Mapping biological to clinical phenotypes during the development (21 days) and resolution (21 days) of experimental gingivitis.

AIM: To characterize and map temporal changes in the biological and clinical phenotype during a 21-day experimental gingivitis study. MATERIALS AND METHODS: Experimental gingivitis was induced over 21 days in healthy human volunteers (n = 56), after which normal brushing was resumed (resolution phase). Gingival and plaque indices were assessed. Gingival crevicular fluid was collected from four paired test and contra-lateral control sites in each volunteer during induction (Days 0, 7, 14 and 21) and resolution (Days 28 and 42) of experimental gingivitis. Fluid volumes were measured and a single analyte was quantified from each site-specific, 30s sample. Data were evaluated by analysis of repeated measurements and paired sample tests. RESULTS: Clinical indices and gingival crevicular fluid volumes at test sites increased from Day 0, peaking at Day 21 (test/control differences all p < 0.0001) and decreased back to control levels by Day 28. Levels of four inflammatory markers showed similar patterns, with significant differences between test and control apparent at Day 7 (substance P, cathepsin G, interleukin-1ß, elastase: all p < 0.03) and peaking at Day 21 (all p < 0.002). Levels of α-1-antitrypsin showed no pattern. CONCLUSIONS: Levels of substance P, cathepsin G, interleukin-1ß and neutrophil elastase act as objective biomarkers of gingival inflammation induction and resolution that typically precede phenotypical changes.

Practical considerations for treatment of patients taking bisphosphonate medications: an update.

UNLABELLED: Osteonecrosis of the jaw--bisphosphonate-related (ONJ-BR) is an established clinical entity associated with both oral and intravenous (IV) bisphosphonate therapy. An update for the general practitioner on the indications for bisphosphonate therapy and both risk assessment and prevalence of ONJ-BR is provided. Management philosophy within a local unit is illustrated through four brief case studies. It is not uncommon to encounter patients on bisphosphonate therapy in the dental practice environment; the vast majority of these will be on oral bisphosphonates as part of their management for osteoporosis. The risk of developing ONJ-BR is rare in these patients compared with those receiving treatment for skeletal complications associated with cancer, many of whom will be managed with IV bisphosphonates. Although rare, it is important to recognize the potential risk of ONJ-BR. Whilst most patients on oral bisphosphonates can be managed no differently from other patients, it should be appreciated that the relative risk of long-term cumulative exposure, comorbidity and other factors are still to be determined. Surgical intervention and extractions can place the patient at risk of ONJ-BR and vigilance is necessary to ensure that healing progresses satisfactorily. Early referral to the local hospital should be sought if there is cause for concern. CLINICAL RELEVANCE: Although the risk of ONJ-BR is low in non-oncological indications, it is important to be aware that it exists and to know how the risk may be minimized.

Crevicular fluid glutathione levels in periodontitis and the effect of non-surgical therapy.

AIM: To quantify reduced and oxidized glutathione (GSH and GSSG) levels in gingival crevicular fluid (GCF) of periodontitis patients pre-therapy (versus periodontally healthy controls) and ascertain whether successful non-surgical therapy alters glutathione levels. MATERIALS AND METHODS: Thirty-second GCF samples (6/subject) were collected on Periopaper() strips from starved, non-smokers (n=20; mean age 43.6 years) with chronic periodontitis, before and 3 months after non-surgical therapy, and periodontally healthy, age- and gender-matched controls (n=20). GSH and GSSG levels were determined using reversed-phase high-performance liquid chromatography with fluorescence detection. RESULTS: Lower concentrations of GSH (p<0.01) and GSSG (p<0.05) were detected in GCF from patients (pre- and post-therapy) than controls and treatment had no significant effect. Amounts per 30-second sample did not differ between patients and controls. However, the amount of GSSG per 30-second sample decreased in patients after therapy (p<0.05). Consequently, therapy increased the GSH:GSSG ratio (p<0.05) in patients compared with the controls (p=0.8). CONCLUSION: These data demonstrate high concentrations of GSH within GCF, which are compromised in chronic periodontitis. While therapy does not appear to fully restore GSH concentrations in GCF, it does restore the redox balance (GSH:GSSG ratio), suggesting that the abnormal redox balance arises secondary to oxidative stress resulting from periodontal inflammation.