Periodontology Lecture Notes PDF

 Pathogenesis of Periodontal diseases What is the definition of pathogenesis? The development of disease and the chain of events that led to that disease. Etiology of periodontal disease -Complex interplay between bacteria in dental plaque and the host tissues. -Bacterial...

 Pathogenesis of Periodontal diseases What is the definition of pathogenesis? The development of disease and the chain of events that led to that disease. Etiology of periodontal disease -Complex interplay between bacteria in dental plaque and the host tissues. -Bacterial plaque induces host inflammatory response = plaque is the initiating factor (Etiology) for periodontal disease. -So, what really causes the periodontal destruction in periodontal disease? The immunity!! In the presence of plaque! Bacterial Plaque -Definition: it is the diverse microbial community found on the tooth surface embedded in a matrix of polymers of bacterial and salivary origin (Marsh and Martin 1992). -Plaque Exist in the form of a biofilm. -The main nutrients for bacterial plaque is derived from saliva and GCF.  plaque disclosing agent Calculus -Calculus covered by plaque and inducing an inflammatory response in periodontal tissues. -Calculus is a predisposing(risk) factor for periodontal disease. Because it is hard and rough. The Plaque Biofilm is Composed of: A- Water (80-90%). B- Microorganisms (70% of dry weight). --> Main component if we removed the water. C- Intercellular matrix (20-30% of plaque mass) consisting of organic (polysaccharides, proteins, glycoproteins,lipids) and inorganic materials (phosphorus and calcium) derived from saliva, GCF and bacterial products. D- Open fluid-filled channels running through the plaque mass. Specificity of the dentition Q- Why does bacteria accumulate for prolonged periods of time on tooth surfaces and thus cause disease, but not on other parts of the body? 1-Because teeth are the only hard organ exposed to the environment (Not covered) 2- Teeth penetrate epithelium (Not covered by epithelium). 3- Also, teeth they are non-shedding surfaces. Plaque formation phases: Mechanism of Plaque formation phases : 1) The formation of a conditioning film (the acquired pellicle) on the tooth surface; 2) A non-specific reversible phase involving physico chemical interactions between salivary bacteria and the acquired pellicle; 3) Short-range specific stereo-chemical molecular interactions between primary bacterial colonisers and host receptor molecules in the acquired pellicle; 4) The attachment of secondary colonisers to already attached primary colonisers (co- aggregation); 5) Growth and the formation of a climax community Now let’s talk about each phase in detail: 1. Formation of acquired pellicle: -As soon as a tooth has been cleaned, host and bacterial molecules are selectively adsorbed on to the enamel surface to form a conditioning film (aquired pellicle) -This film is usually < 1 /um thick, and it takes 90-120 min for the adsorption of molecules to reach a plateau. -The conditioning film (Acquired pellicle) contains proteins, glycoproteins, lipids and glycolipids derived from saliva, as well as extra cellular molecules from bacteria. -These adsorbed molecules can act as receptors or adhesins for oral bacteria, and  therefore selectively influence the pattern of biofilm development. -Note: the bacteria in this phase is planktonic bacteria. 2. a non-specific reversible chemical interactions between salivary bacteria and the acquired enamel pellicle: - Relatively few oral bacteria are motile; generally, microorganisms are transported passively to the tooth surface by the force of saliva flow. The process starts with cocci bacteria--- → then rods. -They are called the primary colonizers. --> They are predominantly gram-positive facultative spp. -As the cell approaches pellicle coated enamel, long range physico- chemical forces combine to provide a weak, non-specific area of attraction. -The strength of this interaction is relatively weak, and this phase of attachment is reversible. 3. Short-range specific stereo-chemical molecular interactions between primary colonisers and host receptor molecules in the acquired pellicle: 4. Attachment of secondary colonisers to already attached primary colonisers (co- aggregation): -Plaque accumulation is enhanced by intra- and inter-genetic co-aggregation between the primary colonisersand the secondary colonizers Some bacteria can act as co aggregation bridges between otherwise non-coaggregating species. -Example: Fusobacteria: This bacteria co-aggregate with the widerange of bacteria Secondary colonizers are gram-negative anaerobic spp: 5. growth and the formation of a climax community (Maturation) : -In a dental biofilm, bacteria are in close proximity with one another and willinteract as a consequence. -Some of the interactions will be beneficial, and facilitate the development of food chains.  -Other interactions may lead to the degradation of complex host molecules. As plaque mass increases, the beneficial buffering and antimicrobial properties of saliva are less able to penetrate and protect enamel. -Also, an antibiotic for example can't enter the biofilm through its channels (Filtration mechanism). The current model of periodontitis pathogenesis -Definition of periodontitis: Tonetti et al 2018, new classification: chronic multifactorial inflammatory disease associated with dysbiotic plaque biofilm that results in progressive periodontal attachment loss and bone destruction. -Disease results from complex interactions between the biofilm and the inflammatory immune response, and it is the latter that is estimated to account for almost 80% of the risk of periodontal tissue damage. -Immune response in gingivitis is proportionate, but here there is dysbiosis. -In Periodontitis, there will be frank dysbiosis and there will be disproportional inflammatory response (hyper inflammatory response). The stages of Pathogenesis of biofilm induced gingivitis and periodontitis Pristine gingiva versus clinically healthy gingiva: Pristine gingivae, free from any histological inflammation are extremely difficult to achieve without extreme measures of fastidious plaque control. ‘Clinically healthy gingiva’ is a term used to describe the level of gingival health attained by patients practising a meticulous standard of oral hygiene. Nevertheless, an initial inflammatory lesion can form at a histological level following plaque biofilm formation even in such motivated patients Initial lesion (Stage 1) Inflammation begins within 24 hours of plaque accumulation, The cellular response develops in 2–4 days. Gingiva appear clinically healthy Early lesion (stage 2): after about 4-7 days of plaque accumulation, the early lesion develops: Mild redness of the gingiva and clinical signs of inflammation. An increase in lymphocytes and neutrophils occurs. Lymphocytes predominate. Early signs of cell and collagen damage. Rete pegs proliferation in junctional epithelium in attempt to maintain the epithelial barrier function. -The early lesion can persist without shifting to established gingivitis. Established lesion (stage III) -It is difficult to predict when this stage of the lesion will develop, but usually it does between 2-3 weeks. it involves the following: Plasma cells & B lymphocytes predominate The junctional epithelium is no longer attached closely to the tooth and has transformed into a pocket epithelium (gingival ‘false’ pocket). This allows the subgingival plaque to extend more apically. Clinical features of gingivitis become obvious. -Established lesion may remain stable or may become active and progress to periodontitis. Advanced lesion (Stage 4) Plasma cells dominate and constitute >50% of the cell types. Loss of periodontal connective tissue attachment. Apical migration of the junctional epithelium and the formation of a true periodontal pocket. Alveolar bone loss. Initial Lesion Early lesion Established lesion Advanced lesion Periodontal Health Recap: 1- No inflammation/ bleeding 2- No recession 3- No deep pockets (1-3 mm sulcus) 4- Distance between bone and CEJ = 2 mm False Pocket (Psuedo pocket): -Pocket > 3 mm -No CAL (attachment loss) -No bone loss. -caused by gingival enlargement -This is not periodontitis. Periodontitis scenario 1: -Clinical attachment loss (CAL) -Deep pocket >3 mm -Bone loss -No recession. Periodontitis Scenario 2: -Clinical Attachment loss (CAL) -No deep pocket (2mm here) -There is recession (2mm for example) -Bone loss. Periodontitis Scenario 3: -No recession (Gingival margin is 1 mm above CEJ) -No deep pocket (the depth of the sulcus is 3 mm) -yet there is 2 mm CAL -There is bone loss. -Happens when the base of the sulcus is below the CEJ! Summary: -CAL (clinical attachment loss) in periodontitis patients may manifest itself in one of the three patterns: 1- deep periodontal pockets. 2- Recession. 3- Combination (Pocket + recession, happens in advanced cases) -However, mild attachment loss (CAL) of 1-2mm may occur without deep pockets or recession, as explained previously.