Unit 22. Gingivitis and periodontitis.pdf

Microbiology Unit 22 Microbiology of gingivitis and periodontitis Ve más allá 1 CONCEPTS  Gingivitis is the inflammation of soft tissues around the teeth, primarily the gum, without extending to the cement, periodontal ligament and alveolar bone.  Periodontitis is the inflammation of the tissue...

Microbiology Unit 22 Microbiology of gingivitis and periodontitis Ve más allá 1 CONCEPTS  Gingivitis is the inflammation of soft tissues around the teeth, primarily the gum, without extending to the cement, periodontal ligament and alveolar bone.  Periodontitis is the inflammation of the tissues supporting the teeth, characterized by a progressively destructive changes with loss of bone and periodontal ligament, by extension of inflammation from the gingiva.  Both entities are called periodontal diseases which are infectious processes affecting the supporting tissues of the teeth. ETIOLOGY OF PERIDONTAL DISEASE Gingivitis Produced by bacterial plaque • Universal, affects the entire population. • Reversible, outbreaks with varying intensity. • Produced by inadequate control of the plaque. • Polymicrobial origin. • The predisposing factors of the host are very important: metabolic disorders, blood dyscrasias, drugs consumption. No plaque-induced • Uncommon. • More often gingivostomatitis than pure gingivitis. • Herpes simplex, herpes zoster, candidosis, syphilis, etc. ETIOLOGY OF PERIDONTAL DISEASE Periodontitis  Adult periodontitis  The most frequent.  Slow evolution.  Porphyromonas gingivalis, Prevotella intermedia/Prevotella nigrescens, less frequent Aggregatibacter (Actinobacillus) actinomycetemcomitans. Early-onset peridontitis  Beginning in children and young people.  Less frequent, more rapid evolution, bad response to treatment.  Predominantly: Aggregatibacter (Actinobacillus) actinomycetemcomitans. Periodontitis associated with systemic diseases  Diseases that alter immunosuppression) the host response (AIDS, diabetes, Necrotizing periodontal diseases  Involvement of various bacterial associations, frequently treponemes and P. intermedia/P. nigrescens. ETIOLOGY OF PERIDONTAL DISEASE • Porphyromonas gingivalis • Aggregatibacter actinomycetemcomitans • Prevotella intermedia/Prevotella nigrescens • Fusobacterium nucleatum • Peptostreptococcus micros • Treponema denticola • Campylobacter rectus • Eikenella corrodens • Eubacterium • Tannerella forsythia • … ETIOLOGY OF PERIDONTAL DISEASE Clusters or microbial complex: • Bacteria act in a synergistic way • Predominates in subgingival plaque • Described by Socransky S. (Periodontology, 2000, 38-185, 20) • 5 microbial groups classified by colors: purple, yellow, green, red and orange • In subgingival plaque: initial colonization is due to the complex yellow and purple; later, green and orange become predominant and make a linkage between the earlier and later colonizers (red) • In advanced stages: orange and red complexes predominate, which are those associated with gingivitis and periodontitis ETIOLOGY OF PERIDONTAL DISEASE Clusters or microbial complex: J Am Dent Assoc 2006;137;10S-15S (Tannerella forsythia = Bacteroides forsythus) TYPES OF PERIODONTAL INFECTIONS ACCORDING TO THE ETHIOLOGY  True infections: Pathogens with high etiological association, that are not usually isolated in healthy areas. Exogenous infections: A. actinomycetemcomitans and P. gingivalis.  Infections by an increase of commensal bacteria: Bacteria of the normal microbiota. Usually nonpathogenic, but they become pathogenic when the load increases. Endogenous infections. P. intermedia, Peptostreptococcus micros, Fusobacterium nucleatum, Campylobacter rectus, Eikenella corrodens, Eubacterium spp., and treponemes.  Superinfection: Unusual pathogens in the oral microbiota together with existing pathogens collaborate on periodontal destruction. Enterobacter spp., E. coli, Pseudomonas spp., Staphylococcus spp., Candida spp. etc. TYPES OF PERIODONTAL INFECTIONS Resident microorganisms P. intermedia F. nucleatum C. rectus E. corrodens Eubacterium, etc. Immunocompromised host Opportunistic infection Infection by overgrowth of commensal bacteria Exogen microorganisms Superinfection E. coli Enterobacter spp. Pseudomonas spp. Staphylococcus spp. Candida spp., etc. Healthy carrier True infection P. gingivalis A. actinomycetemcomitans PATHOGENY OF PERIODONTAL DISEASE Gingivitis  When the accumulation of plaque and supragingival calculus exceed the capacity of defensive response in tissues, an inflammatory process occurs, which is a characteristic of gingivitis.  Cause-effect relationship.  Reversible by removing plaque. Periodontitis  It is a more complex process. It is also infectious but not by the mere accumulation of bacteria.  Involves the presence of certain bacteria in subgingival plaque acting on a susceptible host.  Importance of individual susceptibility.  Importance of biological risk factors and environmental factors. PATHOGENY OF PERIODONTAL DISEASE  Pathogenic mechanisms associated with bacteria  Direct pathogenicity: by the microorganism itself.  Pathogenic mechanisms associated with the host  Indirect pathogenicity: by induction of the immune response  Normal response  Pathological response  Hyperesponse  Hyporesponse  Risk factors in the genesis of periodontitis PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with bacteria  Direct pathogenicity  Tissue damage.  Invasion of tissues.  Ability to evade the host response. PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with bacteria Direct pathogenicity: 1. Tissue damage  Exotoxins: Epitheliotoxins, favor microbial development. Aggregatibacter actinomycetemcomitans, Capnocytophaga spp.  Endotoxins: Initiate the inflammatory process by activating the complement alternative pathway and macrophages.  Exoenzymes: Porphyromonas gingivalis produces gingi-pains that destroy collagen in the periodontal ligament.  