祝愷 譚軍 張紫豪 李文鋒

綜述

腰椎小關(guān)節(jié)骨關(guān)節(jié)炎宏觀及微觀改變的研究進(jìn)展

祝愷 譚軍 張紫豪 李文鋒

脊柱；腰椎；骨關(guān)節(jié)炎，脊柱；綜述

腰椎小關(guān)節(jié) ( facet joint or zygapophyseal joint，F(xiàn)J ) 是整個(gè)脊柱惟一的滑膜關(guān)節(jié)，與同節(jié)段椎間盤共同構(gòu)成一個(gè)功能單位－三關(guān)節(jié)復(fù)合體[1]。相較于其它大的負(fù)重關(guān)節(jié)( 比如膝關(guān)節(jié)、肩關(guān)節(jié)等 )，國(guó)內(nèi)外學(xué)者對(duì) FJ 的研究較少。近些年，由于發(fā)現(xiàn) FJ 與其它脊柱退變性疾病如椎間盤退變、腰椎滑脫等，尤其與腰背痛的密切關(guān)系[2-8]，學(xué)者們對(duì) FJ 退變的研究逐漸增多。FJ 退變最主要的病理過(guò)程是骨關(guān)節(jié)炎 ( osteoarthritis，OA ) 的發(fā)生、發(fā)展，筆者就FJOA 的研究進(jìn)展作一綜述，從宏觀和微觀兩個(gè)層面進(jìn)行歸納和總結(jié)。

一、FJOA 的宏觀結(jié)構(gòu)變化

已有眾多研究結(jié)論表明，F(xiàn)JOA 始于關(guān)節(jié)軟骨、滑膜及關(guān)節(jié)囊。早期表現(xiàn)為關(guān)節(jié)軟骨面由淺及深的纖維化、點(diǎn)蝕、微裂、剝脫，進(jìn)一步發(fā)展為軟骨下骨侵蝕，晚期階段表現(xiàn)為骨贅形成和軟骨下骨的重塑、硬化、骨囊腫形成等，而關(guān)節(jié)間隙變窄是貫穿始終的形態(tài)性改變[9-11]。

1. 小關(guān)節(jié)分區(qū)：研究 FJOA 的宏觀結(jié)構(gòu)首先有必要了解小關(guān)節(jié)的分區(qū)。Tischer 等[12]根據(jù)形態(tài)學(xué)觀察將完整摘除的小關(guān)節(jié)的關(guān)節(jié)面大體分為 5個(gè)區(qū)域：上、下、腹內(nèi)側(cè)、背外側(cè)及中心區(qū)。Simon 等[13]結(jié)合三維 CT 重建、地形圖分析、矢量坐標(biāo)系統(tǒng)等將關(guān)節(jié)面分為內(nèi)側(cè)、外側(cè)、上、下及中心區(qū)，這種分區(qū)在解剖形態(tài)學(xué)上更為準(zhǔn)確。

2. 關(guān)節(jié)軟骨：如前所述，軟骨損害被認(rèn)為是 OA 的早期改變。Tischer 等[12]通過(guò)大體形態(tài)學(xué)觀察發(fā)現(xiàn)，OA 軟骨缺損主要發(fā)生在關(guān)節(jié)邊緣，而中心區(qū)的軟骨相對(duì)存留較好；上、下關(guān)節(jié)突的軟骨缺損位置不同：上關(guān)節(jié)突大部分發(fā)生在上極，而下關(guān)節(jié)突可發(fā)生在關(guān)節(jié)面的各個(gè)邊緣，但最嚴(yán)重的是在下極；無(wú)論上、下關(guān)節(jié)突，腹內(nèi)側(cè)和背外側(cè)區(qū)的軟骨缺損情況較輕；從節(jié)段來(lái)看，L5水平的小關(guān)節(jié)其關(guān)節(jié)軟骨缺損情況最為嚴(yán)重。為了更加準(zhǔn)確地評(píng)價(jià)軟骨退變，Tanno 等[14]通過(guò)對(duì)尸體標(biāo)本的測(cè)量，總結(jié)一種評(píng)價(jià)方法：關(guān)節(jié)囊內(nèi)表面與關(guān)節(jié)表面的面積比 ( the capsule / facet index )。Abd Latif 等[15]則進(jìn)行了方法學(xué)上的探索，作者認(rèn)為通過(guò)軟骨蠕變壓痕實(shí)驗(yàn)結(jié)合有限元模型分析，可以更好地反映小關(guān)節(jié)軟骨的生物力學(xué)特征。

