Aspects of adaptive host response in periodontitis.
OBJECTIVE
To review host response in periodontitis with respect to cellular composition of lesions, T cell receptor (TCR) gene expression, cytokine profiles of T-helper (Th) cells and autoimmune components.


METHODS
The studies included were confined to human material (biopsies, gingival crevicular fluid, blood from subjects with periodontitis).


CONCLUSIONS
In periodontitis lesions, plasma cells are the most common cell type and represent about 50% of all cells, while B cells comprise about 18%. The proportion of B cells is larger than that of T cells and Th cells occur in larger numbers than T cytotoxic cells. Polymorphonuclear cells and macrophages are found in fractions of less than 5% of all cells. Lesions in aggressive and chronic forms of periodontitis exhibit similar cellular composition. Differences in disease severity, however, may reflect increases in plasma cell and B cell densities. B cells serve as important antigen-presenting cells in periodontitis. The periodontitis lesion expresses a unique TCR gene repertoire that is different from that in blood. The role of superantigens in periodontitis is unclear. There are few studies using comparative designs and unbiased quantitative methods regarding Th-1 and Th-2 cells in periodontitis. The relative dominance of B cells and plasma cells in periodontitis lesions cannot entirely be explained by enhanced Th-2 functions but maybe because of an imbalance between Th-1 and Th-2. Autoimmune reactions are evident in periodontitis lesions. The role of auto-antibodies in the regulation of host response in periodontitis, however, needs to be clarified. Auto-reactive B cells occur in larger proportions in subjects with periodontitis than in healthy controls.
Berglundh
Tord
T
Department of Periodontology, Institute of Odontology, The Sahlgrenska Academy at Göteborg University, Göteborg, Sweden. berglundh@odontologi.gu.se
Donati
Mauro
M
D000208:Acute Disease; D000938:Antigen-Presenting Cells / Q000502:physiology; D001323:Autoantibodies / Q000502:physiology; D002908:Chronic Disease; D016207:Cytokines / Q000096:biosynthesis / Q000235:genetics*; D006801:Humans; D007111:Immunity, Cellular / Q000502:physiology*; D016130:Immunophenotyping; D008213:Lymphocyte Activation; D016131:Lymphocyte Subsets / Q000502:physiology*; D008264:Macrophages / Q000502:physiology; D009504:Neutrophils / Q000502:physiology; D010518:Periodontitis / Q000276:immunology* / Q000473:pathology; D010950:Plasma Cells / Q000502:physiology; D011948:Receptors, Antigen, T-Cell / Q000096:biosynthesis / Q000235:genetics*
D001323:Autoantibodies; D016207:Cytokines; D011948:Receptors, Antigen, T-Cell