Toxic metabolites: butyric acid, propionic acid, ammonia, indole etc. Produced by many species but Fusobacterium nucleatum is one of the most butyric acid and sulfur compounds producers. PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with bacteria 2. Tissue invasion  Different bacteria can invade the periodontal tissue  Treponemes invade the connective tissue in acute ulcerative gingivoperiodontitis (ANUG) 3. Evasion of host response  Destruction of PMN by leukotoxins  Chemotactic inhibition of PMN  Destruction of components of the complement system and immunoglobulins  Inhibition of B cells (decrease of antibodies)  Toxic action on monocytes and lymphocytes PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with the host  The indirect pathogenicity of the plaque bacterial flora is related to its ability to induce an inflammatory response in periodontal tissues.  The damage will be related to the balance between factors that trigger harmful phenomena and factors that neutralize them.  Two types of situations:  Normal response.  Pathological response either excessive or deficient. PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with the host Pathological response: Hyperresponsiveness B cell activation: production of Ab Activation of macrophages INFLAMMATION Complement activation When the inflammation occurs:  Bone destruction, osteoclast activation.  Tissue damage by production of proteases, collagenases and elastases. PATHOGENY OF PERIODONTAL DISEASE Pathogenic mechanisms associated with the host Pathological response: hyporesponsiveness The host response is unable to control bacterial activity: Increased aggressiveness, faster evolution. PATHOGENY OF PERIODONTAL DISEASE Risk factors in the genesis of periodontitis  Different individual susceptibility to develop destructive periodontal disease, although the presence of bacteria is the same.  There are some risk factors associated with periodontitis:  Behavioral factors: Smoking (decreased immunity), stress (increased cortisol in saliva), lack of hygiene (plaque development)  Genetic factors: Deficit overproduction of IL-1. of complement, Ig deficiency,  Added factors: Multiple and varied, local and systemic factors. Occlusion trauma, Diabetes, AIDS, leukemia, immunosuppressive therapy etc. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE  The infectious origin of periodontal diseases is well known.  Over 300 species can be isolated from periodontal pockets but only a few are etiologically important.  The polymicrobial nature makes difficult to establish causality.  Socransky established a series of assumptions (adaptation of Koch's postulates) DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE Socransky's postulates: • Association with disease: relative increase of pathogens in the affected tissues in comparison with healthy tissues. • Elimination of the pathogens should interrupt the disease. • Modification of the specific humoral or cellular response to certain species will suggest the participation of these bacteria. • Implantation of the pathogen in the gingival sulcus of an animal will induce the production of some of the characteristics of the disease. • The microorganisms must have some of the virulence factors that justify the initiation and progression of periodontitis. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE So...  The hypothesis of nonspecific plaque (variation only quantitative and not qualitative) has been replaced by the specific plaque hypothesis (a small number of specific bacteria with a low presence in healthy tissues, are those that cause disease). The introduction of more sensitive and specific diagnostic methods help to increase the knowledge about periodontal disease progression. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE Diagnostic methods 1 - Peripheral blood markers. Allows to know aspects of the responsiveness of the host.  Specific antibodies in serum and its avidity for antigens: especially against :  P. gingivalis  A. actinomycetemcomitans. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE Diagnostic methods 2 - Analysis of gingival fluid: Easy to make, minimal patient discomfort.  Detection of PGE2 and interleukins, secreted by macrophages. Related with bone loss and active periodontal lesions.  Proteolytic enzymes such as collagenase, gelatinase, hyaluronidases, chondroitin sulfatases, etc. They are useful as indicators of destruction activity of connective tissue. For example: a trypsin-like positive reaction indicates the presence of Porphyromonas gingivalis, Treponema denticola, and Bacteroides forsythus (BANA test).  Detection of intracytoplasmic enzymes, help to monitor periodontal disease. They are released when cell destruction occurs. Aspartate aminotransferase (AST), lactate dehydrogenase (LDH), alkaline phosphatase, etc. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE Diagnostic methods 3 - Detection of specific bacteria from the periodontal pocket.  There are several techniques: DNA probes, monoclonal antibodies etc.  Establishment of threshold levels of insertion loss. For example 3x104 CUF for A. actinomycetemcomitans or 6x105 CFU for P. gingivalis.  There is no culture of specimens from all patients only those who poorly respond to treatment or implants. DIAGNOSTIC IMPLICATIONS OF PERIODONTAL DISEASE Diagnostic methods 4 - Sampling.  Isolate the area with cotton.  Dry the crown and the gingival margin.  Drag supragingival plaque with sterile cotton and Gracey curettes.  To take the sample:  With an abrasive wire inserted into the periodontal pocket through a hollow needle: The sample is taken after the wire is retracted within the needle to protect from contamination of the oral cavity.  Absorbent paper points or capillaries. Collected by capillarity from the periodontal pockets gingival fluid.  Processed immediately or placed in appropriate transport media. THANKS FOR YOUR KIND ATTENTION! QUESTIONS PLEASE? Ve más allá © Copyright Universidad Europea. Todos los derechos reservados