New technique for the treatment of fresh bony mallet finger: A retrospective case series study.

Background: The bony mallet finger is a tear fracture of the extensor tendon, resulting in a flexion deformity of the finger, which affects both the function of the finger. The classical Ishiguro's method is associated with damage to the cartilage of the distal interphalangeal (DIP) joint and always lead to the joint stiffness. This paper explores a new technique to overcome the shortcomings of the classical Ishiguro's method and achieve better clinical efficacy. Methods: We examined 15 patients with bony mallet fingers, 9 males and 6 females, from February 2020 to June 2022, ranged from 23 to 58 years, including 1 case of index finger, 5 cases of middle finger, 3 cases of ring finger and 6 cases of little finger. The median course of the injury to surgery was 2 days (range, 1∼7 days). All had fresh closed injuries, according to the Wehbe and Schneider classification: 4 cases of type IA, 6 cases of type IB, 3 cases of type IIA and 2 cases of type IIB. All patients were treated surgically by the new technique. Post-operative follow-up was conducted to record the healing of the fracture, the pain of the affected finger and the function of joint movement. Results: The 15 cases were followed up after surgery. The median active range of motion was 65° (range, 55∼75°). The median extension deficit of DIP joint was 0° (range, 0∼11°). The median clinical healing time of the fracture was 6 weeks (range, 6∼10 weeks). None of the patients experienced significant pain. The patients were assessed according to the Crawford criteria at the final follow-up: 11 cases were assessed as excellent, 3 cases were assessed as good and 1 case was assessed as fair. No loss of fracture repositioning, loosening of internal fixation, skin necrosis or infection was observed. Conclusion: The application of the new technique for the treatment of bony mallet fingers has the advantages of good stability, fracture healing and functional recovery of the DIP joint, making it an ideal surgical procedure for the treatment of fresh bony mallet fingers.

Regulation of osteoblast autophagy based on PI3K/AKT/mTOR signaling pathway study on the effect of ß-ecdysterone on fracture healing.

OBJECTIVES: To investigate the effects of ß-ecdysterone on fracture healing and the underlying mechanism. METHODS: MTT assay was used to detect the cell viability. AO/PI and flow cytometry assays were used to determine the apoptotic rate. The expression level of RunX2, ATG7 and LC3 was evaluated by qRT-PCR and Western blot assays. X-ray and HE staining were conducted on the fractured femur. Immunohistochemical assay was used to detect the expression level of Beclin-1 and immunofluorescence assay was used to measure the expression level of LC3 in the fractured femurs. Western blot was utilized to determine the expression level of PI3K, p-AKT1, AKT1, p-mTOR, mTOR, p-p70S6K, and p70S6K. RESULTS: The ALP activity and the expression of RunX2 in fractured osteoblasts were significantly elevated, the apoptotic rate was suppressed by rapamycin, 60, and 80 µM ß-ecdysterone. The state of autophagy both in fractured osteoblasts and femurs was facilitated by rapamycin and ß-ecdysterone. Compared to control, Garrett score was significantly promoted in rapamycin and ß-ecdysterone groups, accompanied by ameliorated pathological state. Lastly, the PI3K/AKT/mTOR pathway both in fractured osteoblasts and femurs was inhibited by rapamycin and ß-ecdysterone. CONCLUSION: ß-ecdysterone might facilitate fracture healing by activating autophagy through suppressing PI3K/AKT/mTOR signal pathway.

Icariin alleviates osteoarthritis by regulating autophagy of chondrocytes by mediating PI3K/AKT/mTOR signaling.

Osteoarthritis (OA) is a chronic degenerative disease that significantly impacts the quality of life of the elderly population. Recently, the pathogenesis of OA has been reported to involve autophagy in chondrocytes. Intriguingly, icariin, one of the main components of epimedium, exerts multiple pharmacological effects, including a protective effect against chondrocyte damage. Thus, we aimed to investigate the therapeutic effect of icariin on OA and its potential underlying mechanism by using a rat model of OA. After treatment with icariin or an autophagy activator (rapamycin) or inhibitor (3-methyladenine), OA chondrocyte viability was measured using the CCK-8 assay, apoptosis in the chondrocytes was evaluated using the acridine orange-propidium iodide assay and flow cytometry, and OA tissue pathological state was assessed using micro-CT scanning and safranin O staining. Furthermore, immunohistochemical staining was used to measure the expression level of Beclin-1 and immunofluorescence labeling was used to visualize LC3 expression, and western blotting was used to determine the expression levels of autophagy proteins and key proteins in the PI3K signaling pathway. The apoptotic rate of OA chondrocytes was markedly elevated by 3-methyladenine and suppressed by rapamycin and icariin; autophagy genes were drastically downregulated in the 3-methyladenine group and upregulated in the rapamycin and icariin groups; and the PI3K/AKT/mTOR signaling pathway was activated by 3-methyladenine and inhibited by rapamycin and icariin. Notably, following treatment with rapamycin and icariin, the severe pathological state in OA cartilage tissues was substantially alleviated, and this was accompanied by activated autophagy and inhibited PI3K signaling in the cartilage tissues. Taken together, these findings indicate that icariin alleviates OA by regulating the autophagy of chondrocytes by mediating PI3K/AKT/mTOR signaling.

