Etiology Of Periodontal Diseases PDF

Etiology Of Periodontal Diseases By/ Shaimaa Hamdy  Introduction Periodontal diseases are an inflammatory disorder in which tissue damage occurs through complex interactions between periodontal pathogens and components of the host mechanisms Periodontal diseases are a persistent polyba...

Etiology Of Periodontal Diseases By/ Shaimaa Hamdy  Introduction Periodontal diseases are an inflammatory disorder in which tissue damage occurs through complex interactions between periodontal pathogens and components of the host mechanisms Periodontal diseases are a persistent polybacterial infection causing chronic inflammation in periodontal tissues Periodontitis is multi-factorial disease that cause tooth loss 2 Definition: Etiology: The cause or origin of a disease or condition. In medical contexts, it involves understanding the various factors that contribute to the onset and progression of illnesses. The term is derived from the Greek words "aitia," meaning cause, and "logia," meaning study. 3 Why etiology of periodontal diseases is needed to be well understood ? because of two major reasons: First, identification of etiological agents of periodontal diseases would help in determination of suitable treatment strategies. Second, it would provide a useful therapeutic approach to control and prevent periodontal diseases, e.g., manufacturing of vaccines. 4 Etiology of periodontal disease Initiating factor Local predisposing factors Systemic predisposing factors 5  Initiating factor Dental plaque (Biofilm( 6  Local predisposing factors 1. Calculus 2. Margins of Restorations 3. Malocclusion 4. Associated With Orthodontic Therapy 5. Habits. 6. Smokeless Tobacco 7. Iatrogenic Factors 7  Systemic predisposing factors Identifying smoking and diabetes as the major potential risk factors that can alter the staging of periodontal disease. Recognition of “periodontitis as a manifestation of systemic disease” such as Papillon Lefèvre Syndrome. Systemic conditions affecting the periodontium when not related to dental plaque will be considered as “Systemic Diseases or Conditions Affecting the Periodontal Supporting Tissues”. 8  Initiating factor bacterial dental plaque(Biofilm) (periodontal microbiology) Definition Types of dental plaque (Biofilm) Composition of dental biofilm Formation of dental biofilm Association of plaque bacteria with periodontal disease Bacteria associated with periodontal health Microorganism associated with specific periodontal diseases The putative periodontal pathogens include 9  1. Dental plaque(Biofilm) definition: Biofilm are defined as matrix enclosed bacterial population adherent to each other and /or to tooth surface. as the soft yellow –grayish, dense, non calcified microbial mass or deposits that form the biofilm firmly adhering to the tooth surface or other hard surfaces in the oral cavity , including removable and fixed restorations. It resist to removed by rinsing or spray. It has to be mechanically removed. Dental plaque is a host – associated biofilm. 10  Dental biofilm may be seen on the teeth after 1 to 2 days with no oral hygiene. During from 5 to 7 days if there is no hygiene of the oral cavity the signs of the inflammation appear. In any one individual, 1 gram of mature dental plaque may contain around 2 × 1011 bacterial cells, belonging to 700 species Dental plaque has to be differentiated from other deposits that found on tooth surfaces such as : Materia alba ,dental pellicle , calculus. 11  Materia alba Dental plaque Calculus White cheese like soft yellow -grayish Hard deposit that forms accumulation deposits that form the by mineralization of A soft accumulation of biofilm firmly adhering to dental plaque salivary proteins ,some the tooth surface Generally covered by a bacteria ,many desquamated Primarily composed of layer of un-minralized epithelial cells ,and bacteria in a matrix of dental plaque occasional disintegrating salivary glycoprotein's and food debris extracellular polysaccharides Lacks organized structure Impossible to remove by and is therefore not as rinsing or the use of sprays complex as dental plaque. Easily displaced with a water spray. 