MODELS OF PATHOGENESIS IN PERIODONTITIS (1).pptx

models of pathogenesis in periodontics, periodontitis, etiopathogenesis

1. MODELS OF PATHOGENESIS IN PERIODONTITIS Presented by- Dr Monika Patil 1 st MDS Department of Periodontics

2. CONTENTS Introduction Different models- Linear Model Basic conceptual model - circa model (1980 model) Critical pathway model Non-linear model Multilevel hierarchical model Polymicrobial synergy and dysbiosis model New Biological systems model Mathematical model Contemporary model- Chapple 2015 IMPEDE Model Models of disease pregression Conclusion References

3. Periodontitis is a complex disease with intricate interactions between various components, each contributing to the dynamic nature of the disease process. Models of pathogenesis help in integrating the data available from current scientific research, which aid in comprehensive understanding of the disease. INTRODUCTION

4. They capture the biologic networks that incorporate disease-initiating, modifying, and resolving mechanisms. This stereotypic representation of a disease in the form of a conceptual model helps in translation of new information into practical applications and further assists in diagnosis and treatment planning.

5. Linear Model Linear model given in 1960 by Loe et al . Modern era of the pathogenesis, prevention, and treatment of periodontal diseases began in the mid- 1960s with human and animal experimental evidences. Microbial deposits causes periodontitis.

6. Abandonment of former concepts, non-bacterial factors, such as trauma from occlusion, systemic conditions, and diet. Changed the prevention and treatment of periodontitis. Drawback: I nnate differences among individuals and environmental factors were not taken into consideration.

7. Basic conceptual model - circa model (1980 model) Given by IvanyiL ,Lehner T , 1980 Role of Gram-negative, anaerobic bacteria Protective and destructive roles of the immune response Polymorphonuclear neutrophils (PMNs) in periodontal disease. Histopathological features of periodontal disease were described. Drawback: No explanation to some clinical disease patterns

8. Critical pathway model Offenbacher in 1996 Includes both bacterial etiology & the host response and attempts to define the critical regulatory modes which determine disease outcome . The term “critical path” refers to the steps along the cellular and molecular pathogenesis which is essential/indispensable for the disease process. Many factors may be involved in inflammation, but only few may be critical to the process, and may be only a handful will be associated with attachment or bone loss.

9. Non-linear model Basic conceptual model revised in 1997 Non-linear model given by Kornman in 1997 . Host immunoinflammatory mechanisms are activated by bacterial products.

10. Host derived enzymes such as matrix metalloproteinase as well as changes in osteoclast activity driven by cytokines and prostanoids cause most of the tissue destruction . The model implied that there were a range of host responses and a range of clinical expressions of disease that were primarily determined by genetic and environmental factors that modified the host response.

11. MULTILEVEL HIERARCHIAL MODEL Given by Kenneth S. Kornman in 2008 This model depicts a graded system to express the various interactions which occur between the gene, protein and metabolite. Each level of this framework can be represented as a separate biological component of the system. Different elements can be studied to understand the summative effect on the biological system

12. BIOLOGIC SYSTEM MODEL Offenbacher S Barros SP and Beck JD 2008 Model outlines the role of different components which may lead to the clinical presentation of a disease. For periodontal disease, the factors playing a key role will be on a person level, a genetic/epigenetic level, the biologic phenotype and the clinical phenotype.

13. Polymicrobial synergy and dysbiosis model Given by HAJISHENGALLIS 2012 It suggest that the pathogenesis of periodontitis involves polymicrobial synergy and dysbiosis. The dysbiosis of the periodontal microbiota signifies a change in the relative abundance of individual components of the bacterial community compared to their abundance in health, leading to alterations in the host–microbe crosstalk sufficient to mediate destructive inflammation and bone loss.

14. KEYSTONE HYPOTHESIS : Certain low-abundance microbial pathogens can orchestrate inflammatory disease by remodeling a normally benign microbiota into a dysbiotic one. Red complex bacteria: P gingivalis , T denticola & T forsythia Involved in dysbiosis Transform the normally symbiotic microbiota into a dysbiotic state that leads to a breakdown in the normal homeostatic relationship with the host. P. gingivalis is keystone pathogen Keystone: species whose effects on their communities are disproportionately large relative to their abundance and which are thought to form the “keystone” of the community‟s structure

15. P. gingivalis has evolved sophisticated strategies to evade or subvert components of the host immune system. Impairs innate immunity in ways that alter the growth and development of the entire biofilm, triggering a destructive change in the normally homeostatic host-microbial interplay in the periodontium. Study showed that, at very low colonization levels P. gingivalis induces periodontitis accompanied by significant alterations in the number and community organization of the oral commensal bacteria. P. gingivalis fails to cause disease in germ free mice.