The facile synthesis of copper oxide quantum dots on chitosan with assistance of phyto-angelica for enhancing the human osteoblast activity to the application of osteoporosis.

Osteoblasts are an important key factor for the pathogenesis of several bone-related diseases, notably in osteoporosis. Osteoporosis is a disorder categorized based on the bone mineral density (BMD) and an alteration in the bone micro-architecture had been considered as the major determinant for increasing the fracture risk. The available medicine for curing the osteoporosis shows a minimal or no activity against the genesis or function of osteoblasts. The present study was conducted to determine the influence of phyto Angelica species (Ang.) mediated synthesized copper quantum dots decorated chitosan on human osteoblast cells for application of osteoporosis. The phyto compound of Angelica sp. was extracted by ethanol as solvent and it has been characterized through spectral analyses. An Angelica sp. mediated synthesized copper oxide quantum dots (CuO QDs) and the presence of CuO QDs on chitosan have been analyzed and exhibited by important spectral investigations. The morphological observation of CuO QDs on the chitosan (CS) was visualized by the microscopic analyses. The MTT assay results showed that cell growth of CuO QDs/CS-Ang. by the concentration dependent. The highest cell growth (87%) was noted at 5 µg/mL followed by 80 and 77% at 15 and 25 µg/mL respectively. The functional groups and potential compounds of Angelica sp. with CuO QDs/CS has been improved the osteoblast cell activity as prophylactic potentials against osteoporosis.

4-Phenylbutyric acid presents therapeutic effect on osteoarthritis via inhibiting cell apoptosis and inflammatory response induced by endoplasmic reticulum stress.

Osteoarthritis (OA) is a common bone and joint disease with a wild range of risk factors, which is associated with endoplasmic reticulum (ER) stress. The aim of our study was to discuss the possible mechanism of ER stress associated with OA in vivo and explore novel therapeutic method against OA. OA-induced damages in cartilage tissues were evaluated by HE, Safranin O/fast green, and TUNEL staining. The inflammatory factors concentration and the expression of FAP, MMP2, MMP9, Bax, Bcl-2, CHOP, and GRP78 were evaluated by ELISA, real-time PCR, and Western blot analyses. As results, 4-phenylbutyric acid (4-PBA)-treated OA cartilage tissues presented alleviated tissue damage with less apoptotic cells and cytokine production in comparison with advanced-OA tissues. Downregulation of Bax/Bcl-2, CHOP, GRP78, inflammatory factors, and reactive oxygen species generation, and the increase of MMP level detected after 4-PBA treatment indicated an inhibitory effect of 4-PBA on cell apoptosis, inflammatory response, and ER stress in OA. In conclusion, we indicate that ER stress causes cell apoptosis and inflammatory response, resulting in the tissue damage within OA. At the same time, 4-PBA exhibited protective effect on cartilage cells against OA through the inhibition of ER stress.

ß­Ecdysterone promotes autophagy and inhibits apoptosis in osteoporotic rats.

Osteoporosis is an aging process of skeletal tissues with characteristics of reductions in bone mass and microarchitectural deterioration of bone tissue. The present study aimed to investigate the effects of glucocorticoid­induced osteoporosis on osteoblasts and to examine the roles of ß­ecdysterone (ß­Ecd) involved. In the present study, an in vivo model of osteoporosis was established through the subcutaneous implantation of prednisolone (PRED) into Sprague­Dawley rats, with or without a subcutaneous injection of ß­Ecd (5 or 10 mg/kg body weight). Expression of Beclin­1 and microtubule­associated protein 1A/1B­light chain 3I/II and apoptosis in lumbar vertebrae tissues was measured by immunofluorescence and TUNEL assays, respectively. Serum concentration of calcium and phosphorus, and the activity of tartrate­resistant acid phosphatase (TRAP) and alkaline phosphatase (ALP) were measured by biochemical assay. Reverse transcription­quantitative polymerase chain reaction and western blotting was used for detect the expression of related genes and proteins. PRED treatment inhibited bone formation by decreasing bone mineral density, and suppressing the expression of Runt­related transcription factor 2 and bone morphogenetic protein 2, while enhancing the activity of alkaline phosphatase, upregulating the expression of receptor activator of nuclear factor-κB ligand, and increasing the serum content of calcium, phosphorus and tartrate­resistant acid phosphatase in rats. Additionally, PRED was revealed to inhibit autophagy through the downregulation of Beclin­1, autophagy protein 5 and microtubule­associated protein 1A/1B­light chain 3I/II expression, whereas it induced the apoptosis, through the activation of caspase­3 and the suppression of apoptosis regulator BCL2 expression. Notably, the PRED­induced alterations in bone formation, autophagy and apoptosis were revealed to be attenuated by ß­Ecd administration. In conclusion, the findings of the present study suggested that ß­Ecd may be a promising candidate for the development of therapeutic strategies for the treatment of osteoporosis, through the induction of autophagy and the inhibition of apoptosis in vivo.