3. 關(guān)節(jié)囊：關(guān)節(jié)囊主要承受小關(guān)節(jié)機(jī)械載荷動(dòng)態(tài)變化時(shí)的壓力、張力和剪切力，并可隨著具體的載荷模式來(lái)改變形態(tài)，這尤其體現(xiàn)在脊柱旋轉(zhuǎn)活動(dòng)中[16-17]。Boszczyk等[18]發(fā)現(xiàn)退變小關(guān)節(jié)的后關(guān)節(jié)囊肥厚，并有明顯的環(huán)繞式纖維軟骨增生；作者解釋這種現(xiàn)象是由于后關(guān)節(jié)囊為了適應(yīng)脊柱旋轉(zhuǎn)載荷對(duì)其下關(guān)節(jié)突附著部帶來(lái)的壓力所導(dǎo)致。Tanno 等[14]發(fā)現(xiàn)關(guān)節(jié)面的表面積隨著關(guān)節(jié)軟骨退變的嚴(yán)重程度而增加，而關(guān)節(jié)囊內(nèi)表面的面積呈相反變化，也就是說(shuō)，關(guān)節(jié)軟骨的退變使關(guān)節(jié)囊縮窄，尤其是背側(cè)部分，而后者又可以加快軟骨退變的進(jìn)展，形成惡性循環(huán)。

4. 軟骨下骨：軟骨下骨作為形態(tài)單元，連接透明軟骨和骨松質(zhì)；作為機(jī)械單元，可以減輕關(guān)節(jié)動(dòng)態(tài)載荷過(guò)程中的沖擊應(yīng)力。Duan 等[19]采用質(zhì)子密度加權(quán)的 MRI 來(lái)分析軟骨下骨，發(fā)現(xiàn)下關(guān)節(jié)突軟骨下骨的骨板較上關(guān)節(jié)突薄，而 FJOA 的軟骨下骨板通常也是變薄的，其結(jié)構(gòu)和密度變化可以反映關(guān)節(jié)炎的進(jìn)展。Botter 等[20]通過(guò)研究大鼠OA 模型發(fā)現(xiàn)，軟骨下骨板變薄與軟骨損害并無(wú)相關(guān)性。Berteau 等[21]通過(guò) micro-CT 及靜態(tài)彈性模量的分析，發(fā)現(xiàn)軟骨下骨礦化密度和孔隙率呈正相關(guān)，這兩項(xiàng)參數(shù)比骨板厚度更能反映 OA 的改變。

5. 小關(guān)節(jié)骨贅：FJOA 骨贅形成不如軟骨損害常見(jiàn)。Tischer 等[22]發(fā)現(xiàn)骨贅多見(jiàn)于上關(guān)節(jié)突的背外側(cè)緣，這里是背側(cè)關(guān)節(jié)囊附著部；而下關(guān)節(jié)突的骨贅較上關(guān)節(jié)突少見(jiàn)，多在下關(guān)節(jié)突的下極出現(xiàn)。作者還發(fā)現(xiàn)無(wú)論上、下關(guān)節(jié)突，腹內(nèi)側(cè)區(qū)的骨贅罕見(jiàn)，認(rèn)為這主要與 FJ 活動(dòng)的生物力學(xué)機(jī)制有關(guān)。

