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BACKGROUND: Patients with hypertrophic scarring tend to experience recurrence after treatment, which often occurs in areas of the body with high skin tension. AIMS: To evaluate better treatments aimed at reducing the risk of scar recurrence in areas of high skin tension. METHODS: Patients were randomly divided into the following three treatment groups: botulinum toxin type A (BTA) via dual-plane micro-drop injections, triamcinolone acetonide (TAC) suspension, and CO2 via fractional CO2 laser. Interventions were implemented in all three groups once a month for three consecutive sessions. After the final treatment, scarring was evaluated at 1, 3, 6, 12, and 24 months using the Patient and Observer Scar Assessment Scale (POSAS). RESULTS: The 3-month POSAS score for each scar indicator in the treatment groups was significantly lower than that in the preoperative groups (p < 0.001). The scar score in the TAC group decreased at 3 months and increased thereafter. For other groups, the scar score continually decreased at all time points according to the Patient Scar Assessment Scale. Based on the Observer Scar Assessment Scale, the scar score continuously decreased at all time points in the BTA group; in the TAC group, it decreased at 1 month and increased thereafter; and in the CO2 group, the scar score decreased at 3 months and subsequently stabilized. CONCLUSIONS: All three treatment methods were effective. However, the BTA group experienced a reduced risk of scar recurrence and maintained long-term treatment effects.

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The processes of hypertrophic scar formation are extremely complex, and current animal models have limitations in terms of the complete characterization of lesions. An ideal animal model is indispensable for exploring the complex progression of scar formation to elucidate its pathophysiology and to perform therapeutic testing. This study aimed to establish a long-term, consistent and easily testable animal model by injecting anhydrous alcohol into the dorsal trunk dermis of rabbits. The rabbits were injected with different amounts of anhydrous alcohol. Anhydrous alcohol was infiltrated into the subcutaneous and superficial fascia. The optimal amount of anhydrous alcohol was determined by measuring the area and thickness of the scar. The typical model was established by determining the optimum dosage, and then we analysed the histological characteristics and fibrosis-associated protein expression. The dermal scar was generated by treating with 2 ml/kg anhydrous alcohol and displayed histopathologic features that characterize human hypertrophic scarring, including a parallel collagen fibre orientation, dermal and epidermal thickening, broad collagen deposition and the loss of dermal adnexal structures. The expression of fibrotic pan-markers was also enhanced. Moreover, the scar features and duration were compared between the anhydrous alcohol model and the rabbit ear model. Our results show that injecting anhydrous alcohol in the rabbit model thickened the dermal tissue, stimulated dermal fibroproliferation and resulted in hypertrophic scars with protein and histologic features similar to those seen in humans. Taken together, the findings from this study show that our model could be a feasible and useful tool for further research on the pathogenesis of hypertrophic scars.

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Traumatic pulsating masses are difficult to make a definitive diagnosis due to anatomic variation of malformed vessels and rarely clinical incidence. It is essentially to recognizing the anatomy of such vessels, otherwise it may lead to an improperly treatment or serious complication. Digital subtraction angiogram (DSA) has a distinct advantage in both diagnosis and treatment of this subject. Here the authors report a case of venous malformation in the supraclavicular fossa with an underlying arteriovenous fistula following nonoperative management of a clavicle fracture in an adult, and discuss how to rule out potential differential diagnoses and get minimally invasive treatment with DSA.

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OBJECTIVE: To investigate the tumor-suppressing effect of microRNA-218 (miR-218) in osteosarcoma (OS) and explore its molecular mechanism. METHODS: We examined the expression levels of miR-218 in 68 pairs of OS and adjacent tissue samples using qRT-PCR. Cultured human OS cell line Saos-2 was transfected with miR-218 mimics or anti-miR-218 mimics, and the cell apoptosis was assessed using CCK-8 assay, annexin V-FITC staining and Western blotting. We also analyzed the potential functional targets of miR-218 in Saos-2 cells using luciferase assay, qRT-PCR and Western blotting. RESULTS: The expression level of miR-218 was lowered by at least 8 folds in OS tissues as compared with the adjacent tissues. In cultured Saos-2 cells, transfection with miR-218 mimics for 24, 36, and 48 h resulted in a significant reduction in the cell viability, while transfection with anti-miR-218 mimics significantly increased the cell viability. The cells transfected with miR-218 mimics showed an obviously enhanced expression of cleaved poly(ADP-ribose) polymerase (C-PARP) as compared with the cells transfected with anti-miR-218 mimics and the control cells. Flow cytometry demonstrated obviously increased apoptosis of the cells following miR-218 mimics transfection. We identified the oncogene B lymphoma mouse Moloney leukemia virus insertion region 1 (BMI-1) as a specific target of miR-218 in Saos-2 cells. BMI-1 expressions at both the mRNA and protein levels were significantly reduced in Saos-2 cells overexpressing miR-218 but increased in the cells with miR-218 knockdown as compared to the control cells. Luciferase reporter assay indicated that miR-218 directly inhibited the expression of BMI-1 via binding to its 3'-UTR in OS cells. CONCLUSION: miR-218 can promote OS cell apoptosis and plays the role as a tumor suppressor by down-regulating BMI-1.

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Congenital muscular torticollis (CMT) is a neck deformity that involves shortening of sternocleidomastoid muscle (SCM) characterized by muscle atrophy and interstitial fibrosis. To investigate wheatear Botulinum toxin type A (BTA) has anti-fibrotic effects in CMT, we established acquired muscular torticollis that mimetics CMT in rabbit by intra-SCM injection of anhydrous alcohol. The treatment groups received BTA (2.5units or 5units) injection into the fibrotic SCM. The shortening and thickening of SCM were recorded by B-mode ultrasound. Changes in Col1A1, Fn, α-SMA expression were determined by immunohistochemistry. In vitro studies, TGF-ß induced NIH3T3 fibroblasts were used to evaluate anti-fibrosis effect of BTA. Expression of the myofibroblast marker α-SMA and fibrosis markers Col1A1 and Fn were detected by Western blotting and quantitative RT-PCR. Our results showed that BTA injection attenuated shortening and thickening of fibrotic SCM. Elevated expression of Col1A1, Fn, α-SMA were confirmed in this fibrotic muscle model but reversed after BTA injection. Similar results observed in TGF-ß induced NIH3T3 fibroblasts in both mRNA and protein levels. In conclusion, our results suggested that BTA could be a promising agent against SCM fibrosis in CMT through regulating fibroblast and inhibiting myofibroblast differentiation.

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