12 2. Types and composition of dental biofilm Based on its relationship to the gingival margin, biofilm is differentiated into two categories : 1. supragingival biofilm 2. subgingival biofilm 14  Types of dental biofilm Subgingival Supragingival biofilm biofilm attached unattached Coronal Marginal biofilm biofilm biofilm biofilm Tooth associated Epithelium associated Connective tissue associated 15  1- Supragingival biofilm Types Supra-gingival biofilm ▪ Clinically detected by: ▪ it can be detected clinically only after it reached a certain thickness after 1 to 2 days with no oral hygiene..small amount of plaque detected by using Disclosing agent. ▪ Color ▪Grey to yellowish-grey ▪ Location ▪At or above the gingival margin ▪ Composition (matrix) ▪50% matrix ▪ Flora ▪Mostly gram positive ▪ Motile bacteria ▪Few ▪ Anaerobic/ aerobic ▪Aerobic unless thick ▪ Metabolism ▪Predominantly carbohydrates ✓ Types ✓Coronal plaque: only on tooth surface ✓Marginal plaque: which is associated with the tooth surface at the gingival margin 16  1- Supragingival biofilm It can be detected clinically only after it has reached a certain thickness. Small amounts of plaque can be visualized by using disclosing agents. The rate of formation and location of plaque vary among individuals and is influenced by: Diet. Age. Salivary secretion oral hygiene. Tooth alignment. systemic diseases and host factors. 17 disclosing agents. 18 19  2- Subgingival biofilm Types Subgingival biofilm ▪ Clinically detected by: ▪ Identified only by running the end of a probe around gingival margin ▪ Color ▪ brown, black or green ▪ Location ▪ Within the gingival sulci or periodontal pocket ▪ Composition (matrix) ▪ Little or no matrix ▪ Flora ▪ mostly gram negative ▪ Motile bacteria ▪ Common ▪ Anaerobic/ aerobic ▪ Highly anaerobic ▪ Metabolism ▪ Predominantly proteins ✓ Types ✓ Unattached ✓ Attached(tooth associated, epithelium associated, connective tissue associated) 20  2-Subgingival biofilm It is usually thin, contained within the gingival sulci or periodontal pocket and thus CANNOT be detected by direct observation. Its presence can be identified only by running the end of a probe around gingival margin 21 22  N.B Plaque can be assessed by Direct vision Supragingival biofilm Using disclosing agents Subgingival biofilm running the end of a probe around gingival margin 23  3. COMPOSITION of dental biofilm Dental plaque is mainly composed of microorganisms. The material present between the bacteria in the dental plaque is called as intermicrobial matrix 1. Bacteria I. Microorganisms 2. non-bacterial 1. Organic material II. Intercellular 2. Inorganic material matrix 24 25  I. Microorganisms Bacterial: There are approximately 700 distinct bacterial species and 1 mg of dental plaque contains approximately 2 × 1011 bacteria. Nonbacterial: 1. Mycoplasma 2. Yeasts 3. protozoa 4. viruses. 26  II. Intercellular matrix: Accounts for 20% to 30% of the biofilm mass Organic and inorganic materials Derived from: 1. Saliva. 2. Gingival crevicular fluid. 3. Bacterial products. 27  Organic components Carbohydrates Proteins Lipids 28 29  4. Formation of dental biofilm The biofilm formation is divided into three phases: 1. Enamel Pellicle formation 2. Initial Adhesion/Attachment of Bacteria 3. Colonization and Biofilm Maturation 30  Location and rate of plaque differ from one person to another depending on : 1. Oral hygiene 2. salivary composition and flow rate 3. diet. 1. Acquired Enamel Pellicle formation ❑ Acquired Enamel pellicle: a homogenous, membranous, acellular film that covers the tooth surface and frequently form the interface between the tooth & the dental biofilm. ❑ Derived from components of: 1. saliva and crevicular fluid 2. as well as bacterial and host tissue cell products 3. and food debris 31 ▪ the initial organic structure that forms on the surfaces of the teeth and artificial prosthesis. ▪ The first stage in pellicle formation involves adsorption of salivary proteins to apatite surfaces. The acquired enamel pellicle provides a substrate on which bacteria can attach. ▪ The mechanism of selective adsorption