”Chronic” is characteristic of most rheumatic diseases, which often present with persistent symptoms and whose pathophysiological properties change over time. For example, pain associated with RA, which may be due to injury sensation, can gradually become central and spread throughout the body as inflammation develops in the joints. This means that over a long period of time, it may be both injury-receptive and central. The degree of pain in patients with rheumatic diseases is highly variable. Osteoarthritis (OA) occurs with age and affects 8 out of 10 men and women over the age of 75. OA primarily affects cartilage and impairs weight-bearing joint function. OA can occur as a result of excessive or repetitive loading of joints, including work-related activities, trauma, inflammation, and persistent stress on joints triggered by chronic obesity. Because pain is the most common symptom of many rheumatic diseases, it should be treated first in the treatment of the underlying disease. patients with RA or other autoimmune diseases, when clinical remission is achieved, the disappearance of peripheral/injury felt pain is often seen. In some cases, however, the pain is clearly central, so that it persists even when inflammation has been suppressed. Current challenges in pain management are: lack of evidence of efficacy for the vast majority of treatments offered to patients; lack of patient awareness of gastrointestinal adverse effects of analgesic medications; inadequate knowledge related to pain management among primary care physicians; and poor multidisciplinary treatment pathways. Try to distinguish between injury-receptive, neuropathic, central, and mixed pain, as central pain may be characterized by any of these. Physicians must understand the impact of the type of pain on the individual patient and develop an appropriate treatment plan. However, in any of these diseases, the presence of mixed pain can make diagnosis and treatment very difficult. For example, patients with RA may present with “central pain” syndromes such as FM, headache, irritable bowel syndrome, TMJ disorder, and interstitial cystitis, which have familial/genetic characteristics. Current evidence suggests that genetic and immunologic factors may contribute to increased pain sensitivity and therefore are more likely to contribute to the development of chronic pain. The most widely accepted causative theory, explaining the correlation between a central pain state and a range of co-occurring somatization symptoms, as well as a higher than expected incidence of mood disorders, is that central neurotransmitters known to be involved in causing pain (low norepinephrine, GABA, 5-hydroxytryptamine, high glutamate levels, and substance P) also have a significant role in controlling sleep, mood, and alertness. Pain is not a problem in a small number of patients and can disappear completely when rheumatic disease is properly treated. Many patients with RA achieve clinical remission with extremely low pain scores. However, the opposite is true in FM with lower extremity pain and fibromyalgia, where pain becomes their particular dilemma and their lifestyle revolves around it. Sometimes intense, persistent and disabling pain is associated with rheumatoid arthritis and spondyloarthritis, often multifactorial, with both central and peripheral origins, and it may be due to currently active inflammation, joint damage, or tissue destruction caused by a previous inflammatory condition. 2. Inflammatory, non-inflammatory and neuropathic pain The main characteristic of inflammatory pain is that normal, harmless stimuli also cause pain. Both physicians and patients need to identify the different types of pain. Chronic noncancerous pain associated with rheumatic disease is associated with early use of nonbiologic disease-modifying antirheumatic drugs (DMARDs) and biologic DMARDs that do not overlap in inflammatory pain conditions. Inflammatory pain conditions can be partially relieved by the use of non-steroidal anti-inflammatory drugs (NSAIDs) or biologic and non-biologic disease-modifying anti-rheumatic drugs (DMARDs). However, many patients still suffer from moderate pain because of alterations in central pain modulation mechanisms, such as chronic widespread pain (CWP) conditions, which are characterized by fibromyalgia. Non-inflammatory pain can also confound the assessment of disease activity, so the goal of treatment should be to relieve painful symptoms while combating inflammatory disease. In patients with rheumatoid arthritis (RA) or spondyloarthritis (SpA), the importance of distinguishing between central and inflammatory pain is that these conditions are currently treated with expensive medications, such as tumor necrosis factor (TNF) inhibitors or other biologic agents, and patients with CWP are directly more costly than those without. The optimal treatment of RA and SpA must include those symptoms such as CWP and overall quality of life. Therefore, a combination program that includes pharmacologic analgesia, biologic and nonbiologic therapy is required. Because although arthroplasty can significantly improve the pain associated with rheumatoid arthritis, it may only be recommended for those patients with their severe progressive disease. Although there is generally no apparent neurological damage, accumulating evidence suggests that neuropathic pain NP symptoms may also be seen in patients with rheumatic diseases such as fibromyalgia or osteoarthritis. The prevalence of neuropathic pain-like features is estimated to be 30% in osteoarthritis and 50%-75% in FM. In recent years, some authors have confirmed the NP component of AS in ankylosing spondylitis as mixed pain in which different pain mechanisms play a role, which may also apply to RA. inflammatory pain is now considered to be a complex mechanism under mechanical, thermal, and chemical transduction modulation through receptors, ion channels, and neurotransmitters or regulatory proteins. Changes in the sensitivity of injury-receptive neurons may underlie the hypersensitivity response of inflamed tissues.