The relationship between body mass index and clinical efficacy of knee arthroplasty in patients with knee osteoarthritis.

Background: Increase body mass index (BMI) is often accompanied by metabolic diseases such as diabetes, which will increase the uncertainty of total knee arthroplasty (TKA) efficacy and the risk of postoperative complications. The present study was to study the relationship between increase BMI and clinical efficacy of knee arthroplasty in patients with knee osteoarthritis. Methods: A total of 97 patients (36 males and 61 females) with knee osteoarthritis (KOA) who underwent TKA surgery were selected. According to the preoperative body mass index (BMI), the patients were divided into a normal group (n=42), overweight group (n=35), and obese group (n=20). All patients received TKA after admission. Seven days after surgery, the American Knee Society (AKS) and the Hospital for Special Surgery (HSS) scales were used to evaluate the recovery of knee function. The recovery was poor if the scores of AKS and HSS were less than 70. Results: Seven days after TKA, the scores of AKS and HSS in different BMI groups were significantly different, and decreased with the increase of BMI (P<0.05). Age, increased BMI, diabetes, preoperative range of motion (ROM), intraoperative blood loss, postoperative C-reactive protein (CRP), postoperative posterior slope angle (PSA), postoperative infection, and postoperative deep vein thrombosis (DVT) of lower extremities were related to AKS score <70 (P<0.05). Diabetes, preoperative ROM, intraoperative blood loss, postoperative CRP, postoperative PSA, and postoperative infection were related to HSS score <70 (P<0.05). Increased BMI, diabetes, postoperative CRP, postoperative infection, and postoperative DVT were independent risk factors for AKS score <70 (HR =3.458, 1.152, 2.960, 1.023, 3.589, P<0.05). Increased BMI, diabetes, postoperative CRP, and postoperative infection were independent risk factors for HSS score <70 (HR =6.891, 1.263, 1.967, 1.235, P<1.235). The area under the curve (AUC) (95% CI) of BMI in diagnosing AKS <70 was 0.740 (0.641-0.839). The AUC (95% CI) of BMI in diagnosing HSS <70 was 0.809 (0.723-0.894). Conclusions: The increase of BMI is an independent risk factor for the poor recovery of knee function after TKA in patients with KOA.

Relationship between Change in Bone Mineral Density of Lumbar Spine and Risk of New Vertebral and Nonvertebral Fractures: A Meta-Analysis.

Studies have shown that the change in lumbar spine bone mineral density with different osteoporosis drugs had a beneficial effect on the frequency of new vertebral and nonvertebral fractures in postmenopausal females, but their results were conflicting. This meta-analysis was performed to evaluate this relationship. A systematic literature search up to May 2020 was performed and 20 studies with 73,390 postmenopausal females were included; of them, a total of 41,980 were treated with osteoporosis drugs and 31,410 with placebo. They reported relationships between the change in lumbar spine bone mineral density and the frequency of new vertebral and nonvertebral fractures in postmenopausal females. Odds ratio (OR) with 95% confidence intervals (CIs) was calculated comparing the osteoporosis drugs to placebo effect on the frequency of new vertebral and nonvertebral fractures in postmenopausal females using the dichotomous method with a random or fixed-effect model. Treatment with osteoporosis drugs had significantly lower frequency of new vertebral fractures (OR, 0.53; 95% CI, 0.45-0.63, P < 0.001) and nonvertebral fractures (OR, 0.82; 95% CI, 0.78-0.87, P < 0.001) compared to placebo in postmenopausal females. Treatment with osteoporosis drugs had a significantly lower frequency of new vertebral and nonvertebral fractures compared to placebo in postmenopausal females. This relationship forces us to recommend osteoporosis drugs in postmenopausal females to avoid any possible new fractures. A cost-effective study is recommended.

Vaccaria hypaphorine impairs RANKL-induced osteoclastogenesis by inhibition of ERK, p38, JNK and NF-κB pathway and prevents inflammatory bone loss in mice.

Osteoclasts are sole bone-resorbing cells which exert a profound effect on skeletal metabolism. The search for medicines that affect the differentiation and function of osteoclasts is crucial in developing therapies for osteoclast-based diseases. Vaccaria hypaphorine, the main active compound of the traditionally used Chinese herb Vaccaria segetalis, has anti-inflammatory activity. The present study demonstrated for the first time that vaccaria hypaphorine could significantly inhibit the receptor activator of nuclear factor kappa B ligand (RANKL)-induced osteoclastic differentiation in vitro and alleviate lipopolysaccharide (LPS)-induced bone loss in vivo. Further study showed that vaccaria hypaphorine decreased osteoclastogenesis in a dose-dependent manner. Furthermore, vaccaria hypaphorine was confirmed to inhibit osteoclasts differentiation at early stage but not at later stage. Pit formation assay and F-actin ring staining showed that vaccaria hypaphorine inhibited the bone-resorbing activity of osteoclasts. Mechanistically, vaccaria hypaphorine impaired RANKL-induced osteoclastogenesis through reduction of extracellular signal-regulated kinases (ERK), p38, c-Jun N-terminal kinase (JNK) and NF-κB p65 phosphorylation. Taken together, our results provided evidences that vaccaria hypaphorine might be considered as potential therapeutic agent for treating osteoclast-based bone loss.

Upregulation of P63 inhibits chondrocyte autophagy thereby enhancing the malignant progression of osteoarthritis.

Loss of autophagy is suggested to play a key role in the progression of osteoarthritis (OA). P63 is a member of the P53 family, which is widely dysregulated in various tumors. However, the specific role of P63 in chondrocyte autophagy has never been fully understood. Here, the expression level of P63 in the articular cartilages of OA patients and chondrocytes treated with 3-MA was explored using western blot. Autophagy was determined using transmission electron microscopy and mRFP-GFP-LC3 assay. Fewer autophagic vesicles were identified in the articular cartilages of OA patients compared with that of normal control. Both the mRNA and protein levels of P63 was markedly increased in the articular cartilages of OA patients compared with that of normal control. MTT assay demonstrated that P63 overexpression markedly reduced chondrocyte viability at 24, 36 and 48 h, while inhibition of P63 inhibited cell viability at 24, 36 and 48 h, respectively. Furthermore, autophagic flux assay showed that transfection of ad-P63 markedly decreased the yellow dots in chondrocytes, while inhibition of P63 induced chondrycyte autophagy. In summary, we first demonstrated that upregulation of P63 in the cartilage tissues of OA patients inhibited chondrocyte autophagy thereby contributing to the malignant progression of OA.