includes electrostatic forces between negatively charged hydroxyapatite and positively changed salivary glycoproteins. ▪ The mean pellicle thickness varies from 100 nm at 2 hours to 500 to 1,000 nm. 32 ▪ The acquired enamel pellicle alters the charge and free energy of the surface which in turn increases the efficiency of bacterial adhesion (attachment). Negative Salivary Charged Phosphate macromolecules group with opposite charged 33  2. Initial Adhesion/Attachment of Bacteria Phase 1: Transport to the Surface Phase 2: Initial Adhesion Phase 3: Strong Attachment Phase 1: Transport to the Surface Bacteria beginning to transport to enamel pellicle by: 1. Brownian motion 2. Sedimentation of microorganisms 34  Phase 2: Initial Adhesion Reversible adhesion. During initial adherence, interactions occur mainly between specific bacteria and the pellicle. They are: 1. Bacterial attachment via electrostatic interaction Oral bacteria bear an overall net negative charge, negatively-charged components of the bacterial surface and negatively-charged components of pellicle become linked by cations such as calcium. 35  2. Bacterial attachment via hydrophobic interaction These interactions are based on the close structural fit between molecules on the pellicle and bacterial surfaces. 36  Phase 3: Strong Attachment Strong irreversible phase Adhesins are protein in nature and have been identified on fimbriae of bacteria. Fimbria are fibrous protein structure extending from bacterial cell surface. Adhesins are able to bind to protein in acquired enamel pellicle so help in bacterial adhesion. Another mean of bacterial adhesion to the tooth surface is the formation of extra-cellular polysaccharides produced by streptococci. 37 38 Bacterial adhesion occur by: 1. Bacteria and pellicle 2. Bacteria and same species 3.Bacteria and different species 4.Bacteria and matrix Then matrix formation occur 39  3. Colonization and Biofilm Maturation Once the bacteria is adhered to the pellicle, subsequent growth leads to bacterial accumulation and increased plaque mass. Dental plaque growth depends on: A.Growth via adhesion of new bacteria B.Growth via multiplication of attached bacteria 40  ❖ Colonization Initial colonizers Secondary colonizers Plaque maturation 41  Initial colonizers by predominantly Gram-positive facultative bacteria. Streptococcus sanguis (Ss) is most dominant & Actinomyces viscosus (Av) are also found in 24 h plaque. ( adhere to pellicle) Initial Secondary Plaque maturation 42  Secondary colonizers These bacteria are not able to initially colonize the tooth surface. Secondary colonizers include Gram –ve anaerobic bacteria such as: Porphyromonas gingivalis, Prevotella intermedia, Fusobacterium nucleatum spp. Campylobacter rectus. Treponema denticola. Tannerella forsythia. 43  They adhere to bacteria already adherent to the tooth by: 1. Coaggregation The ability of planktonic bacteria (un attached) to adhere to one another. The mechanism of coaggregation appears to be mediated by specific receptor-adhesin interaction. i.e. specific protein on the surface of one species (adhesins) attach to specific carbohydrate on the surface of the other (receptor). 44 Well characterized interaction include the coaggregation of: Fusobacterium nucleatum S. sanguis, Prevotella loescheii A. viscosus Capnocytophaga ochraceus A. viscosus 45  2. Co-adhesion is the interaction between a sessile, already adhering organism and planktonic micro- oganisms of a different strain or species Some bacteria are unable to bind directly to the conditioning film, but are able to interact with molecules on bacteria that are already attached (co-adhesion), also by adhesin-receptor interactions. One bacterium, Fusobacterium nucleatum, can co-adhere with almost all other bacteria found in dental plaque, and is considered to be a key bridging organism between early and later colonizers.  Plaque maturation. As a result of ecologic changes, more Gram-negative strictly anaerobic bacteria colonize secondarily and contribute to an increased pathogenicity of the biofilm. 