We investigated oral health of chronic kidney disease (CKD) patients at predialysis state. The hypothesis was that diabetic nephropathy affects oral health more detrimentally than other CKD patients due to the known risk diabetes presents in this regard. We expected worse oral health and particularly poor periodontal health among the diabetic patients. A cross-sectional study was conducted in the Helsinki University Central Hospital, Finland, on 148 patients with different kinds of kidney disease at predialysis state. Data from medical records, clinical oral examination, saliva, and mucosal yeast counts were analyzed and compared between the disease groups. Of the patients, 53 (36%) had diabetic nephropathy (29 patients with type 1, 24 patients with type 2 diabetes). Compared with other CKD patients, diabetic patients had poor glycemic control as expected (mean HbA(1C) 8.0% vs 5.9%, p < 0.01). Diabetic patients also had more dental caries (mean number of carious teeth 5.1 vs 3.1, p < 0.01) and lower salivary flow rates than other CKD patients (stimulated salivary flow 1.2 ml/min vs 1.6 ml/min, p < 0.05). No difference between groups was observed in periodontal health and yeast counts. In conclusion, diabetic nephropathy patients indeed had worse dental health in comparison to CKD group. However, contrary to our expectation, diabetic nephropathy did not seem to affect periodontal health more severely than the other kidney diseases.
Elevated salivary MMP-8 associated significantly with more severe oral/periodontal inflammatory burden among patients with CKD at the predialysis stage. Thus, salivary MMP-8 analysis could give adjunctive information regarding oral health.
We have investigated re-epithelialization following induction of suction blisters in humans in intact blisters, open wounds, i.e. blister roofs removed immediately after blister induction, and calcipotriol-pretreated open wounds. Intact blisters simulate blister healing in bullous disease, while open wounds simulate re-epithelialization during wound healing. Re-epithelialization was clearly faster in open wounds than in intact blisters, and was not affected by calcipotriol pretreatment. Bullous pemphigoid antigen 2 (BP180), bullous pemphigoid antigen 1 (BP230), plectin/hemidesmosomal 1 protein (HD1), laminin 5, laminin alpha5, laminin beta1, type VII collagen, tenascin-C, beta4, alphavbeta5, alpha5 and alpha9 integrins were studied in intact blisters and open wounds by immunohistochemistry. Hemidesmosomal plaque proteins BP230 and plectin/HD1, which connect the keratin cytoskeleton to the hemidesmosome, appeared earlier at the leading edge in intact blisters than in open wounds. Band-like immunostaining in the basement membrane for laminin 5, alpha5 and beta1 chains was continuous in blister bases, but partially discontinuous in open wound bases. The other antigens studied showed similar expression in intact blisters and open wounds. BP180, BP230, plectin/HD1, beta4 integrin, laminin 5 and tenascin-C expression were further studied in calcipotriol-pretreated open wounds. Calcipotriol did not affect the expression of these antigens. The immunohistochemical results suggest that the keratin cytoskeleton is linked to the basal plasma membrane of migrating basal cells via BP230 and plectin/HD1 earlier in the more slowly re-epithelializing blisters than in open wounds. An intact laminin sheath may inhibit keratinocyte migration in intact blisters.
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