Abstract
This study aimed to analyze the effects of fibrin constructs enhanced with laminin-nidogen, implanted in the wounded rat soft palate. Fibrin constructs with and without laminin-nidogen were implanted in 1 mm excisional wounds in the soft palate of 9-week-old rats and compared with the wounded soft palate without implantation. Collagen deposition and myofiber formation were analyzed at days 3, 7, 28 and 56 after wounding by histochemistry. In addition, immune staining was performed for a-smooth muscle actin (a-SMA), myosin heavy chain (MyHC) and paired homeobox protein 7 (Pax7). At day 56, collagen areas were smaller in both implant groups (31.25 ± 7.73% fibrin only and 21.11 ± 6.06% fibrin with laminin-nidogen)) compared to the empty wounds (38.25 ± 8.89%, p < 0.05). Moreover, the collagen area in the fibrin with laminin-nidogen group was smaller than in the fibrin only group (p ˂ 0.05). The areas of myofiber formation in the fibrin only group (31.77 ± 10.81%) and fibrin with laminin-nidogen group (43.13 ± 10.39%) were larger than in the empty wounds (28.10 ± 11.68%, p ˂ 0.05). Fibrin-based constructs with laminin-nidogen reduce fibrosis and improve muscle regeneration in the wounded soft palate. This is a promising strategy to enhance cleft soft palate repair and other severe muscle injuries.
Highlights
Around 46% of all Cleft lip and/or palate (CLP) cases have a cleft in the soft palate, which results in diminished functions such as swallowing and speaking [3,4,5]
In the two days after surgery the rats lost less than 15% of their body weight pre-surgery, which had recovered by day five
This study aimed to evaluate the effects of fibrin constructs with or without lamininnidogen on fibrosis and myofiber regeneration in the wounded soft palate
Summary
Around 46% of all CLP cases have a cleft in the soft palate, which results in diminished functions such as swallowing and speaking [3,4,5]. About 30% of all cases with a cleft in the soft palate experience persistent problems with speech [6]. Craniofacial muscles seem to regenerate less than other skeletal muscles and show extensive fibrosis [7]. This is mainly caused by transforming growth factor-β1 (TGFβ1) that induces the production of large amounts of collagen type I [3,8]. TGFβ1 inhibits the development of new muscle fibers, by reducing the proliferation, differentiation and fusion of satellite cells (SCs), the stem cells of muscle tissue [3,8,9]
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