Er:YAG laser irradiation has been reported to enhance wound healing. However, no studies have evaluated the synthesis of growth factors after laser irradiation. The present study investigated the effects of laser irradiation on the amount of secretion of platelet derived growth factor (PDGF) in the wound, clarifying the effects of the Er:YAG laser on the bone healing. Osteotomies were prepared in the tibiae of 28 rats using an Er:YAG laser (test group). Maximum power of 8 watts, energy per pulse of 700 mJ, and frequency up to 50 Hz were used. The laser was used with external water irrigation, a spot size of 2 mm, energy per pulse of 500 to 1000 mJ/pulse, and energy density of 32 J/cm(2). Twenty eight additional rats served as a control group and their osteotomies were prepared with a drill 1.3 mm in diameter at 1000 rpm, with simultaneous saline irrigation. Two rats from the tested group and 2 from the control group were sacrificed on each day following surgery (1-14 days), and the tissue specimens were prepared for histologic evaluation. Immunohistochemical staining with anti-PDGF was performed after histologic examination. The difference between the PDGF staining intensities of the 2 treatment groups was analyzed using a multivariate logistic regression test. A significant rise in PDGF staining occurred in both groups 2-3 days following surgery. However, while high PDGF counts remained for the 2-week experimental period in the laser group, PDGF levels in the control group returned to baseline levels 8 days post surgery. The 2 groups (laser and control) were found to be different throughout the experiment, and the rat type was found to be a significant predictor (P = .000011). The present study demonstrated that Er:YAG laser irradiation seems to stimulate the secretion of PDGF in osteotomy sites in a rat model. It is possible that the high levels of PDGF are part of the mechanism that Er:YAG irradiation enhances and improves the healing of osteotomy sites.
Hyperglycemic environment alters responsiveness of renal cells to in-vitro simulation of malignant hypertension. The main consequence of either malignant hypertension or hyperglycemia is exaggerated apoptosis. However, the operating mechanisms differ: Malignant hypertension stimulates renal cell apoptosis via increased angiotensin-II, whereas hyperglycemia elicits apoptosis via augmented p53. By contrast to pressure-induced excessive proliferation of normoglycemic cells, hyperglycemia prohibits elevated proliferation in response to pressure. Angiotensin-II production is maximally augmented by hyperglycemic environment and is not stimulated further by pressure application.
The EndoFast Reliant system provides significantly stronger attachment in the immediate postoperative period (0-3 days) compared with trocar-based techniques, and this difference disappeared at day 15 postsurgery.
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