Periodontal disease and inflammatory dermatoses, such as psoriasis, are characterized by the accumulation of dense inflammatory infiltrates immediately beneath the epithelial cell layer of the gingiva and skin, respectively. Dermatologists are increasingly aware that the epidermal keratinocyte probably contributes to inflammatory disease progression by secreting a number of pro-inflammatory cytokines and expressing various adhesion molecules. In psoriatic lesions, it is now believed that epidermal keratinocytes may also act as antigen-presenting cells and participate directly in the superantigenic activation of T-cell clones, some of which may initiate, contribute to, or maintain the disease process. Although the role of the host response in periodontal disease has been extensively studied over the years, very little is known about the contribution of the gingival keratinocyte to the inflammatory response. The available published information is discussed in this review, and we suggest that, like its epidermal counterpart, the gingival keratinocyte may participate actively in the pathogenesis of periodontal disease.

Fusobacterium nucleatum, a Gram-negative anaerobic rod associated with periodontal disease, is also found in healthy individuals and is considered part of the indigenous oral microflora. Although intra-familial transmission of periodontal pathogens has been documented, there are no data relating transmission of F. nucleatum. This study investigated the distribution of F. nucleatum strains in 4 strictly healthy families. 32 F. nucleatum strains were isolated from 19 individuals (8 parents and 11 children aged 1-13 years). DNA was extracted and digested with the restriction endonucleases EcoRI, TaqI and HindIII. The digests were separated by electrophoresis through 0.8% agarose gels at 40 V overnight, in TBE buffer containing 1 microg/ml ethidium bromide, and photographed. The DNA was transferred to nylon filters by Southern blotting and hybridized with a digoxigenin labelled E. coli rRNA probe (Kit Dig DNA Labelling mixture - Boehringer). Probed DNA was visualized colorimetrically (CSPD Luminescent Detection Kit Boehringer) and photographed (Amersham). We found that 10/11 children shared identical ribotypes with at least one of their respective parents. Some of the children also harbored a unique additional ribotype. On the basis of indistinguishable restriction endonuclease and ribotype patterns these results support the hypothesis that intra-familial transmission of F. nucleatum is possible.

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Fusobacterium nucleatum is a Gram‐negative anaerobic rod implicated in the pathogenesis of periodontal disease. However, this organism has also been frequently identified in high numbers in healthy adults. These observations suggest that the species may comprise different clonal types, some of which may participate in disease. The purpose of the present investigation was to use restriction endonuclease analysis (REA) and ribotyping to characterize F. nucleatum clonal types isolated from healthy young adults with optimal plaque control and investigate the stability of some of these clonal types. A group comprising 11 dental students and 11 dental outpatients with optimal plaque control was sampled. Clonal stability was investigated by sampling the dental student group at baseline and at 16 months. One hundred and thirty‐two clinical isolates of F. nucleatum were successfully recovered from 15/22 individuals. For the positive subjects, 29 different clonal types were identified by REA and ribotyping, each subject and site being colonized by 1‐4 clonal types. For the dental students, 9 and 15 different clonal types were identified at baseline and 16 months, respectively. None of the students harboured identical clonal types at both sampling times. Our results show that ribotyping is a useful technique for monitoring the distributions of F. nucleatum clonal types and indicate that healthy individuals with optimal plaque control can be colonized by more than one F. nucleatum clonal type and that these clonal types appear to be unstable.