16. SYNERGISM AMONG PERIODONTAL PATHOGENS: Co‐culture of P. gingivalis with T. denticola induces an alteration in P. gingivalis hemin uptake strategies and changes in the abundance of enzymes involved in glutamate and glycine catabolism. P. gingivalis can provide a source of free glycine and isobutyric acid for T. denticola growth, while T. denticola produces succinic acid which enhances growth of P. gingivalis .

17. MATHEMATICAL MODEL Given by Papantonopoulos 2013 This model hypothesises that periodontitis is a nonlinear chaotic disease . The authors used clinical and immunologic records from patients with periodontitis. They observed that this data fits into 2 separate clinical entities: aggressive periodontitis and chronic periodontitis The authors proved that the disease progression decreased if the level of the host immune response was increased.

18. Patients with chronic and aggressive periodontitis show different immune response. The authors also hypothesized that factors like, genetics, smoking and nutrition may make the system more disordered and random. Drawbacks - Systemic diseases which could be a causal factor for periodontitis were not taken into consideration. localised and generalised forms of periodontitis were not distinguished as separate disease processes.

19. Contemporary model of host–microbe interactions Given by (MEYLE AND CHAPPLE 2015) Periodontal health in an individual is determined by relationship between the microorganisms and the host response. A symbiotic relationship occurs between the two in health, where the microbes derive their nutrients from the host and the peptides released by these organisms leads to a balanced host response. Infrequent disturbance of this causes, strong inflammatory response which increases the nourishment of certain pathogens like P. gingivalis . Called “Incipient Dysbiosis”.

20. “Inflammation-Mediated Polymicrobial-Emergence and Dysbiotic -Exacerbation” (IMPEDE) Given by Thomas Van Dyke et al in 2020. In accordance with 2017 classification Pathogenesis is mainly explained under 3 headings Initiation Exacerbation Resolution This model gives us a holistic understanding of how inflammation is a principal driver of plaque-associated periodontitis.

21. Lee and co-workers described the temporal dynamics of inflammation-induced dysbiosis of the periodontal microbiota and the impact of RvE1 in rat experimental periodontitis. Topical application of RvE1 in rat periodontitis induced significant regeneration of lost periodontal soft tissues and bone. The shifts in the local microbiota induced by inflammation were markedly rescued by RvE1. These results illustrate two biological principles: (1) local environmental conditions impact the composition of the microbiota (2) the impact of inflammation on the microbiome is modifiable. These changes are not observed with inhibition of inflammation with NSAIDs or other inhibitors of inflammation

22. MODELS OF DISEASE PROGRESSION Disease progression can be considered as an indispensable part of periodontal disease pathogenesis. Therefore, the knowledge of models of periodontal disease progression becomes paramount to ensure opportune diagnosis and treatment.

23. CONTINUOUS MODEL The continuous model describes chronic destructive periodontal disease as slow, continual, and progressive in nature. Certain sites are depicted as not changing throughout an individual’s life, and other sites demonstrate the initiation of attachment loss at different times in an individual’s life.

24. RANDOM BURST MODEL The random burst model incorporates the concept of bursts of activity, where the attachment loss is considered as a measure of the cumulative effect of multiple disease episodes. Disease activity is depicted as occurring at random, at any site, where some sites show no activity, while others show one or several bursts of activity.

25. ASYNCHRONOUS MULTIPLE BURST MODEL This model is an extension to random burst model where the major difference from the preceding one is that multiple sites show breakdown within a reasonably short period of an individual’s life with prolonged periods of remission.

26. CONCLUSION Over the past few years a number of models describing the pathogenesis of periodontal disease have been presented based on existing knowledge at that time. The more recently explored biologic systems approach to modeling holds promise for revolutionizing conceptual models of the past by providing a comprehensive view of the disease process as a complex regulatory network. Continuous research is needed to further explore and identify regulatory pathways and molecules at the interface of host and pathogen interactions.

27. This arms us with knowledge to tailor preventive and therapeutic strategies based on an individual’s unique biology and risk profiles. We can hope that the pathogenesis models simplify this while embracing the essential facts and highlighting the key aspects that need the main focus, thus serving the true purpose of these models.

28. REFERENCES Avula H, Chakravarthy Y. Models of periodontal disease pathogenesis: A journey through time. Journal of Indian Society of Periodontology. 2022 May;26(3):204. Kenneth S. Kornman Mapping the Pathogenesis of Periodontitis: A New Look J Periodontol 2008; 79:1560-8 Holt SC, Ebersole JL. Porphyromonas gingivalis , Treponema denticola , and Tannerella forsythia:the “red complex”, a prototype polybacterial pathogenic consortium in periodontitis. Periodontol 2000. 2005; 38:72– 122. Page RC, Kornman KS. The pathogenesis of human periodontitis: An introduction. Periodontol 2000 1997; 14:9-11 Socransky SS, Haffajee AD, Cugini MA, Smith C, Kent RL Jr. Microbial complexes in subgingival plaque. J Clin Periodontol . 1998; 25:134–44

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