Peroxisome proliferator–activated receptor (PPAR) subfamily play an important role in chondrogenesis. Previous study has reported that mixture of GW0742 (PPAR-δ agonist), hyaluronic acid (HA) and mesenchymal stem cells (MSCs) enhance chondrogenesis. The purpose of this study is to compare with efficacies of commercially available HA and demonstrate correlation of PPAR-γ and PPAR-δ. In this experimental study, MSCs were cultured with chondrogenic media and clinical HA gels (Euflexxa®, Synvisc®, Orthovisc® and Supartz®) using micormass culture method. Expression of type Ⅰ, Ⅱ collagen and matrix metalloprotease-13 (MMP-13) was measured by immunoblotting. MSCs were cultured with chondrogenic media and/or HA and/or GW0742 and/or rosiglitazone (PPAR-γ agonist) and/or human osteoarthritis synovial fluid. Immunoblotting was used to measure expression of type Ⅱ collagen and PPAR-γ. To identify the effective dose for chondrogenesis and adipogenesis, either 0.1, 1, 5 or 10 μM of rosiglitazone was added to MSCs in chondrogenic media or adipogenic media. Clinical HA gels inhibited expression of type Ⅰ collagen and enhanced the expression of MMP-13. Type Ⅱ collagen expression was significantly elevated in all treatment groups except Supartz®. GW0742 decreased the expression of PPAR-γ with/without inflammation condition. Rosiglitazone enhanced adipogenesis in a dose-dependent manner and enhanced the expression of type Ⅱ collagen under inflammation condition. Otherwise, the expression of type Ⅱ collagen and formation of chondrocyte spheroids showed a dose-dependent manner with a peak at 1 μM of rosiglitazone. PPAR-γ has a considerable anti-inflammatory effect and a strong pro-adipogenic effect, which inhibits the chondrogenic effect. PPAR-γ is related with PPAR-δ and shows a chondrogenic effect at lower concentrations. And clinical HA gels shows various efficacy of chondrogenesis. This study suggested that PPAR-γ and PPAR-δ are key regulatory factors of chondrogenesis.

Hard palate, developed by embryo neural crest stem cells, is a tissue with strong regenerative abilities. It is considered an abundant source of progenitor cells, forming various mesenchymal tissues. Rabbits are more suitable models than murine animals for regenerative preclinical study of the head and neck, owing to their larger size. However, there are no reports of the existence or characteristics of neural crest stem cells in the hard palate of rabbits. In this study, we demonstrate for the first time the presence of nestin-, Sox2-, and p75-positive neural crest stem cells obtained from the hard palate of rabbits and the properties of these cells. Flow cytometry analysis revealed that CD29, CD44, and CD81 were positive; and CD11b, CD34, and CD90 were negative on the ex vivo expanded palatal progenitor cells. Finally, we differentiated them into cells of mesenchymal lineages (bone, cartilage, and fat) in vitro, and in three-dimensional fabricated polycaprolactone and polycaprolactone–tricalcium phosphate scaffolds. Taken together, our data showed the existence of rabbit palatum-derived mesenchymal progenitor cells, and successful fabrication of progenitor cell-loaded biodegradable scaffold using three-dimensional printing. This study will open avenues for new tissue engineering strategies for cell therapy using three-dimensional printing with scaffolds for reconstruction of head and neck defects.

Purpose: A vascularized bone graft is an option showing a good result to treat scaphoid nonunion. The analysis of the effects of smoking, which affects vascular and union of fracture, has been limited. We tried to analyze the effect of smoking on the outcomes of vascularized bone graft in scaphoid nonunion through meta-analysis Methods: Two researchers analyzed 923 papers searched for ‘scaphoid AND (vascularized OR vascularised OR flap OR pedicled)’ on MEDLINE and Embase (until November 2020). We selected 31 papers which contain that vascularized bone graft was performed for scaphoid nonunion, and the number or proportion of smokers could be confirmed. Through meta-regression analysis and subgroup analysis, whether the smoker’s rate had an effect on union rate, union period, functional score, imaging evaluation, range of motion, and complications rate was analyzedResults: A significant negative correlation between smoking and bone union rate was confirmed in pedicled vascularized bone grafting, and a significant positive correlation between smoking and bone union duration was confirmed in free vascularized bone grafting. Conclusion: It is necessary to have caution for nonunion when considering pedicled vascularized bone graft in smoking patients with scaphoid nonunion.

Sarcopenia and glucocorticoid-induced myopathy are significant forms of muscle atrophy that pose considerable public health challenges. In this regard, preventing muscle atrophy is crucial for enhancing quality of life and increasing life expectancy. In this study, we investigated the effect of recombinant human KAI1 (rhKAI1) on myogenic differentiation and its protective effect against dexamethasone-induced muscle atrophy. rhKAI1 enhanced myogenic differentiation in both murine C2C12 myoblasts and primary human endometrial stromal cells, as evidenced by upregulation of myogenic regulatory factors and increased myotube formation. These effects were accompanied by increased phosphorylation of Akt and AMPK. In a dexamethasone (Dex)-induced atrophy model, rhKAI1 increased myotube diameter, restored MyHC expression, and reduced the expression of the E3 ligase atrogin-1, accompanied by increased phosphorylation of Akt and AMPK. In addition, rhKAI1 administration improved Dex-induced functional impairment in mice, as reflected by increased grip strength and improved rotarod performance. Molecular analyses further showed that rhKAI1 modulated Dex-induced fiber-type-related gene expression by restoring MYH7 (type I) and reducing MYH4 (type IIb) expression. Collectively, our findings demonstrate that rhKAI1 promotes myogenic differentiation and alleviates several functional and molecular features associated with glucocorticoid-induced muscle deterioration. These results support the potential of rhKAI1 as a candidate molecule for further investigation in steroid-induced muscle dysfunction.