Condylar resorption: etiology manifestations and modern restorative treatment

doi:10.3969/j.issn.2095-4344.2014.46.021

Abstract

Abstract:

BACKGROUND: Due to complex etiology, manifestations, symptoms, development and outcomes, there is no article about the detailed introduction of condylar resorption in China.

OBJECTIVE: To analyze the etiology, pathogenesis, clinical manifestations, diagnosis and treatment of condylar resorption, thereby providing a theoretical basis for clinical treatment of condylar resorption.

METHODS: An online computer-based retrieval of PubMed database and CNKI database between January 1990 and January 2014 was performed by the first author. The keywords were “temporomandibular joint, condylar resorption, pathogenesis, diagnosis, treatment” in English and Chinese, respectively. Finally 38 literatures on the etiology, clinical presentation, diagnosis and treatment of condylar resorption were included.

RESULTS AND CONCLUSION: Condylar resorption was subdivided into secondary condylar resorption and primary condylar resorption. Secondary condylar resorption has clear risk factors, including condylar fractures, orthognathic surgery, connective tissue or autoimmune diseases and rheumatoid arthritis. Primary condylar resorption may be associated with lowered serum estradiol concentration. Condylar resorption can be diagnosed by imaging studies combined with clinical manifestations and disease history. Condylar resorption treatment measures mainly include medications, splint treatment, occlusal reconstruction, orthognathic surgery, rib-cartilage transplantation and total joint replacement surgery, in conjunction with orthodontic treatment. Currently, its complex etiology and pathogenesis has not been fully elucidated, and we need to conduct further studies.

中国组织工程研究杂志出版内容重点：组织构建；骨细胞；软骨细胞；细胞培养；成纤维细胞；血管内皮细胞；骨质疏松；组织工程

全文链接：

Key words: jaw, mandibular condyle, alveolar bone loss

CLC Number:

R318

Li Zhen-xing, Chen Chuan-jun. Condylar resorption: etiology manifestations and modern restorative treatment[J]. Chinese Journal of Tissue Engineering Research, 2014, 18(46): 7482-7486.

