Sterilization of Ceramic Sharpening Stones.

Traditionally, periodontal hand instruments are honed or sharpened during patient care as they dull easily during contact with enamel, calculus and cementum. This approach is taught in dental and hygiene schools around the world and remains the standard of care. Recently, some professional organizations have questioned whether this practice should be abandoned because of safety issues. Questions have been raised whether sharpening stones can be properly sterilized and whether the sharpening of contaminated instruments poses a health hazard for the provider. Using bacteria culture techniques and scanning electron microscopy, we tested whether contaminated ceramic sharpening stones can be sterilized. Our results demonstrate that the stones were sterile after being subjected to the manufacturer's sterilization protocol. In addition, over the last year, no incidents related to periodontal instrument sharpening have been reported among nearly 400 students at the faculty of dentistry, University of British Columbia, where chair-side sharpening is taught. Therefore, we conclude that ceramic sharpening stones can be sterilized using normal office protocols and that chair-side sharpening adds little risk beyond routine handling of operatory or periodontal instruments during patient care when proper protocols are followed.

Intra-operative application of chlorhexidine gel reduces bacterial counts in internal implant cavity.

A prospective clinical trial was conducted to assess the bacterial-inhibitory potential of 1% chlorhexidine (CHX) gel in the internal cavity of implant screw holes, when utilized at the time of implant placement. A total of 40 Straumann (S) and Nobel Biocare (N) implants were divided into test (ST or NT; implant + CHX gel) and control (SC or NC; implant only) groups. Total numbers of colony-forming units (CFUs ml(-1) ) were assessed at a minimum of 3 months postsurgery by aerobic and anaerobic culture. A set of specimens was stained with Gram stain. The mean sample-collection time was 110 d for the test population and 98 d for the controls. The use of 1% CHX gel significantly reduced bacterial counts in both the ST and NT samples by over three logs compared with controls. No statistical differences in the numbers of CFUs ml(-1) were evident between aerobic and anaerobic cultures. Differences in the numbers of CFUs ml(-1) between ST and NT groups were not statistically significant. Microscopic analysis showed mainly Gram-positive coccoid species in most samples.

Kindler syndrome and periodontal disease: review of the literature and a 12-year follow-up case.

BACKGROUND: The association of aggressive periodontitis with Kindler syndrome was based on a single case in 1996 and later confirmed with a larger population. Since then, significant research has greatly increased our understanding of the molecular pathology of this disorder. We review recent advances in the molecular mechanisms of the syndrome and present a maintenance case report of a patient who has been followed in our clinic. METHODS: A female patient who was diagnosed with Kindler syndrome and aggressive periodontitis at the age of 16 years has been followed and treated in our clinic for 12 years. Her main treatment has been maintenance therapy following her initial treatment and restorative work previously documented. Gingival biopsies obtained during the recent extraction of hopeless maxillary molars were used for histologic assessment of gingival tissue attachment apparatus and to isolate gingival fibroblasts. Reverse transcription-polymerase chain reaction (RT-PCR) was performed using these cells to confirm the lack of expression of kindlin-1. RESULTS: RT-PCR showed the total loss of kindlin-1 mRNA in cultured gingival fibroblasts, supporting the clinical diagnosis of Kindler syndrome. Tissue biopsies revealed atypical pocket epithelium. Maintenance therapy has been moderately successful. Teeth that were recently lost had a poor prognosis at the initial assessment. The patient's gingiva and oral mucosa continue to be fragile with episodes of sloughing and inflammation. CONCLUSIONS: Periodontitis in Kindler syndrome responds to maintenance therapy, but the gingiva and oral mucosa continue to display an abnormal appearance with white patches. Histologic findings suggest that the junctional epithelium in Kindler syndrome may be abnormal and could explain why these patients have periodontal disease. Attachment loss progressed around teeth with an initial guarded or poor prognosis. Teeth that started with a good or fair prognosis continue to have a fair prognosis. Limited dental implant treatment is being considered.

