Compared to the initial observations, the results suggested that nearly 60% of the condition could be of fibrotic origin. Initial periodontal therapy and curettage resulted in the resolution of the inflammation in CsA-induced GH. Further investigation of the treated patients has shown that 7 out of 15 patients (47%) in the test group responded well and their GH scores decreased below 30% at the end of the study. The treatment in this study was effective in eliminating the necessity of more extensive surgical modes of treatment, such as gingivectomy, in 47% of cases.

Papillon-Lefevre syndrome (PLS) is an autosomal recessive form of palmoplantar ectodermal dysplasia, characterized by palmoplantar hyperkeratosis and severe early-onset periodontitis. The presence of severe periodontitis distinguishes PLS from other palmoplantar keratodermas. As part of our efforts to study the genetic basis of periodontitis susceptibility, we performed a genome-wide search to identify major loci for PLS in 44 individuals (14 affected) from 10 consanguineous PLS families. We have identified evidence for linkage of a PLS gene on 11q14-q21. A maximum two-point logarithm of the odds (LOD) score of 8.24 was obtained for D11S1367 at a recombination fraction of theta=0.00. Multipoint analysis resulted in a LOD score of 10.45 and placed the gene for PLS within a 4-5 cM genetic interval. This genetic interval, flanked by D11S4197 and D11S931, contains more than 50 cDNAs and 200 expressed sequence tags (ESTs). This refinement of the candidate region for a PLS gene is in agreement with other recent reports of linkage for PLS to chromosome 11q14-q21 and should help in identification of the gene for PLS.

HLA-A, B, C and DR antigen frequencies were determined in a group of patients with juvenile periodontitis and rapidly progressive periodontitis. In juvenile periodontitis patients, HLA-A24 and DR4 were found at a significantly higher level than in the control group, and in rapidly progressive periodontitis patients, A9 and DR4 were found at a significantly higher level than the control group. The presence of these antigens gives evidence as to the susceptibility of various forms of early onset periodontitis.

This study has been designed to investigate the immunogenetic susceptibility of Cyclosporine-A (CsA) immunosuppressed renal transplant patients to development of gingival overgrowth, and the amplifying effect of calcium channel blockers on the severity of this clinical entity. 52 renal transplant recipients were selected and initially grouped as follows: group (Gp)1: CsA (n = 7); Gp 2: CsA + verapamil (n = 26); Gp 3: CsA + diltiazem (n = 6); Gp 4: CsA + nifedipine (n = 13). These groups were not found to be significantly different in age, sex, plaque index (PlI), gingival index (GI), calculus index, periodontal probing depth, serum CsA level, or duration of CsA therapy (p > 0.05). No significant (p > 0.05) additive effect of the calcium channel blockers on the gingival overgrowth (GO) was assessed. The main group (n = 52) was evaluated for the correlations between the clinical and the pharmacological variables and the GO. GI (rs = 0.60) and the periodontal probing depth (rs = 0.71) were found to be moderately correlated with the GO. The patients were regrouped based on the severity of overgrowth and recognized as responders (n = 26) and nonresponders (n = 26). Age, sex, calculus index, serum CsA level, duration of the CsA therapy, were not statistically different among these groups (p > 0.05). PlI, GI, periodontal probing depth, and GO were significantly higher in the responder group (p > 0.05). Analysis of HLA distribution of the responders and the nonresponders and comparison with the controls (n = 3731) revealed that a statistically significant (p < 0.001)% of the nonresponders were positive for HLA-DR1. These data would indicate that an immunogenetic predisposition should be suspected in the pathogenesis of the entity, and that HLA-DR1 would have a protective rôle against gingival overgrowth induced by CsA.

