如你有此疾病,請遵照閣下醫生的完整醫療方案;而是否使用多學科復康方案前,你必須咨詢主診醫生的意見,如果閣下的主診醫生不建議您加入補充劑調理組合,請你不要使用。如果你需要尋求其他醫生作第二咨詢,閣下可聯絡我們線上<無邊界醫生>。或你自己城市內的其他專業醫生的再診斷。
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為免錯誤診斷及漏診,請提供最近1個月的專業診斷報告。
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骨關節炎
骨關節炎（OA）的特徵包括關節退行性變、軟骨遺失和軟骨下骨改變。它是最常見的關節炎，發病率最高。它主要影響老年人，但35%的發病率早在30歲就開始了（通常診斷為髕骨軟骨軟化症）。發病率隨著年齡的增長而急劇增加。超過4000萬美國人患有骨性關節炎，其中80%的人年齡在50歲以上。OA負責25%的初級保健醫生的辦公室就診。男性和女性同樣受到影響，但症狀出現得更早，女性似乎更嚴重。
被認為是特定關節骨性關節炎的疾病：手（Heberden和Bouchard淋巴結）、髖部（陳舊性髖關節）、顳下頜關節（coxae senilis）、膝蓋（髕骨軟骨軟化症）和脊柱（强直性長骨刺症、骨間質增生症）。
負重關節、周邊關節和軸向關節主要受到影響。透明軟骨破壞後，關節邊緣硬化並形成大骨刺（鈣化骨贅），導致疼痛、畸形和關節活動受限。炎症通常很輕微。
兩種類型的骨性關節炎：（1）原發性骨性關節炎發生於磨損後的第五和第六個幾十年，沒有誘發异常。幾十年的使用累積效應應力膠原基質。損傷釋放破壞膠原蛋白成分的酶。隨著年齡的增長，合成修復性膠原蛋白的能力下降。（2）繼發性骨性關節炎是退行性變的易感因素。因素包括關節結構或功能的先天性异常（例如，活動過度和關節表面形狀异常）、創傷（肥胖、關節表面骨折、手術）、晶體沉積、軟骨异常、關節炎（類風濕性關節炎[RA]、痛風、化膿性關節炎）。
骨關節炎的嚴重程度與疼痛程度無關。外觀正常的關節，關節間隙很小，會非常疼痛。相反，畸形嚴重的關節可能很少疼痛。事實上，40%的OA x線分級最差的患者沒有疼痛。疼痛的原因是不明確的，但有許多潜在的原因。抑鬱和焦慮會新增OA疼痛的體驗。
If you have this disease, please follow your doctor's complete medical plan. You must consult the attending doctor before using the multidisciplinary rehabilitation plan. If your attending doctor does not recommend you to join the supplement conditioning combination, please do not use it. If you need to seek second opinion from other doctors, you can contact our online "Doctors Without Borders", or another professional doctorin your own city.
Need expert diagnosis
In order to avoid misdiagnosis and missed diagnosis, please provide the professional diagnosis report of the last month.
Osteoarthritis (OA)
Osteoarthritis (OA) characteristics include joint degeneration, loss of cartilage, and alterations of subchondral bone. It is the most common form of arthritis, with the highest morbidity rate of any illness. It primarily affects the elderly, but 35% of its incidence in the knee starts as early as age 30 years (often diagnosed as chondromalacia patellae). The incidence dramatically increases with age. More than 40 million Americans have OA, including 80% of persons older than 50 years. OA is responsible for 25% of all office visits to primary care physicians. Men and women are equally affected, but symptoms occur earlier and appear to be more severe in women.• Diseases thought to be OA of specific joints: hands (Heberden’s and Bouchard’s nodes), hips (malum coxae senilis), temporomandibular joint (Costen’s syndrome), knees (chondromalacia patellae), and spine (ankylosing hyperostosis, interstitial skeletal hyperostosis).
• Weight-bearing joints and peripheral and axial articulations are principally affected. Hyaline cartilage destruction is followed by hardening and formation of large bone spurs (calcified osteophytes) in joint margins, causing pain, deformity, and limited joint motion. Inflammation usually is minimal.
• Two categories of OA: (1) primary OA arises from wear and tear after the fifth and sixth decades, with no predisposing abnormalities. The cumulative effects of decades of use stress collagen matrix. Damage releases enzymes that destroy collagen components. With aging, the ability to synthesize restorative collagen decreases. (2) Secondary OA entails predisposing factors for degeneration. Factors include congenital abnormalities in joint structure or function (e.g., hypermobility and abnormally shaped joint surfaces), trauma (obesity, fractures along joint surfaces, surgery), crystal deposition, presence of abnormal cartilage, previous inflammatory disease of joint (rheumatoid arthritis [RA], gout, septic arthritis).
• OA severity, as determined by radiography, does not correlate with degree of pain. Normal-looking joints, with little joint-space narrowing, can be excruciatingly painful. Conversely, joints with tremendous deformity may have little pain. In fact, 40% of patients with the worst x-ray classification for OA are pain free. The cause of pain is ill defined, but there are numerous potential causes. Depression and anxiety increase the experience of OA pain.
