Immunopathogenesis of Periodontal Disease PDF

Immunopathogenesis of Periodontal Disease WLHSDM Peer Mentoring — Michael Lou 10/19/2023 Contact Info Email: [email protected] Cell phone #: (972) 400-2472 Please feel free to reach out to me anytime for 1-on-1 tutoring! Google drive folder link (presentation & notes) ht...

Immunopathogenesis of Periodontal Disease WLHSDM Peer Mentoring — Michael Lou 10/19/2023 Contact Info Email: [email protected] Cell phone #: (972) 400-2472 Please feel free to reach out to me anytime for 1-on-1 tutoring! Google drive folder link (presentation & notes) https://drive.google.com/drive/folders/1x_6kOWSBZWCQ7as-TwhRMyhG0hZxaEnr?usp=share_link  The attached gingiva is keratinized (but decreases keratin expression upon exposure to bacteria) Periodontitis is characterized by bone loss This bone loss can progress to tooth loss Dental biofilm is the cause (etiologic agent) of both gingivitis and periodontitis  Oral epithelial cells express all 10 types of Toll-like receptors (TLRs) which detect patterns associated with bacteria, leading to the release of IL-1 and IL-8 (implicated in periodontitis)  Oral epithelial cells also express NOD1 and NOD2 pattern recognition receptors which also detect bacteria (NOD1 detects gram negative bacterial cell walls and NOD2 detects both gram + and - cell walls)  Upon activation, immune system tries to defend the body against biofilm pathogens by deploying weapons such as: Complement White blood cells proteins (like neutrophils)  Complement proteins are found in gingival crevicular fluid (secreted into the gingival sulcus)  The complement system is activated upon contact with biofilm bacteria, eventually leading to the release of C3a and C5a (the anaphylatoxins)  C5a and C3a diffuse back into the body where they call for reinforcements (such as neutrophils) to enter the gingival sulcus For these neutrophils to pass through the gingival epithelium to the sulcus, the epithelial barrier needs to become more permeable (aided by damage to the epithelial barrier by bacterial toxins) Biofilm bacteria are resistant to phagocytosis by neutrophils  As a result, neutrophils opt instead to self-destruct, releasing damaging molecules that can cause a lot of collateral damage to the gingiva This self-inflicted damage contributes to gingivitis (sometimes progressing to periodontitis) It’s very hard to predict whether gingivitis will progress to periodontitis However, periodontitis is associated with having a large Th2 and B cell population  There are four stages of periodontitis: 1. Initial lesion (2-4 days) ○ No clinical symptoms yet ○ Complement activation and neutrophil chemotaxis occurs (innate immunity) 2. Early (stable) lesion (4-10 days) ○ Earliest clinical symptoms ○ Lymphocytes arrive (adaptive immunity) ○ Patients may stay in this stage indefinitely  There are four stages of periodontitis: 3. Established (progressive) lesion (2-3 weeks) ○ Plasma cells predominate ○ Bone loss begins (still not overt clinically) ○ Not all patients progress to this stage 4. Advanced lesion ○ Overt loss of bone and clinical attachment (periodontitis) What factors decide if a patient will progress from gingivitis (inflammation only) to periodontitis (bone loss)? ○ Bacterial composition of biofilm P. gingivalis appears to play a role ○ External factors (e.g. smoking) ○ Age ○ Genetics Thank you!! Please scan here to fill out the feedback form! :)