Cyclosporine A (CsA) and verapamil are two agents used in renal transplantation, both of which are suspected of inducing gingival overgrowth. This study was conducted to investigate the effect of verapamil on the severity and prevalence of CsA‐induced gingival overgrowth. Fifty‐one (51) renal transplant recipients (total group) of whom 22 were using only CsA (Group A) and 29 of whom were prescribed CsA + verapamil (Group B) were evaluated for various periodontal and pharmacological parameters. No statistically significant differences were found in age, sex, plaque index, gingival index, calculus index, probing depth, CsA oral dose, CsA whole blood level, duration of CsA therapy, azathioprine dose, and prednisolone dose. Although the prevalence of the gingival overgrowth was more pronounced in CsA + verapamil group compared to CsA group (51.72% vs. 40.91%), the difference was not statistically significant. Similarly, the severity of gingival overgrowth, although more manifest in CsA + Verapamil group than CsA patients (34.24% vs. 28.91%), was not significantly different. Gingival overgrowth scores in the main group, CsA, and CsA + verapamil groups were found to be positively correlated to periodontal probing depths (r = 0.60, r = 0.70, r = 0.52, respectively) and the gingival index (r = 0.60, r = 0.70, r = 0.54, respectively). CsA oral dose, whole blood level, and duration of CsA therapy were not found to be correlated with the gingival overgrowth in either group. Likewise, the dose of verapamil and the duration of verapamil therapy were not correlated with the gingival overgrowth in Group B. This study indicates that verapamil, when prescribed as the calcium channel blocker in renal transplant patients, has no augmenting effect on the severity and the prevalence of CsA‐induced gingival overgrowth. J Periodontol 1996;67:1201–1205.

Glanzmann's thrombasthenia was reported and described as a bleeding diathesis seen in children and characterized by diminished clot retraction. It is an autosomal recessive bleeding disorder. The disease is marked by frequent mucocutaneous hemorrhages either due to defective function of the platelets or lack of fibrinogen binding membrane receptor glycoproteins IIb/IIIa which are located on the surface of the platelets. Case reports on 3 siblings, a girl of 11, and 2 boys of 12 and 16 years old with Glanzmann's thrombasthenia are reviewed. The major complaint of the patients was gingival bleeding. Periodontal treatment was performed under platelet transfusion and proper oral hygiene instruction was given. The patients were followed for 6 months and no periodontal complications developed during this time. Proper periodontal care for such patients is essential both for local and systemic health. J Periodontol 1996;67:816–820.

The clinical and immunological data from 4 patients with generalized prepubertal periodontitis are presented. The peripheral blood neutrophil chemotaxis was measured using zymosan activated sera as the chemoattractant. All of the 4 patients have shown depressed neutrophil chemotaxis compared to those of the healthy controls. Peripheral blood lymphocyte subpopulations were analysed by double-coloured flow cytometry using monoclonal antibodies for the receptors CD2, CD3, CD4, CD8, CD19, CD29, CD45RA+, 34,29dK, CD56. CD11b/CD18. Lymphocytes bearing CD3 receptors showed a significant decrease compared to those of the controls. Natural killer cells were lowered in 3 of the 4 cases. All of the patients showed a higher increase in CD11b/CD18 expression. The evaluation of CD11b/CD18 receptor in peripheral blood leukocytes may be of help explaining the rôle of neutrophils in the pathogenesis of the disease.

Background: Gingival overgrowth is one of the major adverse effects of the immunosuppressive drug cyclosporine A (CsA). Although several studies have attempted to determine the immunological mechanisms of gingival hyperplasia (GO) due to CsA therapy, the pathogenesis remains unclear. In this study, the distribution of the peripheral blood leukocytes in a group of renal transplant patients undergoing CsA therapy was analyzed and possible correlations of periodontal and pharmacological variables to lymphocyte subpopulations, natural killer cells, and monocytes investigated.Methods: Thirty‐six patients were classified into 2 groups of 18 each according to the degree of gingival overgrowth. The periodontal evaluation included plaque index (PI), gingival index (GI), gingival overgrowth (GO), calculus index (CI), and probing depth (PD). The pharmacological variables of current doses of the therapeutic serum levels of CsA were investigated. The peripheral blood leukocytes were studied by 2color flow cytometric analysis using anti‐human CD2, CD3, CD4, CD8, CD11b, CD11c, CD16, CD19, HLA‐DR, and CD3+HLA‐DR+ monoclonal antibodies.Results: Statistical evaluation revealed that none of the pharmacological variables varied between the 2 groups. Responders (GO >30%) had significantly higher GI, PD, and GO scores compared to nonresponders (GO ≤30%). Of the immunological parameters studied, only CD2 was higher in the responder group. None of the clinical parameters correlated to the immunological values.Conclusions: The results of this study may be useful in explaining the underlying mechanisms of drug‐induced gingival overgrowth. Several previously unsuspected cells and accessory activation mechanisms for T lymphocytes could play a role in the pathogenesis. J Periodontol 1998;69:1435–1439.