPTION OF THE NORMAL ANATOMY OF THE CT
•GCF EXUDATES AND PROTEIN CONCENTRATIONS INCREASE
•CT INFILTRATES CHANGE TO LYMPHOCYTES AND MACROPHAGES
•PLASMA CELLS AND ASSOCIATED COLLAGEN DEPLETION

10. HISTOPATHOLOGY OF GINGIVITIS/PERIODONTITIS
•Page and Shroeder -4 descriptions.
•INITIAL LESION------CLINICALLY HEALTHY GINGIVA
•EARLY LESION-------CLINICALLY HEALTHY GINGIVA
•ESTABLISHED LESION-------CHRONIC GINGIVITIS
•ADVANCED LESION-------PERIODONTITIS

11. HISTOPATHOLOGY OF GINGIVITIS/PERIODONTITIS
1.INITIAL LESION
•Plaquein gingival third in 24 hours results in vascular changes and intercellular gap formation and permeability-----leads to exudation in tissues and increased GCF .
•PMN migration is influenced by adhesion molecules ( ICAM-1,ELAM-1) and a strong chemo attractant gradient.
•The time frame for this is between 2-4 days

12. HISTOPATHOLOGY OF GINGIVITIS/PERIODONTITIS
2.EARLY LESION
•More vascular changes occur ( redness as a clinical symptom)
•Fibroblastdegenerate by apoptosisand must be cleared hence more PMN infiltration (PAGE AND SHROEDER, TAKAHASHI)
•Subsequent collagenfiber breakdown-----more space for infiltrates
•Time frame -1 WEEK

13. HISTOPATHOLOGY OF GINGIVITIS/PERIODONTITIS
•3.ESTABLISHED LESION
•Increased GCF flow and leukocyte infiltration. PLASMA CELLS dominate according to PAGE AND SHROEDER. Brecxand Franssonpropose lymphocytes in young people but plasma cells in older people.
•JE +SEthen changes to POCKET EPITHELIUM (PE)- allowing for a more apical migration of the biofilm.
•Pocket epithelium is more permeable and hence bleeds easily

14. HISTOPATHOLOGY OF GINGIVITIS/PERIODONTITIS
4.ADVANCED LESION
•New niche created by the apical migration of biofilm is now an ANAEROBIC eco-niche.
•The Established lesion progresses along with LOSS OF CT ATTACHMENT AND LOSS OF ALVEOLAR BONE.
•Pocket epithelium predominated with PLASMA CELLS and CT infiltrates
NB-this progessionof lesions is influenced greatly by the SUBJECT AND VARIABILITY.

15. SCHEMATIC VIEW OF THE PROGRESSION

16. HOST PARASITE INTERACTION
The inflammatory responses in periodontium is influenced by
•1. MICROBIAL VIRULENCE FACTORS
•2.HOST-DERIVED INFLAMMATORY MEDIATORS
•1.MICROBIAL VIRULENCE FACTORS
•These factors activate the immune inflammatory response
•A.LIPOPOLYSACCHARIDE (LPS)–ENDOTOXIN
•The host has TOLL-LIKE RECEPTORS (TLR) which recognize them and TRIGGERSa CASCADE of events for CYTOKINE PRODUCTION, BLOOD COAGULATION AND COMPLEMENT SYSTEM.

17. HOST PARASITE INTERACTION
•B.ENZYMES AND NOXIOUS PRODUCTS
•Metabolites such as ammonia, indole, hydrogen sulphide, butyric acid are known to induce T and B cell apoptosis and influence cytokine secretion.
•Proteases such as Arg-1 protease by Porphyromonasgingivalisand Leukotoxinby Aggregatibacteractinomycetemcomitans

18. HOST PARASITE INTERACTION
•C.MICROBIAL INVASION
•P. gingivalis, A.a, Fusobacteriumnucleatum
•Translocation of from the biofilm

