Infectious agents causing periodontal diseases

Periodontal Disease Definition An inflammatory disease of the supporting tissues of the teeth caused by specific microorganism, resulting in progressive destruction of the periodontal ligament and alveolar bone with pocket formation, recession or both.

Periodontal Structures Attachment Apparatus: Cementum Bone Periodontal ligament

Periodontal Microbiology 1960’s Spirochete might be the cause of acute necrotizing ulcerative gingivitis (ANUG) Actinobacillus actinomycetemcomitans (A.A.) possible pathogen in localized aggressive periodontitis Porphyromonas Gingivalis suggested to be important in chronic periodontitis. 1960 they observed large numbers of this organisms in sections of lesions of this disease. Returned of the specificity as a fundamental concept of the etiology of periodontal disease

Periodontal Microbiology

Complexity of the problem Technical difficulties Taking of the plaque samples Uncontaminated samples Laboratory diagnosis Cultivation Technical difficulties and the inadequate understanding of the biology of destructive peridontitis, uncontaminated samples from the correct location

Inadequate understanding of Disease Pathogenesis Misclassification of the disease type and status Disease due to different species at different sites Succesive episodes of disease due to different species Mistaken conclusion of samples taken from sites in remission Interprating them as if th ey from sites undergoing active destruction

Complexity of the Problem Pathogens may result from the disease rather than the cause Two or more species act together and cause disease The carrier state of disease can represent a long lag phase prior to detection of disease Differences in clonal types

Approach to Determining Etiologic Agents Koch’s Postulates: 1) The agent must be routinely isolated from diseased individuals and recovered from cases of other forms of disease or healthy individuals 2) The agent must be isolated as a pure culture 3) Produce a similar disease when inoculated into susceptible laboratory animals 4) The agent must be re-isolated from infected animal Third criteria was abandoned by kocks in 1884

Approach to Determining Etiologic Agents In recent years, periodontal researchers have extended Koch’s postulates including: Association Requires that suspected pathogenic species be more frequently detected and at higher level in cases than in the controls Elimination Successful therapy will diminish the level of a pathogen and stop disease progression Host response the organism must have high levels of serum, salivary and gingival fluid antibody against it in periodontally diseased subjects

Approach to Determining Etiologic Agents Virulence factors the organism must be found to produce virulence factors in vitro which can be correlated with clinical histopathology Animal Pathogenicity the organism must mimic similar pathogenic properties in an appropriate animal model

Plus associated with the bacteria

Evolving Concepts Susceptible Host Active Disease Presence of Pathogens S sanguis Absence of Beneficial Species Destructive Periodontal Disease

Evolving Concepts Susceptible Host Impaired Neutrophils Inadequate or unregulated immunological response LPS Responsiveness AIDS Diabetes Smoking Drugs Lps some patient il1react very high to and have high responsivenes to lipopolisacharides,inmmunological response like in papillon lefre

Evolving Concepts Presence of Pathogens Actinobacillus actinomycetemcomitans T. forsythus Eikenella corrodens Fusobacterium nucleatum Peptostreptococcus micros Porphyromonas gingivalis Prevotella intermedia Campylobacter rectus Selenomonas sp. Eubacterium sp. Spirochetes

Evolving Concepts Absence of Beneficial species Actinomyces sp Capnocytophaga ochracea  [] C. ochracea;  [] P. gingivalis Diminished attachment loss S. mitis S. mitis produces H2O2 Kills A. a. Streptococcus sanguis Veillonella parvula

(Bacteroides forsythus ) Veillonella parvula Actinomyces odontolyticus S. mitis S. oralis S. sanguis S. gordonii S. intermedius Campylobacter rectus Campylobacter. showae Eubacterium nodatum Fusobacterium nucleatum Prevotella intermedia Peptostreptococcus micros Prevotella nigrescens Porphyromonas gingivalis Treponema denticola Tannerella forsythensis (Bacteroides forsythus ) Capnocytophaga spp. Eikinella corrodens A. actinomycetemcomitans Red complexes is associated with periodontitis Microbial Complexes in Subgingival Plaque

Role of Disease Susceptibility Microbial species unevenly distributed from subject to subject and from site to site Subjects with widespread disease had more sites showing new attachment loss than subjects with fewer affected sites at baseline Percentages of suspected pathogens is highest in subjects with localized destruction and lowest in widespread disease subjects Subjects with widespread disease and high levels of suspected pathogens had a greater number of active sites than subjects in other groups

Bacterial interactions Different types of microorganisms existing in periodontal pockets may act synergistically to induce disease progression Bacterial interactions may be beneficial to the host

Virulent Clonal Types of Pathogens Multiple clonal types within a pathogenic species Clonal types differ in pathogenicity (A.a.) Some clonal types are associated with health and others with disease

Regulation by the Local Environment Strains of many species may turn virulence factors “on/off”, depending on the nature of their environment: Temperature  subgingival  new attachment loss (appears) Iron [ ] Calcium Magnesium Osmolarity

Conclusions For a disease to result from a pathogen: Be a virulent clonal type Must possess chromosomal/extrachromosomal genetic factors to initiate disease Host must be susceptible to pathogens Pathogen must be in numbers sufficient to exceed threshold for the host Must be located in the right place Other bacterial species must foster or at least not to inhibit the process Local environment must be favorable to disease expression