6. 小關(guān)節(jié)半月盤：FJ 上、下關(guān)節(jié)面之間存在有蒂連于關(guān)節(jié)囊的半月盤樣結(jié)構(gòu)，主要由滑膜皺襞組成，按其組織結(jié)構(gòu)可分為滑膜性、脂肪性、纖維性三種類型，第一種常見(jiàn)，最后一種罕見(jiàn)。在退變小關(guān)節(jié)中半月盤結(jié)構(gòu)明顯，表面粗糙不平，邊緣呈分葉狀或者磨損狀，組織纖維化。這些半月盤的主要作用是增大關(guān)節(jié)面接觸面積，彌補(bǔ)關(guān)節(jié)面之間的吻合不全和填補(bǔ)關(guān)節(jié)腔空隙。Kos 等[23]認(rèn)為在脊柱屈伸、扭轉(zhuǎn)活動(dòng)中，上下小關(guān)節(jié)對(duì)關(guān)節(jié)盤的突然卡壓是導(dǎo)致腰背部疼痛的重要因素。

二、FJOA 的微觀變化

1. 細(xì)胞學(xué)改變：Bleil 等[24]用番紅 O 染色檢測(cè) FJOA軟骨細(xì)胞的蛋白多糖含量，用 caspase 3表達(dá)來(lái)評(píng)定軟骨細(xì)胞的凋亡。發(fā)現(xiàn)退變軟骨細(xì)胞的蛋白多糖含量減少，caspase 3陽(yáng)性軟骨細(xì)胞的比率增加，這種變化最多見(jiàn)于軟骨面表層的中間區(qū)域。作者還發(fā)現(xiàn)軟骨下骨板被纖維組織侵襲，緊鄰骨板的骨髓纖維化，而纖維組織的邊緣可觀察到破骨細(xì)胞的增加。Netzer 等[25]通過(guò)研究腰椎管狹窄患者的 FJOA，發(fā)現(xiàn)骨軟骨交界區(qū)出現(xiàn)大量鵝卵石樣的成骨細(xì)胞，這些成骨細(xì)胞內(nèi)有膠原纖維沉積，未發(fā)現(xiàn)有多核破骨細(xì)胞的存在；另外還發(fā)現(xiàn)，CD34陽(yáng)性的血管結(jié)構(gòu)出現(xiàn)在骨襯細(xì)胞的鄰近，CD68陽(yáng)性巨噬細(xì)胞均勻分布在成骨細(xì)胞及血管結(jié)構(gòu)區(qū)域。結(jié)合上述發(fā)現(xiàn)，作者指出骨軟骨交界處的新骨形成是 OA 組織病理學(xué)上的主要特點(diǎn)；作者進(jìn)一步研究了軟骨下骨的細(xì)胞學(xué)變化，表現(xiàn)為富含 CD68陽(yáng)性巨噬細(xì)胞的骨髓組織內(nèi)，TRAP 陽(yáng)性單核細(xì)胞及多核破骨細(xì)胞增多。Appel 等[26]通過(guò)免疫組織化學(xué)分析，發(fā)現(xiàn)在OA 的小關(guān)節(jié)中，骨保護(hù)素、骨鈣素及骨保護(hù)素配體陽(yáng)性的破骨細(xì)胞比例減少。作者認(rèn)為新骨形成可能是 FJOA 的生理性修復(fù)功能。Boszczyk 等[27]通過(guò)對(duì)細(xì)胞外基質(zhì) ( 包括膠原蛋白 / 糖胺聚糖 / 蛋白聚糖 ) 的免疫組織化學(xué)研究，發(fā)現(xiàn)退變節(jié)段的小關(guān)節(jié)其背側(cè)關(guān)節(jié)囊呈現(xiàn)軟骨性化生的特點(diǎn)，最明顯處位于超出小關(guān)節(jié)固有空間的關(guān)節(jié)囊附著部。

