C-reactive protein in gingival crevicular fluid may be indicative of systemic inflammation.

BACKGROUND AND AIM: Periodontitis is associated with elevated C-reactive protein (CRP) in both serum and gingival crevicular fluid (GCF). Although the liver is the primary source of CRP, extra-hepatic production of CRP has been reported. This study aimed to determine whether CRP in GCF is produced locally in the gingivae. MATERIALS AND METHODS: Gingivae and GCF were collected from non-periodontitis and periodontitis sites. Presence of CRP in gingivae was assessed by immunohistochemistry. CRP in GCF was measured using ELISA. Gene expression for CRP in gingivae was determined using real-time polymerase chain reaction. RESULTS: CRP was found in both the gingivae and GCF. No gingivae had detectable amounts of CRP mRNA. Not all patients with periodontitis had detectable levels of CRP in the GCF. Some non-periodontitis patients had detectable levels of CRP in the GCF. CONCLUSION: CRP in the GCF appears to be of systemic origin, and therefore may be indicative of systemic inflammation from either a periodontal infection or inflammatory disease elsewhere. The correlation between levels of CRP in GCF and serum requires validation in future studies.

Histopathological and ultrastructural features of dermal telangiectasias in systemic sclerosis.

AIMS: To investigate the histological, ultrastructural and immunohistochemical features of the vascular lining of dermal telangiectasia, a characteristic clinical finding in scleroderma. METHODS: Standard histological, electron microscopic and immunohistological techniques were used to examine dermal telangiectasias in five patients with limited scleroderma, the most common scleroderma variant in Caucasian populations. RESULTS: The telangiectasias were dilated postcapillary venules located in the papillary and superficial reticular dermis. The vessel walls consisted of non-fenestrated endothelial cells surrounded by a variable number of pericytes and smooth muscle cells. There were no unique ultrastructural features. Thickened collagen fibres in the reticular or deep dermis were seen in all but one patient, although in variable and generally minimal quantities. Surrounding infiltrating inflammatory cells were scarce. No enhanced endothelial staining was obtained with antibodies directed against endoglin, endothelin, E-selectin and ICAM-1 suggesting a resting or inactivated state. CONCLUSION: The immunohistological and ultrastructural features of the lining endothelium of established telangiectasias in long-standing, limited scleroderma appear benign. It would be of interest to examine telangiectasias in the early phase of their formation. Alternatively, other explanations need to be explored in understanding the aetiopathogenesis of telangiectasia in scleroderma.