Lip piercing: prevalence of associated gingival recession and contributing factors. A cross-sectional study.

BACKGROUND AND OBJECTIVE: Body piercings have increased tremendously in popularity in recent years. For oral piercing, late complications include gingival trauma and localized periodontitis. The purpose of this cross-sectional study was to investigate the prevalence and contributing factors of gingival recession associated with labial piercing. MATERIAL AND METHODS: The test group included 50 subjects with lower-lip studs. Nonpierced controls were matched according to gender, age and smoking status. Clinical examination included plaque and bleeding indices, probing depth, recession, clinical attachment level, width of keratinized gingiva, periodontal biotype, insertion of frenula, evaluation of hard tissues, trauma of occlusion, characteristics of the stud, radiographs and photographs. RESULTS: Gingival recessions were noted on teeth opposite the stud in 68% of the test group compared with 4% of the controls. Localized periodontitis was recorded in 4% of test subjects. Time since piercing and the position of the stud in relation to the cemento-enamel junction were significantly associated with the prevalence of buccal recessions. There were no significant associations between piercing and abnormal tooth wear. CONCLUSION: The prevalence of gingival recessions is associated with labial piercing. The position of the intra-oral disc and time since piercing are associated with a greater prevalence of gingival recession. A narrow width of keratinized gingiva is associated with increased buccal recessions.

Insertional inactivation of the gene for collagen-binding protein has a pleiotropic effect on the phenotype of Staphylococcus aureus.

This report describes phenotypical changes caused by the insertional inactivation of the gene for the collagen-binding protein in Staphylococcus aureus PH100. Insertional inactivation resulted in reductions in the amount of fibronectin-binding protein in PH100 and the ability of intact cells to aggregate in the presence of fibronectin. However, the capacity of PH100 to adhere to immobilized fibronectin remained the same.

Collagen binding of Staphylococcus aureus is a virulence factor in experimental endocarditis.

The role of Staphylococcus aureus collagen binding in the development of experimental endocarditis was studied. Two isogenic strains of S. aureus, 1 carrying an insertional inactivation of the gene encoding collagen-binding protein, were compared in a rat model of catheter-induced infective endocarditis (i.e.). Separate groups of rats with traumatized aortic valves were intravenously challenged with 1 of the strains. In rats sacrificed 24 h after inoculation, the collagen-binding strain significantly outnumbered the mutant strain (P < .001); however, 1 h after challenge, there was no difference in numbers of the 2 strains. The results were substantiated, using a 1:1 mixture of the parent strain and the mutant as an inoculate. Our findings suggest that collagen binding of S. aureus is important in the sustenance of experimental IE and plays a limited role during the initial attachment of the microorganism to traumatized aortic valves.

Reconsideration of the role of fibronectin binding in endocarditis caused by Staphylococcus aureus.

The adherence characteristics in vivo and virulence of two isogenic strains of Staphylococcus aureus differing in fibronectin binding were compared in a rat model of catheter-induced infective endocarditis. No differences were found between the two strains. The results strongly point to the multifactorial nature of bacterial adherence to damaged heart valves and suggest that other binding functions can compensate for the lack of fibronectin binding in S. aureus.

Development and characterization of a new model of hematogenous osteomyelitis in the rat.

Hematogenous osteomyelitis was produced in the tibia or the mandible of rats by drilling a hole into the bone, injecting sodium morrhuate, and inoculating Staphylococcus aureus Phillips into the femoral vein. Animals were sacrificed after 2 weeks and examined. The infection was characterized grossly and radiographically by bone deformation, histopathologically by a characteristic suppurative reaction, and microbiologically by the recovery of S. aureus Phillips from the infected tissue. These findings indicate that the model mimics human osteomyelitis with respect to its inflammatory bone changes. In contrast to earlier rat models in which bacteria were injected directly into the bone, this new experimental model allows study of the initiating events of osteomyelitis such as bacterial attachment and might assist as a model for both prophylactic and therapeutic trials.