ISSN:1049-8885    

DOI:10.1902/jop.1992.63.1.58

出版商:Wiley    

年代:1992

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.1.61

出版商:Wiley    

年代:1992

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.1.63

出版商:Wiley    

年代:1992

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.317

出版商:Wiley    

年代:1992

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.319

出版商:Wiley    

年代:1992

数据来源: WILEY

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.321

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

The interpretation of diagnostic testsfor the detection of subgingival bacterial species is dependent on knowledge of the microbial etiology of destructive periodontal diseases. Specific etiologic agents of these diseases have been sought for over 100 years; however, the complexity of the microbiota, an incomplete understanding of the biology of periodontal diseases, and technical problems have handicapped this search. Nonetheless, a number of possible pathogens have been suggested on the basis of their association with disease, animal pathogenicity, and virulence factors. The immunological response of the host to a species and the relation of successful therapy to the elimination of the species have also been used to support or refute suspected periodontal pathogens. Current data suggest that pathogens are necessary but not sufficient for disease activity to occur. Factors which influence activity include susceptibility of the individual host and the presence of interacting bacterial species which facilitate or impede disease progression. Recent studies have attempted to distinguish virulent and avirulent clonai types of suspected pathogenic species and seek transmission of genetic elements needed for pathogenic species to cause disease. Finally, the local environment of the periodontal pocket may be important in the regulation of expression of virulence factors by pathogenic species. Thus, in order that disease result from a pathogen, 1) it must be a virulent clonal type; 2) it must possess the chromosomal and extra‐chromosomal genetic factors to initiate disease; 3) the host must be susceptible to this pathogen; 4) the pathogen must be in numbers sufficient to exceed the threshold for that host; 5) it must be located at the right place; 6) other bacterial species must foster, or at least not inhibit, the process; and 7) the local environment must be one which is conducive to the expression of the species' virulence properties.J Periodontol 1992; 63:322‐331.

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.322

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

The oral microbiota playsa primary role in the initiation and progression of the most common forms of periodontal disease. Because of the multiplicity of factors that control the establishment and long‐term evolution of the oral microbiota, a great deal of heterogeneity exists in the composition of the periodontal microbiota among individual subjects. Despite these individual differences and the complex interactions between bacteria and the host and among bacteria, an association has been demonstrated between certain species and various forms of periodontal disease. However, the predictive value of either positive or negative tests for selected bacterial species has not proved to be high enough for routine use in clinical practice. Nevertheless, bacteriological tests have been of value in the management of patients with juvenile Periodontitis and refractory forms of periodontal disease. The increasing availability of diagnostic laboratory services and diagnostic kits for office use will make it easier for the practitioner to select appropriate antimicrobial treatments and monitor patients undergoing antimicrobial therapy.J Periodontol 1992; 63:332–337

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.332

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

In periodontal diseases, bacteria trigger inflammatoryhost responses which, along with the direct destructive effects of the bacteria, cause most of the tissue destruction. Periodontal inflammatory responses are, by and large, immunologic, and our understanding of these reactions has been advanced by the explosion of knowledge in immunobiology, some of which is discussed in this review. Understanding the role of immune cells and their regulatory cell surface molecules such as the MHC, CD antigens, and receptors, as well as knowledge of effector systems set into motion such as phagocytes and cytotoxic T‐cells, and the effector molecules such as antibodies, complement, and cytokines, have led to better understanding of the complex pathogenesis of periodontal disease. The role of mediators including the matrix metalloproteinases, proteoglycans, the kinins and anaphylatoxins, and low molecular weight mediators including products of arachidonic metabolism is beginning to be elucidated in periodontal disease. Important avenues of research for development of diagnostic tests based upon host response are apparent. For example, tissue products released during periodontal inflammation including the metalloproteinases, elastase, cytokines, prostaglandins, antibodies, and complement components may provide the basis for future diagnostic indicator tests. The recognition that the neutrophil/antibody/complement axis is critical for protection against periodontal bacteria and that abnormalities in this system often lead to increased periodontal susceptibility provide approaches for the development of diagnostic tests assessing risk. A group of factors which are negative regulators of inflammation including TGF‐β, gamma‐interferon, and IL‐1 receptor antagonist provide potential for assessment of periodontal disease in remission or in the healing phase. Finally, factors such as HLA associations and the molecular basis for neutrophil abnormalities may provide genetic markers for periodontal disease susceptibility. Diagnostic factors based upon host response measures offer great potential for predicting host susceptibility and will likely be used in combination with microbial diagnostics which identify specific infecting organisms.J Periodontol 1992;63:338‐355.

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.338

出版商:Wiley    

年代:1992

数据来源: WILEY

摘要:

Extensive data collected over the past decadedemonstrate clearly that diseaseactive and disease‐inactive periodontal pockets exist, disease progression is infrequent and episodic, and most progression occurs in a small proportion of highly susceptible individuals. Furthermore, traditionally used diagnostic procedures do not identify susceptible individuals nor distinguish between disease‐active and disease‐inactive periodontal sites. New diagnostic tests based on host response factors that will aid in resolving these problems appear to be possible. Sources of material for use in such tests include gingival crevicular fluid (GCF), blood cells, and blood serum. Of these, components in GCF are most promising, at least in the immediate future. Although more than 40 GCF components have been studied, efforts that attempt to relate the presence and amount of a given component to an independent measure of active disease are very few in number. As a consequence, we do not yet know the potential for most GCF components as the basis of diagnostic tests. Those components that have been documented to associate with active disease as measured by attachment loss of 2 mm or greater include alkaline Phosphatase, β‐glucuronidase, prostaglandin‐E2, aspartate aminotransferase, and IgG4antibody subclass. Even in these cases, the data base is small and additional clinical studies are needed to document claims. At the present time, tests based on β‐glucuronidase, nonspecific neutral proteases, and aspartate aminotransferase are being commercialized. One test has received FDA approval. Tests based on blood cells have limited application for patients with adult periodontitis, but are useful for patients with earlyonset forms of periodontitis. An abnormality in the leukocyte adherence molecules on the surfaces of neutrophils is diagnostic for generalized prepubertal periodontitis, and defects in chemotactic receptor numbers and in a surface molecule designated as GP110 are found on the neutrophils of most but not all localized juvenile periodontitis patients. Recent data indicate that enhanced unstimulated or stimulated release of PGE2and Interleukin‐1 by peripheral blood monocytes may be an indicator of susceptibility to severe periodontitis. Assessment of the humoral immune response as reflected by serum antibodies to antigens of periodontopathic bacteria shows little promise as the basis for tests diagnostic of site‐specific disease activity. However, the capacity of an individual to mount an IgG2subclass response to carbohydrate antigens may have potential as an indicator of disease susceptibility.J Periodontol 1992; 63:356–366.

ISSN:1049-8885    

DOI:10.1902/jop.1992.63.4s.356

出版商:Wiley    

年代:1992

数据来源: WILEY