19. HOST DEFENCE PROCESS
•Two branches 1. NON-SPECIFIC/ INNATE2.SPECIFIC/ ADAPTIVE
•1. INNATE IMMUNITY-
•Redness, swelling, heat, pain and loss of function.
•Saliva, GCF, epithelial keratinocytes, Normal flora. Concept of TOLL-LIKE RECPTORS.
a.SALIVA-antibodies, histatins, cystatins, lactoferrin, lysozyme, mucins, peroxidases

20. HOST DEFENCE PROCESS
a.GCF-FLUSH /DILUTION effect and the medium for transporting blood components to the crevice
b. EPITHELIAL TISSUES-barrier function of oral mucosa. Junctional epithelium ( non-keratinized, high turnover ) Host interaction with fimbriae of P.gingivalis
c.PATHOGENRECOGNITION AND ACTIVATION OF CELLULAR INNATE RESPONSE-Pattern Recognition Receptors (PRR) on macrophages and dendrites recognize MICROBE-ASSOCIATED MOLECULAR PATTERNS ( MAMPS) to signal an immune response

21. HOST DEFENCE PROCESS
2. SPECIFIC IMMUNITY
•Proteinases, Protease inhibitors, Matrix Metalloproteases (MMP), Cytokines ( Interleukins and Prostaglandins)
•a. Proteinases-Endopeptidases and Exopeptidases
b. Protease inhibitors -Alpha-2-macroglobulin (A2- M) and Alpha-1 antitrypsin (A1-AT)
C. MMP-responsible for tissue repair and remodeling. Neutrophil collagenase—pdlis the most metabolically active tissue and collagen metabolism represents most of its activity. Degrades ELASTIN,GELATIN, GAG.

22. •d. CYTOKINES –soluble proteins serving as messenger molecules that initiate /maintain an immune response.
•1.INTERLEUKIN 1 FAMILY CYTOKINES.
•IL-1 BETA ---synergizes PGE2 to induce BONE RESORPTION
•TUMOUR NECROSIS FACTOR ALPHA------ osteoclast induction
•IL-6-----monocyte differentiation to osteoclast
•PGE2----induce MMPs
•MMP-----Up regulates IL-1 beta

23. LINKING PATHOGENESIS TO CLINICAL SIGNS OF DISEASE
•FACT-bacteria in the pocket are never fully ELIMINATED!!!
•END RESULT-----ALVEOLAR BONE
•RESORPTION
•This progression will be strongly
influenced by the concentration of the
mediators
•and the penetration of bacteria into alveolar bone
•BONE MODELLING SYSTEM---RANK/RANK-L/OPG.

24. LINKING PATHOGENESIS TO CLINICAL SIGNS OF DISEASE
•RESOLUTION OF INFLAMMATION
•If the initial and early lesions do not progress to the established and advanced lesions, the gingivitis may resolve
•New agonists in this concept, LIPOXINS , RESOLVINS AND PROTECTINS function ACTIVELY as anti- inflammatory agents and inhibitors of neutrophil infiltration.

25. LINKING PATHOGENESIS TO CLINICAL SIGNS OF DISEASE
•A. LIPOXINS (LXA4, LXB4) –inhibit PMN recruitment, chemotaxis and adhesion, signal macrophages to phagocytize .
•B. RESOLVINS AND PROTECTINS—inhibit neutrophil infiltration and transmigration, inhibit production of pro-inflammatory mediators, and REDUCE cytokine expression

26. Summary and conclusion.
•Pathogenesis of periodontal disease is strongly influenced by the interplay of host-parasite interaction as well as the host response to the irritating factor.
•Gingivitis does not always progress to Periodontitis
•There is a wide variability in terms of progression in different subjects/individuals.
•Variations occur from tooth to tooth and from site to site.

27. Summary and Conclusion
•These events are site specific and are not usually associated with pain and this makes them more sinister.
•These conditions are preventablewith re-enforced oral hygiene instructions and client motivation.
•Visit your dentist twice a year for routine check-up and scaling and polishing prevent periodontal diseases.

28. THANK YOU!!