As an aging population and a growing prevalence of obesity, the number of individuals affected by OA is expected to rise. The investigation into the etiology and pathogenesis of OA is gaining increasing attention. Our research team conducted a meta-analysis[12] and revealed a correlation between weather factors and OA pain. However, it is noteworthy that the majority of literature exploring the relationship between weather and osteoarthritis concentrated on the assessment of pain severity, largely overlooking the bone structure and levels of proinflammatory cytokines associated with OA. However, these factors hold great significance in the pathophysiology of osteoarthritis and might indeed contribute to weather-induced pain[13, 14]. Hence, a comprehensive investigation of the relationship between meteorological variables and not only clinical symptoms but also biological features is imperative to better understand the effects of weather on KOA.
Drawing upon these findings, our research team designed this cohort study. This is the first longitudinal study to explore the relationship between weather factors and OA pain, BMA, and inflammatory factors simultaneously. Our results showed that temperature was negatively associated with pain scores, IL-1β, and IL-6 levels.
Our pain score findings are in accordance with 3 preceding studies.These studies encompassed conditions such as rheumatoid arthritis (RA)[15] and fibromyalgia (FM)[16], extending beyond the scope of OA. The contribution of our study lies in augmenting the existing body of evidence by finding low temperature is also associated with inflammatory levels, which may have a mediating effect between weather changes and joint pain. The underlying mechanism regarding the impact of temperature on KOA is complex and not fully understood. We speculate that this may be related to inflammatory cytokine groups, which could lead to the loss of joint tissue metabolic homeostasis by promoting catabolic metabolism and cartilage destruction processes [17, 18]. Both in vitro[19] and in vivo[20] studies indicate that low temperatures can stimulate the elevation of inflammatory cytokines such as IL-1, IL-6, IL-8, and tumor necrosis factor-alpha (TNF-α), and elevated percentage of neutrophils in the peripheral blood. The thermosensitive transient Receptor Potential (Thermo-TRP) channels may play an important role in this process [21], particularly TRPA (ankyrin) grousps [22]. When exposed toexternal temperature stimuli, the activation of TRPA1 not only elicits action potentials that are transmitted to the central nervous system, resulting in the sensation of pain, but also releases inflammatory neuropeptides into the nearby damaged tissue, thereby initiating a neurogenic inflammatory response[23]. The ambient temperature is also linked to season[24] and sun exposure, subsequently influencing the production of vitamin D. Vitamin D plays a significant role in the restoration of chondrocyte functionality and viability, and is associated with the symptoms and cartilage damage in KOA [25]. In addition, irregular temperature fluctuations might be more likely to disrupt clock genes and affect chondrocyte function [26]. Overall, temperature factors are related to pain perception and proinflammatory cytokine levels. This indicates that the impact of weather on KOA is not just a psychological or mental "illusion". Therapies and treatment targets related to temperature are worthy of further attention[27].
Moreover, humidity and wind speed were found to have no association with KOA. Atmospheric moisture, as a participant in heat stress and hydration state, is associated with the incidence and mortality rates of various diseases such as cardiovascular disease, pulmonary disease, and infectious diseases. Some researches provided evidence indicating that high humidity increases the sensitivity of the body to mechanical stress and promotes the production of inflammatory cytokines in chondrocytes[28, 29], as well as altering metabolic products in arthritic mice[30]. Clinical studies have also confirmed the association between high humidity and arthritis pain, stiffness, and erythrocyte sedimentation rate levels[31, 32]. In this study, relative humidity did not demonstrate a significant impact on patients with KOA. This could be attributed to the shielding effect provided by the tissues such as the skin, adipose layers, and joint capsules, which prevent direct external exposure to the bones and joints, rendering them less susceptible to humidity compared to organs like the lungs. As for the wind speed, some studies[15, 33] have pointed out that it has no association with KOA, which is similar to the results obtained in our study. A potential explanation could be attributed to the meticulous measurement of wind speed data, in contrast to the comparatively less precise assessment of pain and BMA data.
Additionally, it was observed that there was no correlation between BMA and meteorological factors. This absence could be attributed to the fact that observable bone marrow alterations necessitate substantial and prolonged effects of pathogenic factors[34]. For example, in animal models of KOA, bone marrow injury only manifested at least 2 weeks post interventions like anterior cruciate ligament (ACL) surgery[35]. However, the weatherl data collected in this study was limited to the three days preceding the investigation, possibly insufficient to induce changes in the bone marrow level.
Our findings are based on the results of a prospective longitudinal study and have a number of advantages compared to the previous researches. The study has for the first time concurrently assess the associations between subjective clinical performance (pain), objective clinical performance (BMA), inflammatory factors, and weather factors. Also,this study employed an appropriate statistical approach (multivariate linear regression models) to analyze the associations and adjust for confounding factors, including age, gender, BMI, and disease course.
This research also has some limitations. Primarily, our study is constrained by limited geographical representation. As our data originates from China, a region where disease culture emphasizes the significance of wind, cold, and dampness, participants may have been influenced by regional beliefs. Additionally, this study used meteorological station data as a substitute for individual exposure levels to environmental factors, essentially introducing inaccuracies in the collected exposure data. Moreover, the study population selection also exhibits a limitation as it predominantly comprises individuals of older age, who may possess distinct perceptions of weather variations in contrast to younger cohorts.