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The safety and efficacy of a degradable, subgingivally placed drug delivery system containing 2.5 mg chlorhexidine (CHX) were evaluated in a randomized, blinded, multi-center study of 118 patients with moderate periodontitis. A split-mouth design was used to compare the treatment outcomes of scaling and root planing (SRP) alone with the combined use of SRP and the CHX in pockets with probing depths of 5 to 8 mm. The two maxillary quadrants were used for the two treatment arms of the study. Scaling and root planing was performed at baseline only, while the CHX was inserted both at baseline and at 3 months. Clinical and safety measurements including probing depth (PD), clinical attachment level (CAL), and bleeding on probing (BOP) as well as gingivitis, plaque, and staining indices were recorded at baseline, and at 1, 3, and 6 months. The average PD reduction in the CHX-treated sites was significantly greater than in the sites receiving SRP alone at both 3 and 6 months with a mean difference of 0.42 mm (P < or = 0.01) at 6 months. The reduction in CAL at the treated sites was greater than at the SRP sites, although the difference was statistically significant at the 6-month visit only. An analysis of patients with initial probing depths of 7 to 8 mm (n = 56) revealed a significantly greater reduction in PD and CAL in those pockets treated with CHX compared to SRP at both 3 and 6 months. The mean differences between test and control sites at 6 months were 0.71 mm and 0.56 mm PD and CAL respectively.

Of the many palmoplantar keratoderma (PPK) conditions, only Papillon-Lefèvre syndrome (PLS) and Haim-Munk syndrome (HMS) are associated with premature periodontal destruction. Although both PLS and HMS share the cardinal features of PPK and severe periodontitis, a number of additional findings are reported in HMS including arachnodactyly, acroosteolysis, atrophic changes of the nails, and a radiographic deformity of the fingers. While PLS cases have been identified throughout the world, HMS has only been described among descendants of a religious isolate originally from Cochin, India. Parental consanguinity is a characteristic of many cases of both conditions. Although autosomal recessive transmission of PLS is evident, a more "complex" autosomal recessive pattern of inheritance with phenotypic influences from a closely linked modifying locus has been hypothesised for HMS. Recently, mutations of the cathepsin C gene have been identified as the underlying genetic defect in PLS. To determine if a cathepsin C mutation is also responsible for HMS, we sequenced the gene in aVected and unaVected subjects from the Cochin isolate in which both the PLS and HMS phenotypes appear. Here we report identification of a mutation of cathepsin C (exon 6, 2127A→ G) that changes a highly conserved amino acid in the cathepsin C peptide. This mutation segregates with HMS in four nuclear families. Additionally, the existence of a shared common haplotype for genetic loci flanking the cathepsin C gene suggests that aVected subjects descended from the Cochin isolate are homozygous for a mutation inherited "identical by descent" from a common ancestor. This finding supports simple autosomal recessive inheritance for HMS in these families. We also report a mutation of the same exon 6 CTSC codon (2126C→T) in a Turkish family with classical PLS. These findings provide evidence that PLS and HMS are allelic variants of cathepsin C gene mutations. (J Med Genet 2000;37:88-94)

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