Osteoporosis is a systemic disease with progressive bone loss. The bone loss is associated with an imbalance between bone resorption via osteoclasts and bone formation via osteoblasts. Other cells including T cells, B cells, macrophages, and osteocytes are also involved in the pathogenesis of osteoporosis. Different cytokines from activated macrophages can regulate or stimulate the development of osteoclastogenesis-associated bone loss. The fusion of macrophages can form multinucleated osteoclasts and, thus, cause bone resorption via the expression of IL-4 and IL-13. Different cytokines, endocrines, and chemokines are also expressed that may affect the presentation of macrophages in osteoporosis. Macrophages have an effect on bone formation during fracture-associated bone repair. However, activated macrophages may secrete proinflammatory cytokines that induce bone loss by osteoclastogenesis, and are associated with the activation of bone resorption. Targeting activated macrophages at an appropriate stage may help inhibit or slow the progression of bone loss in patients with osteoporosis.

Systemic lupus erythematosus (SLE) is a chronic systemic inflammatory disease associated with a high prevalence of cardiovascular disease (CVD). Hydroxychloroquine (HCQ) is commonly used to control disease activity in patients with SLE. We evaluated its potential additional therapeutic effect for reducing CVD in SLE patients. We conducted a retrospective cohort study, in which one million participants were sampled from 23 million beneficiaries and data were collected from 2000 to 2013. In total, 826 SLE patients receiving HCQ medication were included after exclusion for previous CVD. The total number of SLE patients was 795 after follow-up for more than one year. After adjusting for chronic comorbidity, a significantly decreased hazard ratio (HR) for coronary artery disease (CAD) was found among SLE patients with a high usage of HCQ for at least 318 days (HR = 0.31, 95% confidence interval, CI: 0.12–0.76). A low HR for CAD was observed in SLE patients with a high cumulative dose of at least 100,267 mg HCQ (HR = 0.25, 95% CI: 0.09–0.66). However, there was no significant lowering of the HR for stroke. Long-term HCQ therapy decreases the HR of CVD in SLE patients. The cardiovascular protective effect of HCQ therapy was associated with decrease in CAD, but not stroke.

Rheumatoid arthritis (RA) is a systemic inflammatory disease with different etiologies in different areas. Our study focused on the prevalence of RA in Taiwan from 2001 to 2011. This study contained longitudinal enrollment files, claims data, catastrophic illness files, and treatment registries from Taiwan Longitudinal Health Insurance Research Database. We identified RA patients by ICD-9-CM code 714.0. The demographical variables including age, sex, income and area of registration were evaluated. The multivariate Poisson regression was applied to calculate relative risk for developing RA. In Taiwan, the ratio of female to male was about 5:1. From 2001 to 2011, significant increasing prevalence of RA, from 0.07% to 0.14%, was found in women. The prevalence of RA was increasing 6% per year in both sex groups. The annual incidence rate (per 10,000 person years) ranged from 1.62 to 2.02 (female: 2.30–3.14; male: 0.71–1.17) from 2003 to 2011. City area had lowest incidence rate of RA compared with suburban or rural area. Higher incidence of RA was observed among lower socioeconomic status. The prevalence of RA was rising from 0.07% in 2001 to 0.14% in 2011. Incidence was about 2/10,000 person-years and female to male ratio was 5:1. Lower socioeconomic status and living rural region might be a risk factor for developing RA.

Background: Advanced glycation end-products (AGEs) can accumulate in organs and tissues during ageing and diabetes. Increased levels of AGEs are found in the bone tissue of patients with osteoporosis. The purpose of this study was to evaluate circulating AGEs in patients with osteoporosis.

Gout is a common systemic inflammatory disease with a male predominance. This study aimed to determine the relationship between serum total testosterone level and hyperuricemia. Data on 1899 men, collected from 2007 to 2017, were included in the analysis. Serum testosterone and urate (SU) were measured on enrolment. The primary endpoints were SU levels ≥ 7 mg/dL and ≥9 mg/dL. On enrolment, participants had a mean age of 45.6 years and mean total testosterone and SU levels of 510 ng/dL and 6.6 mg/dL, respectively. The mean total testosterone levels were 533 and 470 ng/dL in patients with SU levels < 7 mg/dL and ≥7 mg/dL, respectively (p < 0.001); and 515 and 425 ng/dL in patients with SU levels < 9 mg/dL and ≥9 mg/dL, respectively (p < 0.001). After adjusting for age, body mass index, creatinine, serum lipid, fasting blood glucose, systolic blood pressure, and diastolic blood pressure, low testosterone level (<400 ng/dL) was significantly associated with an SU level ≥ 7 mg/dL (hazard ratio: 1.182, 95% confidence interval: 1.005–1.39) and ≥9 mg/dL (hazard ratio: 1.905, 95% confidence interval: 1.239–2.928). In men, a low testosterone level may be associated with an increased risk of hyperuricemia.

Context: Osteoarthritis (OA) is a degenerative joint disease with damage to the articular cartilage. Active production of inflammatory cytokine/chemokine and matrix metalloproteinases may be found during the progression of OA. Isorhamnetin had the effects of anti-inflammatory, antioxidant, anti-ischemia, anti-atherosclerotic hepatoprotective and anticancer activities. Objective: Our study was focused on the effects of isorhamnetin treatment in OA. Materials and methods: We used monosodium iodoacetate (MIA)-induced OA rats to evaluate the effects of isorhamnetin related anti-inflammatory process. The rats in all groups were sacrificed on four weeks post-MIA injection. The measurements of knee joint swelling, histological analysis, serum inflammatory biomarkers and western blot were evaluated. Results: We found that isorhamnetin may reduce MIA-induced knee swelling by significantly reduction of articular cartilage damage.in rats. Suppression of pro-inflammatory cytokines production was found after isohamnetin treatment. Isorhamnetin inhibited the production of NO and PGE2, and the expression of iNOS and COX-2. The production of COMP, CTX-II and osteopontin (OPN) were also inhibited in MIA-induced OA rats. Discussion and conclusions: Isorhamnetin may modulate the inflammatory progression of OA in MIA-induced OA rats. The prevention of cartilage damage was found in OA after adequate isorhamnetin treatment. Isorhamnetin may serve as a potential agent for the management of OA.