Background. Postoperative pain management remains a significant challenge for all healthcare providers. A randomized controlled trial was conducted to examine the adjuvant effects of auricular acupressure on relieving postoperative pain and improving the passive range of motion in patients with total knee replacement (TKR). Method. Sixty-two patients who had undergone a TKR were randomly assigned to the acupressure group and the sham control group. The intervention was delivered three times a day for 3 days. A visual analog scale (VAS) and the Short-Form McGill Pain Questionnaire were used to assess pain intensity. Pain medication consumption was recorded, and the knee motion was measured using a goniometer. Results. The patients experienced a moderately severe level of pain postoperatively (VAS 58.66 ± 20.35) while being on the routine PCA. No differences were found in pain scores between the groups at all points. However, analgesic drug usage in the acupressure group patients was significantly lower than in the sham control group (P < 0.05), controlling for BMI, age, and pain score. On the 3rd day after surgery, the passive knee motion in the acupressure group patients was significantly better than in the sham control group patients (P < 0.05), controlling for BMI. Conclusion. The application of auricular acupressure at specific therapeutic points significantly reduces the opioid analgesia requirement and improves the knee motion in patients with TKR.

Anterior cruciate ligament (ACL) tear can lead to osteoarthritis (OA). However, parathyroid hormone (PTH)-(1-34) was found to alleviate OA progression in a papain-induced OA model. Autophagy is a protective mechanism in normal cartilage, and its aging-related loss is linked with chondrocyte death and OA. Thus we examined the roles of autophagy in PTH treatment in OA after ACL transection (ACLT). Thirty-six rats were randomized into three groups: control group, ACLT-induced OA (OA) group, and OA with intra-articular PTH-(1-34) treatment (OA+PTH) group. Weight-bearing and treadmill tests were evaluated. Cartilage matrix was determined by a histological evaluation of glycosaminoglycan (GAG), Osteoarthritis Research Society International (OARSI) score, chondrocyte apoptosis, and immunohistochemistry. Rats in the OA group had significantly decreased weight bearing and running endurance. The histological results indicated that GAG, collagen type II, and chondrocyte autophagy had decreased but that the OARSI score, terminal differentiation markers (collagen type X and Indian hedgehog), and chondrocyte apoptosis had increased in the OA group. Additionally, PTH-(1-34) treatment significantly improved weight bearing and treadmill endurance, preserved GAG and collagen type II, and reduced the OARSI score and terminal differentiation markers. Finally, PTH-(1-34) ameliorated chondrocyte apoptosis by regulating the expression of autophagy-related proteins, through reducing mechanistic target of rapamycin (mTOR) and p62 and enhancing microtubule-associated protein-1 light chain 3 (LC3) and beclin-1. Reconstructive surgery after ACL rupture cannot prevent OA occurrence. Intra-articular PTH-(1-34) treatment can alleviate OA progression after ACLT and histological molecular changes. Possible mechanisms are reducing chondrocyte terminal differentiation and apoptosis, with increasing autophagy. NEW & NOTEWORTHY Anterior cruciate ligament (ACL) tear can lead to osteoarthritis (OA). Intra-articular parathyroid hormone (PTH)-(1-34) significantly improved weight bearing and treadmill endurance, preserved glycosaminoglycan and collagen type II, and reduced Osteoarthritis Research Society International (OARSI) score and terminal differentiation. Finally, PTH-(1-34) ameliorated chondrocyte apoptosis by regulating the expression of autophagy-related proteins, through reducing mechanistic target of rapamycin (mTOR) and p62 and enhancing microtubule-associated protein-1 light chain 3 (LC3) and beclin-1. PTH-(1-34) can alleviate OA progression after ACL transection. Possible mechanisms are reducing chondrocyte terminal differentiation and apoptosis, with increasing autophagy.