Effects of Low Intensity Pulsed Ultrasound Stimulation on the Temporal Dynamics of Irradiated Bone Tissue Healing: A Histomorphometric Study in Rabbits.

The present study evaluated the influence of Low-Intensity Pulsed Ultrasound (LIPUS) on the regeneration processes of non-critical-size bone defects in irradiated and non-irradiated rabbit tibias. Bone defects were surgically created on both tibiae of six rabbits. The control group had no additional treatment. In one intervention group, one tibia was irradiated with 15 Gy in a single dose. A second group was treated with LIPUS, and a third with a combination of both treatments. The control samples showed 83.10% ± 17.79% of bone repair after 9 weeks, while the irradiated bone had regenerated significantly less during the same period (66.42% ± 29.36%). The LIPUS treatment on irradiated bones performed a 79.21% ± 21.07% bone fill and could not significantly improve the response compared to the non-treated irradiated specimens. However, LIPUS treatment on non-irradiated bone showed bone formations beyond the size defect (115.91% ± 33.69%), which was a highly significant increase when compared to the control group or any irradiated group. The application of ultrasound to healthy bone produced highly significant and enhanced bone formations with 36.70% more regenerated bone when compared to the same application on irradiated bone. LIPUS vibration stimuli may be considered as a promising complementary treatment approach in non-irradiated bone regeneration procedures to shorten the treatment and enhance bone healing. In irradiated bones, the effect of ultrasound application is less clear, and further studies are needed to refine the dynamics of the present results.

Further evidence of the association between periodontal conditions and coronary artery disease.

BACKGROUND: There is increasing evidence that chronic infections, such as periodontal diseases, could play a role in the initiation and development of coronary artery disease (CAD). The present study was intended to test for a possible association between presence and severity of periodontitis and coronary artery disease in a Belgian population. METHODS: A total of 108 CAD patients (mean age 59.2 +/- 11 years) and 62 presumably healthy controls (mean age 57.7 +/- 9 years) were enrolled in the study. Probing depth, periodontal pocket bleeding index (PPBI), plaque index, furcation involvements, and tooth mobility were evaluated to compare periodontal health in both groups. The subjects were also ranked according to a novel index of periodontitis severity, the periodontal index for risk of infectiousness (PIRI), aimed at quantifying the risk of release of proinflammatory mediators from the periodontal sites. RESULTS: Periodontitis was significantly more frequent in CAD patients than in controls (CAD patients: 91%; controls: 66%). The mean number of pockets was 18 +/- 17.1 in cardiac patients versus 7.6 +/- 12.7 in controls (P < 0.0001), despite the fact that the mean number of missing teeth was significantly greater in cases than in controls (14 +/- 7.1 versus 9 +/- 5.2; P < 0.0001). Furthermore, proportions of mobile teeth, bleeding sites, periodontal pockets, and involved furcations were significantly higher in CAD patients than in controls. In addition, the extent of the periodontal disease present was also greater in cases than in controls. A logistic model, adjusted for known cardiovascular risk factors, showed a strong association between CAD and periodontitis (odds ratio [OR] = 6.5). Moreover, there was a significant dose-response relationship between increasing scores of the periodontal risk of infectiousness and the presence of CAD (adjusted OR = 1.3 per PIRI unit). CONCLUSION: In the present study, periodontitis was revealed to be a significant risk factor for CAD after adjusting for other confounding factors, with the level of association increasing with the individual extent of the periodontal lesions.

Systemic release of endotoxins induced by gentle mastication: association with periodontitis severity.

BACKGROUND: Periodontitis has recently been identified as a potential risk factor for systemic pathologies such as cardiovascular disease, the hypothesis being that periodontal pockets could release pro-inflammatory bacterial components, for instance endotoxins, into the bloodstream. It is known that the oral cavity can be a source of circulating bacteria, but this has never been shown for bacterial endotoxins, and no evidence exists so far that the risk of systemic injury is related to the severity of periodontitis. The aim of the present study was to test the influence of gentle mastication on the occurrence of endotoxemia in patients with or without periodontal disease. METHODS: A total of 67 subjects were periodontally examined and grouped according to their periodontal status. This classification was based on an original index of severity of periodontal disease (periodontal index for risk of infectiousness, PIRI) aimed at reflecting the individual risk of systemic injury from the periodontal niches. Thus, the patients were classified into 3 risk groups: low, PIRI = 0; n = 25; moderate, 1 < or = PIRI < or = 5, n = 27; and high 6 < or = PIRI < or = 10, n = 15. Blood samples were collected before and 5 to 10 minutes after a standardized session of gentle mastication for detection of circulating endotoxins. Blood samples were tested with a chromogenic limulus amoebocyte lysate assay. RESULTS: Overall, blood levels of endotoxin after mastication were found to be significantly higher than before mastication (0.89 +/- 3.3 pg/ml versus 3.0 +/- 5.8 pg/ml; P= 0.0002). Likewise, the incidence of positive endotoxemia rose from 6% before mastication to 24% after mastication (P = 0.001). When accounting for the PIRI index, endotoxin levels and positive endotoxemia proved to be significantly higher in patients with severe periodontal disease than in the subjects with low or moderate periodontitis. CONCLUSIONS: Gentle mastication is able to induce the release of bacterial endotoxins from oral origin into the bloodstream, especially when patients have severe periodontal disease. This finding suggests that a diseased periodontium can be a major and underestimated source of chronic, or even permanent, release of bacterial pro-inflammatory components into the bloodstream.