Intra-socket application of medical-grade honey after tooth extraction attenuates inflammation and promotes healing in cats.

OBJECTIVES: Dental diseases are a major problem in cats and often necessitate tooth extraction. Medical-grade honey (MGH) has antimicrobial and wound-healing properties, and therefore the aim of this study was to investigate whether intra-socket application improved healing after tooth extraction. It was postulated that applying MGH would reduce inflammation, improve the viability of the surgical flap and enhance healing following tooth extraction. METHODS: A prospective randomised controlled trial was performed in client-owned cats undergoing bilateral tooth extractions of the same element of the canine or (pre)molar tooth. A split-mouth design was used in which every animal served as its own control. After surgical extraction of the elements, the sockets on one side were filled with an MGH-based ointment (L-Mesitran Soft), whereas the contralateral side received no treatment (control). A mucoperiosteal flap was used on both sides, and simple interrupted monofilament sutures were placed. No antimicrobial drugs were administered. Clinical parameters (inflammation/redness, flap viability and wound healing) were subjectively analysed on days 3 and 7 post-extraction by a veterinarian blinded to the treatment. RESULTS: Twenty-one cats were included. MGH significantly decreased signs of inflammation (P <0.01), improved mucoperiosteal flap viability (P <0.01) and promoted wound healing (P = 0.01), at both time points. MGH was easy to apply and there were no adverse events. CONCLUSIONS AND RELEVANCE: Intra-socket application of MGH after tooth extraction positively affects the surgical wound, as it reduces redness, improves flap viability and enhances wound healing. Applying MGH represents a potent adjuvant therapy to support intra-oral wound healing after tooth extraction.

Retinoic acid effects on in vitro palatal fusion and WNT signaling.

Retinoic acid is the main active vitamin A derivate and a key regulator of embryonic development. Excess of retinoic acid can disturb palate development in mice leading to cleft palate. WNT signaling is one of the main pathways in palate development. We evaluated the effects of retinoic acid on palate fusion and WNT signaling in in vitro explant cultures. Unfused palates from E13.5 mouse embryos were cultured for 4 days with 0.5 µM, 2 µM or without retinoic acid. Apoptosis, proliferation, WNT signaling and bone formation were analyzed by histology and quantitative PCR. Retinoic acid treatment with 0.5 and 2.0 µM reduced palate fusion from 84% (SD 6.8%) in the controls to 56% (SD 26%) and 16% (SD 19%), respectively. Additionally, 2 µM retinoic acid treatment increased Axin2 expression. Retinoic acid also increased the proliferation marker Pcna as well as the number of Ki-67-positive cells in the palate epithelium. At the same time, the WNT inhibitors Dkk1, Dkk3, Wif1 and Sfrp1 were downregulated at least two-fold. Retinoic acid also down-regulated Alpl and Col1a2 gene expression. Alkaline phosphatase (ALP) activity was notably reduced in the osteogenic areas of the retinoic acid- treated palates. Our data suggest that retinoic acid impairs palate fusion and bone formation by upregulation of WNT signaling.

Remote ischaemic preconditioning by brief hind limb ischaemia protects against renal ischaemia-reperfusion injury: the role of adenosine.

BACKGROUND: Remote ischaemic preconditioning (RIPC) is a strategy to protect a target organ against ischaemia-reperfusion injury (IRI) by inducing short-term ischaemia/reperfusion (I/R) in a remote organ. RIPC of the kidney by temporary limb occlusion would be a safe, inexpensive and noninvasive method to prevent renal damage in, e.g., transplantation and aortic surgery. We investigated whether brief hind limb occlusion can protect against renal IRI and whether this protection is adenosine dependent. METHODS: Rats underwent either no RIPC, unilateral RIPC or bilateral RIPC. The preconditioning stimulus was either continuous (12'/12' I/R) or fractionated (three times 4'/4' I/R). After the last reperfusion period, we induced 25' ischaemia in the right kidney. RESULTS: After 24 h of reperfusion, renal function was improved by 30-60% in both bilateral RIPC groups and in the fractionated unilateral group. Renal tubule damage and kidney injury molecule-1 expression were reduced in three of four RIPC groups. Treatment with the adenosine receptor blocker 8-(p-sulfophenyl)theophylline had no effect on fractionated or continuous RIPC. CONCLUSIONS: Brief hind limb ischaemia induces protection against renal IRI, which makes this a promising strategy to prevent renal IRI in a clinical setting. Bilateral RIPC was more effective than unilateral RIPC, and this protection occurs via an adenosine-independent mechanism.