The periodontal status of patients with reduced immunocapacity was assessed. Gingival inflammation, periodontal destruction, and plaque accumulation were compared in three groups--renal transplant patients, dialysis patients, and normal individuals. The levels of all parameters were similar in the three groups indicating that immunosuppression does not affect the clinical appearance of periodontal disease when measurements are made in a single examination. In the transplant group, however, there is a lack of correlation between P.I. and G.I. and between P.I. and P.D.I., indicating a dissociation between plaque accumulation and the tissue response. Long-term longitudinal studies of periodontal disease in such patients are needed in order to obtain more meaningful information on the role of the immune system in affecting the rate of periodontal destruction. This study suggests that nonimmune mechanisms such as the direct effect of bacterial products on supporting tissues can account for at least some of the clinical manifestations of periodontal disease.

The periodontal status of renal transplant patients on immunosuppressant drug therapy was compared with that of an age matched normal group over a period of 2 to 4 1/2 years. Gingival Index, Plaque Index, and Periodontal Destruction Index were used as measures of comparison. Over this period of time the Gingival Index of the immunosuppressed patients increased significantly when compared to the normals. There was a significant increase in the mean Plaque Index for both groups during the study period. The increase was greater in the immunosuppressed group. However, the difference in the Plaque Index for the two groups was not significant. There was little change in the Periodontal Destruction Index in both groups over time. The results of this study indicate that there is little difference in the rate of periodontal destruction between patients taking immunosuppressant drugs and normal patients. These findings, taken in conjunction with other recent reports, would seem to indicate that T cells play a minor role in the etiology of periodontal disease.

Refractory cases of periodontitis were assayed for chemotaxis of polymorphonuclear neutrophilic leukocytes using an in vivo assay. 9 refractory patients and 9 normal patients were studied. When cell counts were plotted against time, normal patients showed a single peak at 25-30 min after casein (chemo-attractant) challenge, whereas refractory patients showed 2 and 3 peaks of PMN's at varying time intervals. 5 of the refractory patients showed this pattern in tests of normal sulci as well as deep periodontal pockets. 4 of the refractory cases showed a double peak in tests of deep periodontal pockets. This suggests that some refractory cases have an intrinsic chemotactic defect of polymorphonuclear neutrophils while in others the defect may be a secondary phenomenon. It appears that patients with refractory periodontitis have the characteristic cell response that was reported for LJP.

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