“醫(yī)學(xué)英語(yǔ)閱讀：關(guān)節(jié)炎性疼痛綜合征骨關(guān)節(jié)炎”相信是準(zhǔn)備學(xué)習(xí)醫(yī)學(xué)英語(yǔ)的朋友比較關(guān)注的事情，為此，醫(yī)學(xué)教育網(wǎng)小編整理內(nèi)容如下：

osteoarthritis has traditionally been described as“wear and tear”joint degeneration attributable to the aging process.pain due to osteoarthritis constitutes the most common joint complanint for which patien is seek medical attention.primary osteoarthritis affects the articular cartilage of otherwise normal joints.secondary osteoarthritis occurs as a sequela of trauma，joint disease such as legg-perthes disease，or subtle anomalies such as mild acetabular dysplasia resulting in long-standing joint incongruity.

骨關(guān)節(jié)炎被傳統(tǒng)地描述為由于老年化過(guò)程而出現(xiàn)的磨損性關(guān)節(jié)變性。由骨關(guān)節(jié)炎引起的關(guān)節(jié)能疼痛是病人就醫(yī)時(shí)最多的主訴。原發(fā)性骨關(guān)節(jié)炎犯其他正常侵犯其他正常的骨關(guān)節(jié)軟骨面。繼發(fā)性骨關(guān)節(jié)炎是作為創(chuàng)傷、關(guān)節(jié)病（如legg-perthe?。┗蜉p微畸形（如輕度髖臼發(fā)育不良導(dǎo)致長(zhǎng)期關(guān)節(jié)不交合）的后遺癥而發(fā)生的。

osteoarthritis is the most common of all arthropathies，affecting roughly 30-50%of the entire population.heritability has not been demonstrated.women are more often affected than men，though virtually all persons overage 55 have some x-ray evidence of this disease.fortunately，less than half of patients with x-ray changes will experience joint symptoms.onset of symptomatic disease is usually in the sixth decade.

骨關(guān)節(jié)炎是所有骨關(guān)節(jié)病中最常見(jiàn)，整個(gè)人群中約有30~50%受累。遺傳性未得到證實(shí)。女性較男性患者多。事實(shí)上超過(guò)55歲的人都有一點(diǎn)患此病的x線證據(jù)，幸而只有不到一半有x線證變化的病人感到有關(guān)節(jié)癥狀，通常是在60歲開(kāi)始出現(xiàn)。

though the specific in citing agent remains unclear，the earliest histopathologic change in osteoarthritic joints is loss of mucopolysaccharide ground substance in the outermost layers of articular cartilage.as a result the mechanical properties of the cartilage are altered and resistance to deformation is lowered.the weakened superficial layers of cartilage develop fissures in response to increased deformation by normal loads.this results in uneven distribution of stress transmission to deeper layers of cartilage and to the underlying subchondral bone.this concentration of stress further accelerates cartilage wear with thinning of outer layers and propagation of cracks and fissures in the deeper layers.cartilage debris within the joint results in low-grade chronic inflammatory synovitis and joint effusion.

雖然特異性刺激因素尚不清楚，但是在骨關(guān)節(jié)炎關(guān)節(jié)中最早的組織病理學(xué)變化是在關(guān)節(jié)軟骨的最外層中喪失粘液多糖基質(zhì)。結(jié)果是軟骨的機(jī)械性能發(fā)生改變，對(duì)變形的耐受力下降。變?nèi)醯谋韺榆浌且驅(qū)φＸ?fù)荷增加變形而發(fā)生裂隙。這導(dǎo)致應(yīng)力分布不均勻地傳導(dǎo)至深層軟骨及其下面的軟骨下骨。集中的應(yīng)有盡有力進(jìn)一步加速外民支軟骨磨損及變薄，也加速深層碎裂和裂隙的擴(kuò)布。在關(guān)節(jié)內(nèi)軟骨碎片導(dǎo)致低度慢性囊炎和關(guān)節(jié)積液。

if weight bearing or stress loading of the affected joint continues，thinning of the cartilage may progress to eventual full-thickness cartilage loss.the subchondral bone bears progressively greater loads as cartilage destruction evolves.increased loading of bone stimulates bone remodeling and new bone deposition，manifested by marginal osteophyte formation and sclerosis within the overloaded subchondral bone incite a chronic inflammatory response replacement of nercrotic bone by fibrous tissue results in subchondral cyst formation.

如果受損的關(guān)節(jié)持續(xù)負(fù)重或承受應(yīng)力，軟骨變薄可進(jìn)行下去，直到最后全層軟骨消失。軟骨破壞過(guò)程中，軟骱下骨胳的負(fù)荷逐漸加重，骨負(fù)荷加重刺激骨胳重新塑和新骨沉積，表現(xiàn)為邊緣的骨贅形成和軟骨下骨質(zhì)硬化。過(guò)度負(fù)荷的軟骨下骨質(zhì)中的細(xì)微骨折激起慢性炎癥反應(yīng)，壞死的骨骼被纖維組織替代導(dǎo)致軟骨下囊腫形成。

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