T. Irie, D. Takahashi, T. Asano, R. Arai, M. A. Terkawi, N. Iwasaki, Department of Orthopedic Surgery, Hokkaido University Graduate School of Medicine, Sapporo, Japan Y. M. Ito, Department of Biostatistics, Hokkaido University Graduate School of Medicine, Sapporo, Japan.
Clin Orthop Relat Res. 2018 Jul;476(7):1455-1465. doi: 10.1097/01.blo.0000533619.50951.e3.
The definitive treatment of borderline-to-mild dysplasia remains controversial. A more comprehensive understanding of the etiology of osteoarthritis (OA) and clarification of any possible association between borderline-to-mild dysplasia and the pathogenesis of OA are essential.
QUESTIONS/PURPOSES: (1) Does the distribution of acetabular subchondral bone density increase according to dysplasia severity? (2) Is there an association between borderline-to-mild dysplasia and OA pathogenesis?
We evaluated bilateral hips of patients with developmental dysplasia of the hip who underwent eccentric rotational acetabular osteotomy (ERAO) for inclusion in the dysplasia group and contralateral hips of patients with unilateral idiopathic osteonecrosis of the femoral head (ONFH) who underwent curved intertrochanteric varus osteotomy (CVO) for the control group. ERAO was performed in 46 patients and CVO was performed in 32 patients between January 2013 and August 2016 at our institution. All patients underwent bilateral hip CT. The study included 55 hips categorized according to dysplasia severity: (1) borderline-mild, 19 hips (15° ≤ lateral center-edge angle [LCEA] < 25°); (2) moderate, 20 hips (5° ≤ LCEA < 15°); (3) severe, 16 hips (LCEA < 5°); and (4) control, 15 hips. Thirty-seven dysplastic hips (age < 15 or > 50 years old, prior hip surgery, subluxation, aspherical femoral head, cam deformity, and radiographic OA) and 17 control hips (age < 15 or > 50 years old, bilateral ONFH, LCEA < 25° or ≥ 35°, cam deformity, and radiographic OA) were excluded. CT-osteoabsorptiometry (OAM) predicts physiologic biomechanical conditions in joints by evaluating subchondral bone density. We evaluated the distribution of subchondral bone densities in the acetabulum with CT-OAM, dividing the stress distribution map into six segments: anteromedial, anterolateral, centromedial, centrolateral, posteromedial, and posterolateral. We calculated the percentage of high-density area, which was defined as the upper 30% of Hounsfield units values in each region and compared least square means difference estimated by the random intercept model among the four groups.
In all regions, the percentage of high-density area did not differ between the borderline-mild group and the control (eg, anterolateral, 16.2 ± 5.6 [95% CI, 13.4 to 18.9] versus 15.5 ± 5.7 [95% CI, 12.4 to 18.5, p = 0.984]; centrolateral, 39.1 ± 5.7 [95% CI, 36.4 to 41.8] versus 39.5 ± 4.7 [95% CI, 36.6 to 42.5, p = 0.995]; posterolateral, 10.9 ± 5.2 [95% CI, 8.0 to 13.8] versus 15.1 ± 6.8 [95% CI, 11.7 to 18.5, p = 0.389]). In the anterolateral region, a smaller percentage of high-density area was observed in the borderline-mild group than in both the moderate group (16.2 ± 5.6 [95% CI, 13.4-18.9] versus 28.2 ± 5.1 [95% CI, 25.5-30.9], p < 0.001) and the severe group (16.2 ± 5.6 [95% CI, 13.4-18.9] versus 22.2 ± 6.8 [95% CI, 19.2-25.2, p = 0.026).
Our results suggest that the cumulative hip stress distribution in borderline-to-mild dysplasia was not concentrated on the lateral side of the acetabulum, unlike severe dysplasia.
Based on the stress distribution pattern, our results may suggest that there is no association between borderline-to-mild dysplasia and the pathogenesis of OA. Further studies are needed to evaluate the association between borderline-to-mild dysplasia and instability of the hip.
对于边缘型至轻度发育不良，其明确的治疗方法仍存在争议。更全面地了解骨关节炎（OA）的病因，并阐明边缘型至轻度发育不良与 OA 发病机制之间的任何可能关联至关重要。
问题/目的：（1）髋臼软骨下骨密度的分布是否会随发育不良的严重程度而增加？（2）边缘型至轻度发育不良与 OA 发病机制之间是否存在关联？
我们评估了在我院接受偏心旋转髋臼截骨术（ERAO）的发育性髋关节发育不良患者双侧髋关节（纳入发育不良组）和在我院接受曲形转子间内翻截骨术（CVO）的单侧特发性股骨头坏死（ONFH）患者对侧髋关节（纳入对照组），以纳入研究。2013 年 1 月至 2016 年 8 月，共对 46 例患者进行了 ERAO，对 32 例患者进行了 CVO。所有患者均接受了双侧髋关节 CT 检查。本研究共包括 55 个髋关节，根据发育不良的严重程度进行分类：（1）边缘型-轻度，19 个髋关节（外侧中心边缘角[LCEA]15°≤<25°）；（2）中度，20 个髋关节（5°≤LCEA<15°）；（3）重度，16 个髋关节（LCEA<5°）；（4）对照组，15 个髋关节。排除了 37 个发育不良髋关节（年龄<15 岁或>50 岁、有髋关节手术史、半脱位、非球形股骨头、凸轮畸形和放射学 OA）和 17 个对照组髋关节（年龄<15 岁或>50 岁、双侧 ONFH、LCEA<25°或≥35°、凸轮畸形和放射学 OA）。CT-骨吸收测定（OAM）通过评估软骨下骨密度来预测关节的生理生物力学状况。我们使用 CT-OAM 评估髋臼软骨下骨密度的分布，将应力分布图分为六个节段：前内侧、前外侧、中央内侧、中央外侧、后内侧和后外侧。我们计算了高密度区域的百分比，定义为每个区域 Hounsfield 单位值的上 30%，并通过随机截距模型比较了四组之间最小平方均值差异的估计值。
在所有区域中，边缘型-轻度组与对照组的高密度区域百分比没有差异（例如，前外侧，16.2±5.6[95%CI，13.4 至 18.9]与 15.5±5.7[95%CI，12.4 至 18.5，p=0.984]；中央外侧，39.1±5.7[95%CI，36.4 至 41.8]与 39.5±4.7[95%CI，36.6 至 42.5，p=0.995]；后外侧，10.9±5.2[95%CI，8.0 至 13.8]与 15.1±6.8[95%CI，11.7 至 18.5，p=0.389]）。在前外侧区域，与中度组（16.2±5.6[95%CI，13.4-18.9]与 28.2±5.1[95%CI，25.5-30.9]，p<0.001）和重度组（16.2±5.6[95%CI，13.4-18.9]与 22.2±6.8[95%CI，19.2-25.2，p=0.026）相比，边缘型-轻度组的高密度区域百分比较小。
我们的结果表明，与重度发育不良不同，边缘型至轻度发育不良的累积髋关节应力分布并未集中在髋臼的外侧。
根据应力分布模式，我们的结果可能表明边缘型至轻度发育不良与 OA 发病机制之间没有关联。需要进一步的研究来评估边缘型至轻度发育不良与髋关节不稳定之间的关联。