47  Streptococcus oralis Primary colonizers Streptococcus sanguinis Actinomyces naeslundii Actinomyces oris Actinomyces viscosus ▪ Porphyromonas gingivalis Secondary colonizers ▪ Treponema denticola ▪ Fusobacterium nucleatum spp. ▪ Aggregatibacter actinomycetemcomitans ▪ Prevotella intermedia ▪ Tannerella forsythia. ▪ Campylobacter rectus. 48  Factors that influence complexity of plaque maturation and ecology: a) Oxygen levels: With increasing thickness of dental plaque diffusion of oxygen into the biofilm becomes more and more difficult so favor the growth of anaerobic bacteria. b) Nutritional sources: Dietary products dissolved in saliva are an important source of nutrients for bacteria in the supragingival plaque. Saccharolytic bacteria can ferment sugar to provide energy for their growth and multiplication. 49  c) Interbacterial relation: Beneficial interactions between bacteria may be in the form of: 1) One species provides growth conditions favorable to another. Obligate aerobes utilize oxygen for growth so provide suitable environment for growth of anaerobes. 2) One species facilitates attachment of another resulting in the formation of different morphological structures as corn-cobs. 3) One species provides growth factor utilized by other species such as analogs of vitamin K. 50 Antagonistic interactions between bacteria may be in the form of: 1) Competition for nutrients. 2) Competition for binding sites. 3) Production of substances by one species which limit growth of another one: Streptococcus sanguis produces H2O2 which inhibits the growth of A. actinomycetemcomitans 51  Clinical significance of plaque Accumulation of plaque along the gingival margin leads to an inflammatory reaction of the soft tissue. The presence of this inflammation has a profound influence on local ecology. The availability of blood and gingival fluid components, associated with inflammation, promotes the growth of Gram –ve bacterial species. The bacteria breakdown these host molecules to amino acids and utilize them for growth. 52  5. Association of plaque bacteria with periodontal disease It is clear that periodontal disease is associated with the presence of dental plaque. However, some individuals may show massive plaque accumulation and signs of gingival inflammation (gingivitis) but never change into periodontitis. Based on these observations three theories have been proposed to explain the association between periodontal diseases and bacteria in dental plaque. 53  The three theories ….. (1)Specific theory (2) Non-specific theory (3)Unified theory: “Multiple pathogen or mixed infection theory” 20XX 54  (1)Specific theory It states that, not all plaque is pathogenic and its pathogenicity depends on the presence of certain specific microbial pathogens in plaque. This is based on the fact that, the specific microorganisms responsible for periodontal diseases release certain damaging factors that mediates the destruction of the host tissue. treatment would be directed toward the elimination of the specific pathogen from the mouth with appropriate narrow- spectrum antibiotic. Thus plaque control would no long be necessary since plaque without the specific pathogen would be non-pathogen. 55  2. Non-specific theory ▪ According to pure non-specific theory the inflammatory periodontal disease develops when bacterial proliferation exceeds the threshold of host resistance, the composition of plaque was not considered. i.e. there is a direct relation between the total number of accumulated bacteria and the magnitude of tissue destruction. ▪ If this was the case, why some patients have lifelong contained gingivitis without developing periodontitis in spite of continuous plaque accumulation? Based on bacteria quantity 56  3. Unified theory: “Multiple pathogen or mixed infection theory” It states that 6-12 bacterial species may be responsible for the majority of destructive periodontal disease through synergistic interaction. In acute necrotizing ulcerative gingivitis, synergy exists between spirochetes and fusobacterium. Also, in chronic periodontitis, synergy exists between fusobacterium nucleatum, Tannerella forsythus and campylobacter recuts 57  6. Bacteria associated with periodontal