Diseases of periodontium. Markéta Hermanová toothdiagram nGingivitis: inflammatory lesions confined to marginal gingiva n nPeriodontitis: lesions associated with destruction of the connective tissue attachment of the tooth and loss of alveolar bone n gingivitis Gingivitis-0-400-0-400 Epidemiology of periodontal disease nEarly periodontitis involves some of the teeth in the majority of adults nThe prevalence of pocketing/loss of attachment increases with age nThe proportion of teeth affected by periodontitis increases with age nAdvanced periodontal disease affects only a small percentage of the population Classification of plaque-associated periodontal diseases nGingivitis -Associated with dental plaque only -Modified by systemic factors -Modified by medication -Modified by malnutrition nChronic periodontitis -Localised -Generalised nAggressive periodontitis -Localised -Generalised nPeriodontitis in systemic diseases -Immunocompromised patients -Genetic disorders n Based on International Workshop for a Classification of Periodontal Diseases and Conditions, 1999 Plaque microorganisms in health, gingivitis, and periodontitis Main species % aerobic/ anaerobic % Gram+/ Gram - Motile/ non-motile Healthy gingiva Streptococcus Actinomyces 75/25 90/10 1:40 Chronic gingivitis Actinomyces Streptococcus Porphyromonas Prevotella 60/40 65/35 Number of motile rods and spirochaetes increases with disease Chronic periodontitis Actinobacillus Porphyromonas Bacteroides Prevotella Fusobacterium 20/80 25/75 1:1 Abundant motile rods and spirochaetes Summary: microbiology of periodontal disease nGram-positive cocci decrease as gingivitis progresses to periodontitis nGram-negative anaerobic bacilli increase as disease progresses nMotile forms increase as disease progresses nPeriodontal disease involves interactions of mixtures of bacteria forming complexes in plaque nCertain species (periodontal pathogens) are prevalent in destructive lesions Other risk factors for periodontal diseases nLocal factors -pre-existing anatomy of the teeth, gingiva, and alveolar bone -alignment and occlusal relationships of teeth nSystemic factors -Diabetes mellitus -Pregnancy and sex hormones -Nutrition (avitaminosis C) -Blood diseases -Drugs -AIDS -Smoking n Drugs affecting periodontal tissues and the activity of periodontal disease Anti-epileptics Phenytoin Gingival hyperplasia Immunosuppressants Azathioprine Corticosteroids Cyclosporin Equivocal reduction of disease activity Gingival hyperplasia Non-steroidal anti-inflammatory drugs Indomethacin Ibuprofen Equivocal reduction of disease activity Calcium channel blockers Nifedipine Verapamil Gingival hyperplasia Sex hormones Oestrogen Progesterone Exacerbation of pre-existing gingivitis Host-parasite equilibrium at the plaque-gingival interface: chronic periodontal disease = disturbance of this balance = a dynamic process reflecting changes in the balance of the host-parasite relationship with time Microbial plaque Host defences Direct injury Toxic products Enzymes Antigenic challange Salivary factors Crevicular fluid Epithelial barrier Migrating neutrophils Immune response Potential for tissue regeneration and repair Initial gingivitis nMicroscopic area around base of gingival sulcus nAcute inflammatory changes -Cellular exudate: enhanced migration of neutrophils -Fluid exudate: increased crevicular fluid flow -Number of chemical mediators of inflammation responsible n Early gingivits nLymphocytic infiltration nImpairment of barrier function of junctional epithelium nGingival pocket formation; growth of subgingival plaque Established gingivitis nExpansion of area of inflammation and destruction of gingival connective tissue nPredominance of plasma cells in inflammatory infiltrate nDeepening of gingival pocket; thining/ulceration of pocket epithelium Chronic periodontitis nApical extension of destructive inflammation nLoss of connective tissue attachment and destruction of alveolar bone nApical migration of junctional epithelium and pocket formation nPeriods of quiscence/stability; random bursts of destructive activity Degradation of the extracellular matrix (ECM) of gingiva, periodontal ligaments, and the destruction alveolar bone nMatrix metallo-proteinases (MMPs) degrade ECM nTissue inhibitors of metalloproteinases (TIMPs) inhibit MMPs nActivity of MMPs and TIMPs in balance in health nIncreased MMPs activity in disease; reflects fluctuations in cytokine activity (IL-1) nLocal mediators affecting bone resorption: -Cytokines (IL-1, IL-6, TNF) -Prostaglandins (PGE2) -Growth factors (e.g. from osteblasts which regulate the osteoclast recruitment) n n Pathogenesis of periodontal disease nDisturbance of host-parasite balance nActivation of host inflammatory and immune response nEnhanced synthesis of inflammatory mediators/cytokines nPeriodontal connective tissue degradation/bone resorption nNew equilibrium in host-parasite realtionship as host response contains the challange for plaque bacteria n Clinical forms of periodontitis nChronic periodontitis nAggressive periodontitis nPeriodontitis in systemic disease Aggressive periodontitis nUsually juvenile nF>M nRapid destruction of alveolar bone, vertical bone loss, deep intrabony pockets nFirst molars and/or maxillary incisors nPathogenesis obscure; inflammatory and bacterial plaque??? (G-anaerobic rods (Actinobacillus actinomycetemcomitans), genetic factors, abnormalities in cell-mediated immunity) n Necrotizing ulcerative gingivitis/parodontitis/stomatitis/noma nPolymicrobial, endogennous infection: anaerobic bacteria, particularly Fusobacteria and spirochete species (Treponema, Prevotella, Porphyromonas, Selenomonas, Fusonacterium sp) n nPredisposing factors: -poor oral hygiene, preexisting gingivits -smoking -poor nutrition -psychological stress -weakened immune system, immunodeficiences, dysfunctions of neutrophils n nMalaise, fever, cervical lymphadenopathy n n (NOMA) Periodontitis in systemic diseases nDiseases associated with major abnormalities of neutrophils -Agranulocytosis -Cyclic neutropenia (AD, mutation in the gene for neutrophil elastase) -Chediak-Higashi syndrome (AR, mutation in lysosomal trafficing regulatore gene) -Job syndrome (hyper IgE syndrome, hereditary) nDiseases in which there may be associated neutrophils dysfunctions -Papillon-Lefevre syndrome (palmar and plantar hyperkeratosis, severe periodontal destruction; AR, mutation in lysosomal enzyme cathepsin C gene) -Down syndrome -Juvenile-onset diabetes mellitus nOther systemic diseases -Hypophosphatasia -Langerhans cell histiocytosis (histiocytosis X) -Ehlers-Danlos syndrome Gingival enlargement nFibrous overgrowths -Gingival fibromatosis (hereditary, AD) -Chronic hyperplastic gingivitis -Drug associated hyperplasia (epanutin (anti-epilepticum), verapamil, nifedipin (cardiovascular diseases), cyclosporin (immunosuppressive drug)) nOedematous enlargement n- Oedematous gingivitis in puberty, pregnancy, oral contraceptives, scurvy (avitaminosis C) nSystemic disease -Acute leukaemias -Wegener´s granulomatosis Desquamative gingivitis nGingival manifestation of several different diseases: -Mucous membrane pemphigoid -Lichen planus -Local hypersensitivity reaction -Orofacial granulomatosis (in Crohn´s disease, sarcoidosis, other causes of granulomatous inflammation (infection, foreign bodies), idiopathic, Melkersson-Rosenthal syndrome (recurring facial paralysis, swelling of the face and lips, and the development of folds and furrows in the tongue), allergic reaction,…) Thank you for your attention …