An immunoperoxidase technique was used to examine CD28, CD152. CD80 and CD8
6 positive cells in gingival biopsies from 21 healthy/gingivitis and 26 per
iodontitis subjects. The samples were placed into 3 groups (small, intermed
iate. large) according to the size of the infiltrate. The percent CD28 + T
cells in the connective tissue infiltrates was highly variable with no diff
erences between the healthy/gingivitis and periodontitis groups. While ther
e was an increase in positive sails in intermediate infiltrates from both h
ealthy/gingivitis (28.5%) and periodontitis (21.4%) patients compared with
small infiltrates (8.6% and 11.8% respectively), this was not significant,
although the percent CD28 + T cells did increase significantly in tissues w
ith increased proportions of B cells relative to T cells (p =0.047). A mean
of less than 5% infiltrating T cells were CD152 + which was significantly
lower than the mean percent CD28 + T cells in intermediate healthy/gingivit
is lesions (p = 0.021). The mean percent CD80 + and CD86 + B cells and macr
ophages was 1-7% and 8-16%, respectively, the difference bring significant
in intermediate healthy/gingivitis tissues (p=0.012). Analysis of these cel
ls in relation to increasing numbers of B cells in proportion to T cells an
d also to macrophages, suggested that CD80 was expressed predominantly by m
acrophages while CD86 was expressed by both macrophages and B cells. Few en
dothelial cells expressed CD80 or CD86, Keratinocytes displayed cytoplasmic
staining of CD80 rather than CD86 although the numbers of positive specime
ns in the healthy/gingivitis and periodontitis groups reduced with increasi
ng inflammation. In conclusion, percentages of CD28, CD152, CD80 and CD86 d
id not reflect differences: in clinical status. However, the percent CD28 T cells increased with increasing size of infiltrate and with increasing p
roportions of B cells suggesting increased T/B cell interactions with incre
asing inflammation. The percent CD152 + cells remained low indicating that
CD152 may not be involved in negative regulation of T cells in periodontal
disease. CD80 and CD86 have been reported to promote Th1 and Th2 responses,
respectively, and the higher percent CD86 + cells suggests a predominance
of Th2 responses in both healthy/gingivitis and periodontitis tissues. Neve
rtheless, other factors including cytokines themselves and chemokines which
modulate T cell cytokine profiles must be monitored to determine the natur
e of Th1/Th2 responses in periodontal disease.