Detection of high-risk groups and individuals for periodontal diseases: laboratory markers from analysis of saliva.

The use of saliva as a source of components that may identify subjects at risk of developing destructive periodontitis, or provide markers of disease potential or activity, has been reviewed. It was concluded that bacteria, their constituents or products are unlikely to be rewarding and that host-derived salivary factors such as enzymes cannot identify risk, as deficiency states for these do not exist. Secretory IgA, plasma IgA and IgG isotype levels and specific antibodies may be associated with risk, but probably only if levels fall below those which are protective or a specific antibody response is absent. More work is needed to distinguish between monomeric and dimeric IgA antibodies and to identify IgG antibodies in longitudinal clinical studies. In general, although saliva may prove to be useful as a source of indicators of current disease activity or as a means of assessing responses to treatment, it is unlikely to provide evidence for the existence of risk factors.

[1]  N. Johnson,et al.  Detection of high-risk groups and individuals for periodontal diseases. , 1989, International dental journal.

[2]  J. Sterne,et al.  Detection of high-risk groups and individuals for periodontal diseases. Clinical assessment of the periodontium. , 1988, Journal of Clinical Periodontology.

[3]  J. Sterne,et al.  Detection of high-risk groups and individuals for periodontal diseases. Systemic predisposition and markers of general health. , 1988, Journal of clinical periodontology.

[4]  J. Sterne,et al.  Detection of high-risk groups and individuals for periodontal diseases. Evidence for the existence of high-risk groups and individuals and approaches to their detection. , 1988, Journal of clinical periodontology.

[5]  P. Goldschmidt-Clermont,et al.  Qualitative and quantitative studies of Gc (vitamin D-binding protein) in normal subjects and patients with periodontal disease. , 1987, Journal of periodontal research.

[6]  A. J. Laws,et al.  Suspected periodontopathic microorganisms and their oral habitats in young children. , 1987, Oral Microbiology and Immunology.

[7]  J. Jespersen,et al.  Characterization of Plasminogen Activators in Unstimulated and Stimulated Human Whole Saliva , 1987, Journal of dental research.

[8]  I. Olsen,et al.  Salivary IgG, a parameter of periodontal disease activity? High responders to Actinobacillus actinomycetemcomitans Y4 in juvenile and adult periodontitis. , 1987, Journal of Clinical Periodontology.

[9]  K. Okuda,et al.  Detection of specific antibody in adult human periodontitis sera to surface antigens of Bacteroides gingivalis , 1987, Infection and immunity.

[10]  M. Kilian,et al.  Interference of IgA Protease with the Effect of Secretory IgA on Adherence of Oral Streptococci to Saliva-coated Hydroxyapatite , 1987, Journal of dental research.

[11]  F. Eggert,et al.  Measuring the Interaction of Human Secretory Glycoproteins with Oral Bacteria , 1987, Journal of dental research.

[12]  D. B. Ferguson Current Diagnostic Uses of Saliva , 1987, Journal of dental research.

[13]  R. Miller,et al.  The first component of complement as a constituent of human salivary sediment. , 1987, Archives of Oral Biology.

[14]  R. Gibbons,et al.  Fibronectin-degrading enzymes in saliva and their relation to oral cleanliness. , 1986, Journal of periodontal research.

[15]  D. Fine,et al.  Indicators of periodontal disease activity: an evaluation. , 1986, Journal of clinical periodontology.

[16]  S. Syrjänen,et al.  Salivary IgA, lysozyme and β‐microglobulin in periodontal disease , 1986 .

[17]  P. Nair,et al.  Duct-associated lymphoid tissue (DALT) of minor salivary glands and mucosal immunity. , 1986, Immunology.

[18]  H. Larjava,et al.  Immunoglobulins and Innate Antimicrobial Factors in Whole Saliva of Patients with Insulin-dependent Diabetes Mellitus , 1986, Journal of dental research.

[19]  P. Vilja,et al.  Antimicrobial factors in whole saliva of human infants , 1986, Infection and immunity.

[20]  R. Lockey,et al.  Defective antimicrobial functions of oral secretions in the elderly. , 1986, The Journal of infectious diseases.

[21]  J. Slots,et al.  Effect of periodontal therapy on salivary enzymatic activity. , 1985, Journal of Periodontal Research.

[22]  R. Ellen,et al.  Fluctuations in crevicular and salivary anti-A. viscosus antibody levels in response to treatment of gingivitis. , 1985, Journal of clinical periodontology.

[23]  J. Mestecky,et al.  Immunoglobulin A subclass distribution of naturally occurring salivary antibodies to microbial antigens , 1985, Infection and immunity.

[24]  J. Ebersole,et al.  Salivary IgA antibody to Actinobacillus actinomycetemcomitans in a young adult population. , 1985, Journal of periodontal research.

[25]  S. Dreskin,et al.  Immunoglobulins in the hyperimmunoglobulin E and recurrent infection (Job's) syndrome. Deficiency of anti-Staphylococcus aureus immunoglobulin A. , 1985, The Journal of clinical investigation.

[26]  M. K. Basu,et al.  Changes in salivary peroxidase activity observed during experimentally-induced gingivitis. , 1984, Journal of clinical periodontology.

[27]  R. Reiff Serum and salivary IgG and IgA response to initial preparation therapy. , 1984, The Journal of Periodontology.

[28]  L. Sandholm,et al.  Salivary immunoglobulins in patients with juvenile periodontitis and their healthy siblings. , 1984, The Journal of Periodontology.

[29]  K. Jima,et al.  Collagenase Activity in Human Saliva , 1983, Journal of dental research.

[30]  J. Slots,et al.  Salivary enzymes. Origin and relationship to periodontal disease. , 1983, Journal of periodontal research.

[31]  J. Rambaud,et al.  IgA subclasses in various secretions and in serum. , 1982, Immunology.

[32]  J. Olsson,et al.  Association between bacterial agglutinins and immunoglobulin A in human saliva. , 1981, Acta Odontologica Scandinavica.

[33]  W. C. Berry,et al.  Salivary antibodies in acute gingivitis. , 1980, Journal of periodontology.

[34]  S. Low,et al.  Measurement of serum and salivary antibodies to the oral pathogen Bacteroides asaccharolyticus in human subjects. , 1980, Archives of Oral Biology.

[35]  J. Wilton Suppression by IgA of IgG-mediated phagocytosis by human polymorphonuclear leucocytes. , 1978, Clinical and experimental immunology.

[36]  Griffiss Jm,et al.  Immunoepidemiology of Meningococcal Disease in Military Recruits. II. Blocking of Serum Bactericidal Activity by Circulating IgA Early in the Course of Invasive Disease , 1977 .

[37]  S. Marklund,et al.  Lactoperoxidase Activity in Human Milk and in Saliva of Newborn Infants , 1975, Infection and immunity.

[38]  R. Lundblad,et al.  Oral leukocytes and gingivitis in the primary dentition. , 1974, Journal of periodontal research.

[39]  R. Stallard,et al.  Endotoxin determinations in gingival inflammation. , 1972, Journal of periodontology.

[40]  J. Klinkhamer,et al.  Correlation Between Gingivitis and Orogranulocytic Migratory Rate , 1969, Journal of dental research.

[41]  P. Brandtzaeg,et al.  Adsorption of Immunoglobulin A onto Oral Bacteria In Vivo , 1968, Journal of Bacteriology.