Chlorhexidine là gì? Các công bố khoa học về Chlorhexidine

The recent paradigm that endogenous collagenolytic and gelatinolytic activities derived from acid-etched dentin result in degradation of hybrid layers requires in vivo validation. This study tested the null hypothesis that there is no difference between the degradation of dentin bonded with an etch-and-rinse adhesive and that in conjunction with chlorhexidine, an MMP inhibitor, applied after phosphoric-acid-etching. Contralateral pairs of bonded Class I restorations in primary molars of clinical subjects were retrieved after a six-month period of intra-oral functioning and processed for transmission electron microscopy. Hybrid layers from the chlorhexidine-treated teeth exhibited normal structural integrity of the collagen network. Conversely, abnormal hybrid layers were seen in the control teeth, with progressive disintegration of the fibrillar network, to the extent that it was beyond detection by collagen staining. Self-destruction of collagen matrices occurs rapidly in resin-infiltrated dentin in vivo and may be arrested with the use of chlorhexidine as an MMP inhibitor.

Matrix metalloproteinases (MMPs) are a host cell-derived proteolytic enzyme family which plays a major role in tissue-destructive inflammatory diseases such as periodontitis. The aim of the present study was to evaluate the inhibitory effect of chlorhexidine (CHX) on MMP-2 (gelatinase A), MMP-9 (gelatinase B), and MMP-8 (collagenase 2) activity. Heat-denatured type I collagen (gelatin) was incubated with pure human MMP-2 or -9 activated with p -aminophenylmercuric acetate (APMA), and the proteolytic degradation of gelatin was monitored by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and Coomassie blue staining. The effect of CHX on MMP-8 activity was also studied with a cellular model addressing the ability of phorbol myristate acetate (PMA)-triggered human peripheral blood neutrophils (polymorphonuclear leukocytes [PMNs]) to degrade native type I collagen. CHX inhibited the activities of both gelatinases (A and B), but MMP-2 appeared to be more sensitive than MMP-9. Adding calcium chloride to the assay mixtures almost completely prevented the inhibition of MMP-9 activity by CHX, while the inhibition of MMP-2 activity could be reversed only when CHX was used at a low concentration. This observation suggests that CHX may act via a cation-chelating mechanism. CHX dose-dependently inhibited collagenolytic activity of MMP-8 released by PMA-triggered PMNs. MMP-8 without APMA activation was inhibited clearly more efficiently than APMA-activated MMP-8. Our study suggests that the direct inhibition of the MMPs’ activities by CHX may represent a new valuable effect of this antimicrobial agent and explains, at least in part, the beneficial effects of CHX in the treatment of periodontitis.

Host-derived proteases have been reported to degrade the collagen matrix of incompletely-resin-infiltrated dentin. This study tested the hypothesis that interfacial degradation of resin-dentin bonds may be prevented or delayed by the application of chlorhexidine (CHX), a matrix metalloproteinase inhibitor, to dentin after phosphoric acid-etching. Contralateral pairs of resin-bonded Class I restorations in non-carious third molars were kept under intra-oral function for 14 months. Preservation of resin-dentin bonds was assessed by microtensile bond strength tests and TEM examination. In vivo bond strength remained stable in the CHX-treated specimens, while bond strength decreased significantly in control teeth. Resin-infiltrated dentin in CHX-treated specimens exhibited normal structural integrity of the collagen network. Conversely, progressive disintegration of the fibrillar network was identified in control specimens. Auto-degradation of collagen matrices can occur in resin-infiltrated dentin, but may be prevented by the application of a synthetic protease inhibitor, such as chlorhexidine.

Loss of hybrid layer integrity compromises resin-dentin bond stability. Matrix metalloproteinases (MMPs) may be partially responsible for hybrid layer degradation. Since chlorhexidine inhibits MMPs, we hypothesized that chlorhexidine would decelerate the loss of resin-dentin bonds. Class I preparations in extracted third molars were sectioned into two halves. One half was customarily restored (etch-and-rinse adhesive/resin composite), and the other was treated with 2% chlorhexidine after being acid-etched before restoration. Specimens were stored in artificial saliva with/without protease inhibitors. Microtensile bond strengths and failure mode distribution under SEM were analyzed immediately after specimens’ preparation and 6 months later. With chlorhexidine, significantly better preservation of bond strength was observed after 6 months; protease inhibitors in the storage medium had no effect. Failure analysis showed significantly less failure in the hybrid layer with chlorhexidine, compared with controls after 6 months. In conclusion, this in vitro study suggests that chlorhexidine might be useful for the preservation of dentin bond strength.

Trong một đợt bùng phát nhiễm Serratia marcescens tại bệnh viện của chúng tôi, chúng tôi đã phát hiện sự nhiễm bẩn rộng rãi của dung dịch rửa tay chlorhexidine 2% bởi S. marcescens. Khảo sát bằng kính hiển vi điện tử các mặt của chai chứa dung dịch này cho thấy vi sinh vật đã bám vào một ma trận sợi. Vi khuẩn tự do trong chất lỏng cho thấy hình thái học bất thường, với vách tế bào bị phá vỡ hoặc có biến đổi về nguyên sinh chất. Hơn nữa, các vi khuẩn bám vào thành chai trữ và nằm trong ma trận sợi này cũng có nguyên sinh chất bị biến dạng. Mặc dù có những thay đổi này, các sinh vật S. marcescens còn sống vẫn được thu hồi từ chất lỏng trong suốt thời gian lưu trữ kéo dài 27 tháng. Nồng độ chlorhexidine cần để ức chế các dòng Serratia này là 1.024 microgram/ml; tuy nhiên, vi sinh vật có thể sống sót trong nồng độ lên tới 20.000 microgram/ml. Cần nghiên cứu thêm để xác định cơ chế cho phép vi khuẩn này nhiễm bẩn và sống sót trong các dung dịch khử trùng.

Although it is known that chlorhexidine application may preserve resin–dentin bonds from degradation, the lowest optimal concentration and application time have yet to be established. This study evaluated the effects of different concentrations of chlorhexidine digluconate and different application times on the preservation of resin–dentin bonds formed using two etch‐and‐rinse adhesives. In experiment 1, after acid etching, the occlusal demineralized dentin was rewetted either with water or with 0.002, 0.02, 0.2, 2, or 4% chlorhexidine for 60 s. In experiment 2, the surfaces were rewetted with water, or with 0.002% or 2% chlorhexidine for 15 or 60 s. After this, both adhesives and composite resin were applied and light‐cured. Bonded sticks (0.8 mm²) were tested under tension (0.5 mm min⁻¹) immediately or after 6 months of storage in water. Two bonded sticks from each tooth were immersed in silver nitrate and analyzed quantitatively using scanning electron microscopy. Reductions in microtensile bond strengths and higher silver nitrate uptake were observed for both adhesives when the rewetting procedure was performed with water. Stable bonds were maintained for up to 6 months under all chlorhexidine conditions tested, irrespective of the chlorhexidine concentration and application time. The use of 0.002% chlorhexidine for 15 s seems to be sufficient to preserve resin–dentin interfaces over a 6‐month period.