Subpontic osseous hyperplasia: a case series and literature review.

A subpontic osseous hyperplasia (SOH) is a slow-growing, non-neoplastic bone growth that uniquely affects mandibular posterior edentulous ridges underneath pontics of fixed partial dentures. An SOH can result in significant periodontal and restorative complications, however, it is usually corrected by surgical excision. This report presents a series of SOH cases, illustrates SOH management approaches, and reviews the literature on SOH clinical presentations.

Tobacco smoking affects bacterial acquisition and colonization in oral biofilms.

Recent evidence suggests that smoking affects the composition of the disease-associated subgingival biofilm, yet little is known about its effects during the formation of this biofilm. The present investigation was undertaken to examine the contributions of smoking to the composition and proinflammatory characteristics of the biofilm during de novo plaque formation. Marginal and subgingival plaque and gingival crevicular fluid samples were collected from 15 current smokers and from 15 individuals who had never smoked (nonsmokers) following 1, 2, 4, and 7 days of undisturbed plaque formation. 16S rRNA gene cloning and sequencing were used for bacterial identification, and multiplex bead-based flow cytometry was used to quantify the levels of 27 immune mediators. Smokers demonstrated a highly diverse, relatively unstable initial colonization of both marginal and subgingival biofilms, with lower niche saturation than that seen in nonsmokers. Periodontal pathogens belonging to the genera Fusobacterium, Cardiobacterium, Synergistes, and Selenomonas, as well as respiratory pathogens belonging to the genera Haemophilus and Pseudomonas, colonized the early biofilms of smokers and continued to persist over the observation period, suggesting that smoking favors early acquisition and colonization of pathogens in oral biofilms. Smokers also demonstrated an early proinflammatory response to this colonization, which persisted over 7 days. Further, a positive correlation between proinflammatory cytokine levels and commensal bacteria was observed in smokers but not in nonsmokers. Taken together, the data suggest that smoking influences both the composition of the nascent biofilm and the host response to this colonization.

Host-bacterial interactions during induction and resolution of experimental gingivitis in current smokers.

BACKGROUND: Changes in clinical profiles, microbial succession, and immune mediator fluctuations have all been separately examined during onset and resolution of experimental gingivitis in smokers. However, because both the bacterial challenge and the host response contribute to periodontal disease, the purpose of this investigation is to simultaneously examine clinical, bacterial, and immune changes that occur during the onset and resolution of disease in smokers. METHODS: Experimental gingivitis was induced in 15 smokers for 21 days, followed by treatment with a sonic toothbrush for 21 days. Marginal and subgingival plaque and gingival crevicular fluid samples were collected at baseline; after 7, 14, and 21 days of undisturbed plaque formation; and 21 days after reinstitution of brushing. 16S cloning and sequencing was used for bacterial quantification, and multiplexed bead-based flow cytometry was used to quantify the levels of 27 immune mediators. RESULTS: Onset of clinical gingivitis was preceded by significant changes in the marginal and subgingival biofilms, with a decrease in the abundance of early colonizers, namely, Streptococcus, Veillonella, and Pseudomonas, and an increase in levels of periodontopathogens, such as Treponema, Selenomonas, Parvimonas, Dialister, and Campylobacter. This was accompanied by a decrease in anti-inflammatory, chemokine, and T-helper 2 (Th2) responses and altered Th1/Th2 ratios. Although the bacterial communities continued to shift in the same direction after onset of clinical gingivitis and returned to baseline levels after resolution of disease, the anti-inflammatory, chemokine, and Th2 profiles demonstrated an increase from day 14 that continued even after clinical health was evident. CONCLUSION: Both marginal and subgingival biofilms in smokers are characterized by early acquisition of pathogenic organisms, which elicit a sustained host response that persists even after removal of the bacterial challenge.