Clinical and microbiologic study of periodontitis associated with Kindler syndrome.

BACKGROUND: Little is known about the onset and prevalence of periodontal disease in patients with the rare Kindler syndrome, a genodermatological disorder. This study investigated the level of clinical periodontal attachment in relation to age and presence of putative periodontopathogenic bacteria in individuals with Kindler syndrome. METHODS: Eighteen individuals diagnosed with Kindler syndrome and 13 control subjects, aged 4 to 37 years, from rural Panama received a limited clinical periodontal examination. Subgingival samples were collected for identification of putative periodontal pathogens by polymerase chain reaction. RESULTS: Mild to severe gingivitis was a common finding in all adults of the study population. Seventy-two percent (13/18) of the Kindler patients and 46% (6/13) of the control subjects showed mild to severe periodontal disease (P = 0.001, chi-square test). The onset of periodontitis was earlier and the progression occurred at a faster rate in the Kindler group. There was a strong correlation (r = 0.83) between the level of attachment loss and age in the Kindler group and a weaker correlation (r = 0.66) in the control group. The appearance of gingival tissues suggested atypical periodontitis with spontaneous bleeding and fragile, often desquamative, gingiva. In periodontitis patients, Porphyromonas gingivallis and Diallster pneumosintes tended to occur more frequently in control individuals compared to those with Kindler syndrome. CONCLUSIONS: In the Kindler group, periodontitis had an onset in early teenage years and progressed more rapidly compared to non-Kindler individuals of the same geographic and ethnic group. Clinical and microbiological findings suggest atypical periodontitis in Kindler patients. We propose to include Kindler syndrome in the category of medical disorders predisposing to destructive periodontal disease.

Intentional angulation of an implant to avoid a pneumatized maxillary sinus: a case report.

This case report describes placement of an implant in the posterior maxilla so as to avoid a pneumatized sinus and also to avoid the need for a sinus lift procedure. An 81-year-old woman presented with an edentulous span in the upper right posterior maxilla. She had been missing teeth in this area for many years, and there was a combination of resorption of the alveolar ridge and pneumatization of the maxillary sinus. Eleven years previously, implants had been placed anterior to this region, but the patient was told that implants could not be placed posteriorly unless a sinus lift was done. At the time of the current presentation she was still unwilling to undergo a sinus lift procedure but wanted to know if implants could be placed in the posterior right maxilla. A tomogram obtained with a radiographic stent in place indicated that there was insufficient bone height to allow placement of implants at the usual angulation without a sinus lift. Therefore, to avoid the need for a sinus lift, 2 implants were placed with palatal angulation as guided by a tomographically determined surgical stent. The treatment planning and surgical and restorative techniques are reviewed here. A postoperative tomogram was obtained to determine the final position of the implants. The outcome has been favourable for the patient and the clinicians. In situations where there is sufficient palatal bone medial to the maxillary sinus, placing implants at an angle may prevent the need for a sinus lift procedure, assuming that proper development of an occlusal restorative scheme is possible.

Loss of kindlin-1, a human homolog of the Caenorhabditis elegans actin-extracellular-matrix linker protein UNC-112, causes Kindler syndrome.

Kindler syndrome is an autosomal recessive disorder characterized by neonatal blistering, sun sensitivity, atrophy, abnormal pigmentation, and fragility of the skin. Linkage and homozygosity analysis in an isolated Panamanian cohort and in additional inbred families mapped the gene to 20p12.3. Loss-of-function mutations were identified in the FLJ20116 gene (renamed "KIND1" [encoding kindlin-1]). Kindlin-1 is a human homolog of the Caenorhabditis elegans protein UNC-112, a membrane-associated structural/signaling protein that has been implicated in linking the actin cytoskeleton to the extracellular matrix (ECM). Thus, Kindler syndrome is, to our knowledge, the first skin fragility disorder caused by a defect in actin-ECM linkage, rather than keratin-ECM linkage.