Figures/Tables 1

2.1 髁突吸收的分类 De Bont等[6]依据其是否存在明确发病诱因分为继发性髁突吸收(secondary condylar resorption)和原发性髁突吸收，其中原发性髁突吸收又称特发性髁突吸收。继发性髁突吸收有明确的致病因素，分为局部和全身因素。局部因素包括骨关节炎、颞下颌关节功能结构紊乱、肿瘤、创伤、正畸治疗史、正颌外科手术史等；全身因素包括类风湿关节炎、硬皮病、系统性红斑狼疮、舍格伦综合征、强直性脊柱炎、胶原血管病和类固醇的使用等。与其对应的不明原因的髁突吸收或称为特发性髁突吸收，主要特点为：多青春期发病，女性为主(男女比例为1∶9)；无关节区创伤及正畸正颌治疗等影响关节结构功能的病史及治疗史；无全身其他部位关节病及风湿、类风湿病史；全身健康状况良好[2-5，7]。 Hoppenreijs等[8]根据前牙的咬合关系将髁突吸收分为深覆牙合性和开牙合性两类。髁突上端吸收为深覆牙合性吸收，开牙合性吸收为髁突上端和前端发生吸收，其中特发性髁突吸收属于开牙合性髁突吸收。 2.2 髁突吸收的病因及机制 2.2.1 继发性髁突吸收的病因及机制髁突骨折：国内外大量临床研究发现髁突骨折治疗后出现髁突吸收，这可能与骨折类型、髁突是否发生移位、骨折位置、年龄和治疗方法等因素有关[9-11]。髁突头部骨折出现吸收的概率比髁突颈部骨折高，骨折后发生移位出现髁突吸收的比例高于未移位的骨折，复合型或复杂型骨折发生吸收约为单纯型的34倍，25岁以下患者骨折后出现髁突吸收约为25岁以上患者的27倍。Hlawitschka等[11]发现开放性治疗(例如切开内固定复位)的患者下颌支高度降低发生率约为1.3%，远低于封闭性功能治疗的患者(约为8.2%)，且相比封闭治疗发生髁突严重形变，其吸收多较轻微。髁突骨折后发生髁突吸收可能是由于髁突的负荷发生了改变。正颌手术：国外大量文献报道正颌手术诱导髁突吸收发生，依据患者所受到的不同手术和非手术因素影响，其发生率在1%-31%之间[12-19]。非手术风险因素包括正颌手术前的颞下颌关节功能紊乱、髁突向后倾斜、髁突头部小而薄、高下颌平面角，后面部与前面部高度比小，另外开牙合的患者比深覆牙合患者更容易发生髁突吸收。Ow和Cheung[18]统计1957至2007年发表的文章，发现下颌骨牵张成骨术术后发生髁突吸收约为1.4%，远低于双侧矢状劈开截骨术术后(约为6.1%)。而单侧矢状劈开截骨术术后髁突吸收发生率与双侧矢状劈开截骨术并无明显区别[13]。在牵张成骨手术中下颌骨一次性前徙固定较渐进性前徙更容易发生髁突吸收。且髁突吸收通常发生于下颌前徙超过5 mm或术后实行颌间固定的患者中。如果正颌手术术后前几月内颞下颌关节出现异常声音和疼痛，或术后6个月后患者出现下颌前移或下颌骨自动旋转等症状，都可能预示着髁突吸收的发生。这种吸收与正颌手术增加肌肉张力导致髁突负荷加重有关。结缔组织和自身免疫性疾病：硬皮病、舍格伦综合征、系统性红斑狼疮、皮肌炎和强直性脊柱炎等结缔组织和自身免疫性疾病都可能诱发髁突吸收[1，20]。硬皮病是一种小动脉和微血管内膜增厚、管腔狭窄或闭塞等原因导致的全身性结缔组织病。关节组织常被累及，导致骨侵蚀，骨质溶解，肌肉萎缩，这可能是由缺血性骨损伤引起的[20]。通常双测发生病变，疾病初期下颌骨就被累及并发展迅速，发生率为20%-33%，且多发于女性。类风湿性关节炎：依据不同的临床和影像诊断标准，类风湿性关节炎患者中累及颞下颌关节的占4.7%- 84%，而这些病例中大部分患者髁突出现退行性变，发生吸收[21]。其他因素：Balasubramaniam等[22]报道了1例血小板增多症女性患者在接受颞下颌关节穿刺术后，发生髁突吸收。这可能与血小板升高时手术继发性出血和血栓形成有关。提示临床医生对血小板增多症患者进行颞下颌关节手术应谨慎，并尽可能将血小板控制在正常范围。 Sansare等[23]检查4例口腔结核病例发现有髁突吸收，下颌骨边缘吸收或牙槽骨疏松等骨吸收表现，其中两例发生髁突吸收。这种吸收与一般原因诱导髁突出现扁平状或侵蚀状吸收不同，其范围更广泛，并在吸收区域发现了证明结核存在的上皮细胞肉芽肿。因此临床医生遇到髁突吸收等下颌骨病变时应考虑口腔结核的可能性。继发性髁突吸收发病机制：由于髁突吸收诱因的复杂性，关于其发病机制也有不同观点。Arnett等[24]观点是加载于颞下颌关节的异常负荷诱导髁突发生压力性吸收，这些异常的负荷通常来源于颞下颌关节功能结构紊乱、创伤、正畸正颌治疗、调牙合和不稳定牙合关系等局部因素。适度的负重对维持关节的正常结构和功能有重要意义，但过度或异常的负重，超出生理限度会造成关节退行性变甚至破坏导致髁突吸收。