Three-Dimensional Volumetric Changes After Socket Augmentation with Deproteinized Bovine Bone and Collagen Matrix.

PURPOSE: Socket augmentation decreases the magnitude of alveolar ridge resorption, but the literature is limited in respect to quantifying soft tissue remodeling. The aim of this study was to determine the volumetric and linear dimensional changes at the buccal surface for both hard and soft tissues after socket augmentation treated with a xenogeneic collagen matrix in combination with bone grafting. MATERIALS AND METHODS: Twenty-four individuals indicated for tooth extraction were enrolled in this investigation. Each participant was randomly assigned to one of two groups: (1) deproteinized bovine bone + collagen plug, or (2) deproteinized bovine bone + xenogeneic collagen matrix. A cone beam computed tomography scan was taken prior to extraction and at 6 months postextraction. Intraoral scanning images were taken at baseline, 3 months, and 6 months postextraction. Hard and soft tissue analyses were performed to compare linear ridge remodeling and volumetric changes by noncontact reverse-engineering software. RESULTS: Both groups showed bone and soft tissue remodeling. For hard tissue remodeling, there was no significant difference between the collagen plug and collagen matrix groups. For soft tissue remodeling, the collagen matrix group showed a reduced soft tissue loss compared with the collagen plug group. The volumetric analysis demonstrated that the mean buccal soft tissue volume loss for the collagen matrix group was 68.6 mm3 compared with 87.6 mm3 found in the collagen plug group (P = .009) over a 6-month period. CONCLUSION: This clinical investigation provides early evidence of using the total tissue volume to compare soft and hard tissue remodeling after socket augmentation. The results of this study demonstrated that the use of a xenogeneic collagen matrix reduced the buccal soft tissue loss after tooth extraction, but additional studies are necessary to evaluate the clinical significance of soft tissue augmentation after tooth extraction.

Role of inflammasomes in the pathogenesis of periodontal disease and therapeutics.

Inflammasomes are a group of multimolecular intracellular complexes assembled around several innate immune proteins. Recognition of a diverse range of microbial, stress and damage signals by inflammasomes results in direct activation of caspase-1, which subsequently induces the only known form of secretion of active interleukin-1ß and interleukin-18. Although the importance of interleukin-1ß in the periodontium is not questioned, the impact of inflammasomes in periodontal disease and its potential for therapeutics in periodontology is still in its very early stages. Increasing evidence in preclinical models and human data strongly implicate the involvement of inflammasomes in a number of inflammatory, autoinflammatory and autoimmune disorders. Here we review: (a) the currently known inflammasome functions, (b) clinical/preclinical data supporting inflammasome involvement in the context of periodontal and comorbid diseases and (c) potential therapies targeting inflammasomes. To clarify further the inflammasome involvement in periodontitis, we present analyses of data from a large clinical study (n = 5809) that measured the gingival crevicular fluid-interleukin-1ß and grouped the participants based on current periodontal disease classifications. We review data on 4910 European-Americans that correlate 16 polymorphisms in the interleukin-1B region with high gingival crevicular fluid-interleukin-1ß levels. We show that inflammasome components are increased in diseased periodontal tissues and that the caspase-1 inhibitor, VX-765, inhibits ~50% of alveolar bone loss in experimental periodontitis. The literature review further supports that although patients clinically present with the same phenotype, the disease that develops probably has different underlying biological pathways. The current data indicate that inflammasomes have a role in periodontal disease pathogenesis. Understanding the contribution of different inflammasomes to disease development and distinct patient susceptibility will probably translate into improved, personalized therapies.