health Condition Micro-organism Periodontal ▪ Gram +ve 90%: 1. S. sanguis, health 2. S. mitis, 3. A. viscosus. ▪ Gram –ve 10%: 1. Prevotella intermedia, 2. fusobacterium nucleatum, 3. Capnocytophaga 58  7. Microorganism associated with specific periodontal diseases Gingivitis Gram +ve 50%: S. sanguis, A. viscosus. Gram –ve 50%: P. intermedia, F. nucleatum. periodontitis Gram –ve 75%, the anaerobes 90% Gram –ve anaerobes such as. Prevotella intermedia,. Porphyromonas gingivalis,. Fusobacterium nucleatum,. A. actinomycetemcomitans,.Tannerella forsythia. Spirochetes 30% 59 Periodontal Fusobacterium nucleatum abscesses Prevotella intermedia Tannerella forsythia Porphyromonas gingivalis 60  Criteria For Defining Periodontal Pathogens 1. The microorganisms must be constantly present in every lesion of the disease. 2. Elimination of the suspected organism should be eliminated or decreased in sites where clinical resolution of disease with treatment has occurred. 3. Microbe should be able to demonstrate an altered host humoral or cellular immune response. 4. Potential pathogens should be capable of producing virulence factors, which cause destruction of the periodontal tissues. 5. Pathogens should be capable of causing the same disease in experimental animal models  8. The putative periodontal pathogens include: Aggrigatibacter actinomycetemcomitans (A.a) Porphyromonus gingivalis Tannerella forsythia Spirochetes (Treponema denticola) Prevotella intermedia  Aggrigatibacter actinomycetemcomitans (A.a) It's a G-ve facultative anaerobe (microaerophilic) non-motile coccoid bacillus. It correlates with periodontitis. - It has several virulence factors; - a) Leukotoxins, which kill or impair neutrophils & monocytes function, - b) Epitheliotoxins. - c) Toxins affecting fibroblast function (Fibroblast cytotoxicity factor). - d) Capsule which resists phagocytosis & lysis by the complement. 63 - e) They possess fimbriae (adhesion factor) & attach well to oral surfaces. - f) Lipopolysaccharide endotoxin which has a potent bone resorbing activity & interfere with neutrophil function. - g) Hydrolytic enzymes, & collagenase. - h) May be tissue invasive, no fimbriated variants also may not attach to granulocytes, thereby resisting phagocytosis & allowing invasion of periodontal tissues. - i) Epithelial cell destruction, affecting their integrity. 64  Porphyromonus gingivalis It is a G-ve, anaerobic, non-motile assachrolytic short rods. It forms black- brown colonies on blood agar. It's isolated from diseased mouth. a) It produces numerous virulence factors or damaging toxins including; collagenase, protease, fatty acids, ammonia, and H2S. b) It forms membrane vesicles carrying with them the secreted proteases (gingipain). c) It has the ability to attach to epithelial cells, and invade soft tissues. d) It has a carbohydrate capsule. e) It forms the red complex with both (treponema denticola & tannerella forsythia), that is highly associated with severe forms of periodontitis. 65 Tannerella forsythia: It's a G–ve anaerobic, spindle shaped pleomorphic rod, found in higher numbers at sites of periodontitis rather than gingivitis. It produces proteolytic enzymes that are able to destroy immunoglobulins and complement components. Spirochetes (Treponema denticola) They are spiral, anaerobic motile microorganisms. In advanced periodontal disease may constitute up to 47% of the observable bacteria in plaque. It's associated with ANUG, periodontitis. They produce potent hydrolytic enzymes, including collagenase, proteases, & peptidase T. denticola produce extracellular membrane vesicles, which have hemagglutinating activity. Spirochetes release destructive metabolic end products as ammonia & H2S, which easily, permeates the tissues. 67 Prevotella intermedia: G-ve anaerobic, black pigmented, short rod that can ferment both carbohydrates & proteins. It resists phagocytosis (probably by its capsule). Its lipopolysaccharide (cell wall) contains unusual fatty acids having marked effects on immune & bone cells. It also secretes toxins acting on epithelial cells. It correlates with ANUG, periodontitis. Presentation title