Chuong等[25]认为髁突吸收发病机制可能与股骨头缺血性坏死相似。小血管管腔内或管腔外阻塞破坏动静脉壁，骨髓内脂肪细胞和骨细胞增大导致骨内压力增大，抑制髁突血运循环，导致缺血性坏死，产生吸收。 2.2.2 特发性髁突吸收病因及机制在特发性髁突吸收患者中，并未发现明确的致病因素。但国内外流行病学调查均显示特发性髁突吸收患者具有明显青春期女性发病倾向[2-5]，因此许多学者怀疑其发病机制与雌激素参与髁突软骨和骨组织代谢有关。国外一组关于特发性髁突吸收回顾性病例分析发现：所有病例均为年轻女性、均有雌二醇水平低下，且伴有口服避孕药或卵巢早衰史[26]。提示雌激素异常可能是诱发特发性髁突吸收的主要原因。但是目前雌激素如何诱发髁突吸收的机制并不清楚，还需要进一步实验探究。 2.3 临床表现当患者出现下述症状时，应高度怀疑髁突发生吸收：①髁突形态改变，变扁变平。②髁突高度降低。③面部后侧高度降低。④下颌位置后移。⑤前牙渐进性开牙合、覆盖加深、Ⅱ类错牙合[1]。髁突吸收有时伴有颞下颌关节症状，出现弹响杂音，关节区疼痛，其多双侧同时发生，而单侧发生时，下颌则偏向患侧。但是特发性髁突吸收患者一般无明显颞下颌关节症状，多因咬合关系异常或面部外观改变前往口腔正畸科寻求正畸治疗才被发现[2-5，7]。 2.4 影像学检查髁突吸收影像学检查一般包括全景片、X射线检查、磁共振检查、放射性同位素扫描检查、CBCT检查等[27-29]。①全景片显示：髁突体积减小、表面不规则、髁突颈变短、下颌支高度降低。②头颅侧位片显示：前牙开牙合、Ⅱ类错牙合和下颌支高度降低；当吸收处于活动期时，髁突骨皮质消失，吸收停止1年以上，骨皮质可再次出现。③磁共振成像显示：磁共振可以早期发现髁突骨皮质变薄或消失，关节盘前移位或伴有穿孔。④锝同位素骨扫描可明确髁突吸收是否处于静止期或活跃期。当放射性同位素的摄取量比正常值高2个标准差时，提示髁突吸收处于活跃期。⑤CBCT检查利用三维成像原理，更为直观地观察患者颞下颌关节和咬合关系的改变，定性定量分析髁突吸收的程度和进展变化。相对于传统的多层螺旋CT扫描，其扫描时间短，辐射剂量低，精确度高，是一种很有前途的评估髁突吸收的方法[28-29]。 2.5 诊断通过影像学检查(髁突形态变扁变平，高度降低)结合临床表现及病史即可诊断髁突吸收[1]。髁突吸收前和开始吸收之后，患者面部外观会发生改变，观察和比较患者面部不同时期的照片，将有助于诊断髁突吸收和评估病变的进展。同时，临床医生应当仔细询问患者的相关病史，如颞下颌关节外伤史、正颌正畸治疗史、全身系统性疾病史和类固醇类用药史等，进一步明确病因，去除致病因素，制定个性化治疗方案。 2.6 治疗治疗原则：积极去除致病因素；改善咬合关系、改进面部外观；缓解关节疼痛、尽可能改善颞下颌关节功能和防止关节进一步损害。对于有明确致病因素的继发性髁突吸收，应首先去除诱因。服用类固醇类药物，进行髁突治疗前应停药；正畸诱导髁突吸收的患者需立即停止正畸治疗；患有系统性全身疾病时，患者应积极治疗全身性疾病，待好转后再进行髁突治疗。对于病因不明的特发性髁突吸收则直接实施髁突治疗。目前对于髁突吸收治疗有多种不同措施，包括保守治疗和手术治疗。保守疗法包括药物治疗、夹板治疗和咬合重建[30-32]。当发生髁突吸收时，可首先采用肌肉松弛剂或夹板治疗，减轻颞下颌关节不适、缓解肌张力、防止进一步吸收。髁突吸收较轻时，如果髁突已经停止吸收1年以上，影像学检查髁突软骨完整或锝同位素骨扫描确定髁突吸收处于静止期，可以通过咬合重建利用颞下颌关节的自我修复能力改善颞下颌关节功能。保守治疗后应随访观察，如果髁突再次吸收或吸收加重，出现面部畸形或颞下颌关节症状影响咀嚼、言语、呼吸和唇闭合；或者髁突严重吸收致下颌支高度明显降低，保守治疗后不能代偿，此时应采用手术治疗。手术治疗主要包括正颌外科、肋骨-软骨移植和全关节置换术，同时配合正畸治疗[33-37]。为了减少创伤和术后疼痛，可辅助应用关节镜[35]。常规正颌手术虽然可以立即改善髁突吸收患者的面型，但因颞下颌关节发生病理性改变，术后可能导致关节不稳，髁突负荷异常，使其吸收再次活跃。由于髁突吸收具体发病机制尚未阐明，特别是特发性髁突吸收患者，一般保守治疗或正颌手术治疗无法保证髁突吸收是否再次发生，所以部分学者认为肋骨-软骨移植或全关节置换是最优的治疗方法，其可确保髁突吸收不再复发[1，33，36-37]。必要时辅以手术前和手术后正畸治疗。同时当患者伴有关节盘移位应行关节盘复位修补术，关节盘穿孔较大则行关节盘切除术[7]。"

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