2. 分子水平改變：Igarashi 等[28]應(yīng)用 ELISA 和 CLEIA技術(shù)研究 FJOA 的關(guān)節(jié)囊和滑膜中的炎性因子，發(fā)現(xiàn)α-TNF 主要出現(xiàn)在滑膜組織中，IL-6多量出現(xiàn)在軟骨組織中，但滑膜組織也可見(jiàn)，而 IL-1β 在滑膜和關(guān)節(jié)軟骨中均為少量存在。Xu 等[29]則進(jìn)一步研究了 FJOA 的炎性機(jī)制，認(rèn)為關(guān)節(jié)軟骨和滑膜組織中的 MMP-1( IL-1β 誘導(dǎo) )過(guò)表達(dá)，可能是導(dǎo)致小關(guān)節(jié)退變的炎性機(jī)制；作者還在體外實(shí)驗(yàn)中證實(shí)了軟骨細(xì)胞中 MMP-1mRNA 對(duì) IL-1β 的刺激反應(yīng)呈時(shí)間和劑量依賴性。Boszczyk 等[18]通過(guò)對(duì)比腰椎和胸椎的背側(cè)小關(guān)節(jié)囊中的分子組成，發(fā)現(xiàn) II 型膠原、6-硫酸軟骨素、蛋白多糖和連接蛋白只在腰椎小關(guān)節(jié)囊中檢測(cè)到，而且主要分布于關(guān)節(jié)囊的附著部，尤其是關(guān)節(jié)囊繞過(guò)下關(guān)節(jié)突的后緣處。作者認(rèn)為這種分子組成及分布特點(diǎn)體現(xiàn)了腰椎小關(guān)節(jié)囊的生物力學(xué)特點(diǎn)。Kim 等[30]則對(duì)退變小關(guān)節(jié)囊做了更為詳盡的分子水平的檢測(cè)，包括：促炎因子 ( INF-γ、IL-1β、IL-17、TNFα、IL-1α 等 )、抗炎因子 ( IL-10、IL-13)、疼痛相關(guān)因子 ( iNOS、Cox-2、EP 家族 )、MMP 家族 ( 軟骨降解 )、TIMPs 家族 ( 抗軟骨降解 )、VEGF ( 血管生長(zhǎng)因子 )、NGF / TrkA ( 調(diào)節(jié)神經(jīng)生長(zhǎng) ) 等，作者分別從 mRNA 和蛋白水平證實(shí)了這些分子的表達(dá)呈現(xiàn)不同程度的上調(diào)。值得注意的是，在上述系列因子中有兩種亞型例外，其中 TIMPs-1的表達(dá)沒(méi)有上調(diào)，EP2表達(dá)反而是下降的。Kim 總結(jié)上述發(fā)現(xiàn)后推斷 FJOA與腰背痛的內(nèi)在聯(lián)系：( 1) 退變關(guān)節(jié)囊過(guò)表達(dá)疼痛相關(guān)因子，可能導(dǎo)致背根神經(jīng)節(jié)對(duì)疼痛刺激的敏感性增加；( 2)伴隨血管生成涌入的炎性因子會(huì)進(jìn)一步加重 FJ 退變和疼痛；( 3) 血管生成本身也促進(jìn)了新的感覺(jué)神經(jīng)纖維長(zhǎng)入，而引起疼痛敏感性增加。對(duì)于 FJOA 所致的腰背痛的機(jī)制，Surace 等[31]做出了相似的研究結(jié)論。Pecchi 等[32]則發(fā)現(xiàn)機(jī)械應(yīng)力、IL-1β、細(xì)胞外脂素和煙酰胺磷酸核糖轉(zhuǎn)移酶 ( nicotinamide phosphoribosyl transferase，NAMPT ) 可以刺激關(guān)節(jié)軟骨細(xì)胞過(guò)表達(dá)和釋放 NGF，這可能與關(guān)節(jié)炎性疼痛有密切聯(lián)系，而關(guān)節(jié)軟骨的機(jī)械負(fù)荷的增加可能介導(dǎo)這種聯(lián)系。

三、總結(jié)

目前，關(guān)于 FJOA 的宏觀改變的研究，主要包括解剖形態(tài)學(xué)、生物力學(xué)、病理生理學(xué)、影像學(xué)幾大方面。尤其是隨著影像學(xué)技術(shù)和計(jì)算機(jī)技術(shù)的飛速發(fā)展，使我們?cè)诜椒▽W(xué)上可以更加準(zhǔn)確、全面地評(píng)價(jià) FJOA，從而為進(jìn)一步的微觀研究打下基礎(chǔ)。在細(xì)胞及分子學(xué)層面，我們能深入探究 FJOA 的發(fā)生、發(fā)展機(jī)制，從而為預(yù)防、治療 FJOA提供科學(xué)依據(jù)。對(duì)于 FJOA 的分子機(jī)制研究，主要集中在疼痛介質(zhì)及炎性因子兩方面，這顯然反映出研究者們對(duì)于FJOA 引起的臨床癥狀的關(guān)注。然而容易忽略的是，相比于其它脊柱單位 ( 椎間盤、椎管、椎間孔、椎體等 )，對(duì)FJ 的研究還遠(yuǎn)遠(yuǎn)不足；將 FJOA 放到整個(gè)脊柱退變的模式和進(jìn)程中來(lái)看，F(xiàn)JOA 與其它脊柱退變性疾病有著千絲萬(wàn)縷的聯(lián)系，其中某些研究結(jié)論充滿矛盾。比如 FJOA 和椎間盤退變，究竟哪種退變是始動(dòng)因素或者主要因素[33-35]？再比如對(duì)于 FJOA 所致的腰痛的診斷及治療仍有諸多爭(zhēng)議[7-8,36-39]。因此，對(duì)于無(wú)癥狀性 FJOA 和有癥狀性 FJOA的演變機(jī)制及差異，可能是下一步應(yīng)該集中關(guān)注的領(lǐng)域。

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Progress of research on macroscopic and microscopic changes of lumbar facet joint osteoarthritis

ZHU Kai,TAN Jun, ZHANG Zi-hao, LI Wen-feng.
Department of Spine Surgery, Shanghai East Hospital of Tongji University,Shanghai, 200120, China

s】Lumbar facet joint ( FJ ) is a unique synovial joint of the spine, which forms a functional unit-“three joint complex” with the intervertebral disc of the same spinal segment. The primary pathological process of FJ degeneration is the development of osteoarthritis ( OA ). At present, the research methods on macroscopic changes of FJOA mainly include anatomical morphology, biomechanics, pathophysiology and imaging. With the rapid development of imaging technology and computer technology, we have heen able to evaluate FJOA more accurately and comprehensively, so as to lay the foundation for further micro-research. At the cellular and molecular level, we can investigate the mechanisms of FJOA, which may provide scientific basis for the prevention and treatment of this disease. Many previous researches have focused on pain mediators and inflammatory factors revealed the close relationship between low back pain and FJOA. The mechanisms and differences in the evolution of asymptomatic and symptomatic FJOA should be considered in future studies.

Spine; Lumbar vertebrae; Osteoarthritis, spine; Review

TAN Jun, Email: dr.tan@189.com

10.3969/j.issn.2095-252X.2017.10.009

R684.3

200120 上海，同濟(jì)大學(xué)附屬東方醫(yī)院脊柱外科 ( 祝愷、譚軍 )；100048 北京，解放軍總醫(yī)院第一附屬醫(yī)院骨科 ( 張紫豪、李文鋒 )

譚軍，Email: dr.tan@189.com

2016-11-25)

( 本文編輯：王萌 )