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. 2018 Apr 26;476(7):1455–1465. doi: 10.1097/01.blo.0000533619.50951.e3

Is There an Association Between Borderline-to-mild Dysplasia and Hip Osteoarthritis? Analysis of CT Osteoabsorptiometry

Tohru Irie 1,2,, Daisuke Takahashi 1,2, Tsuyoshi Asano 1,2, Ryuta Arai 1,2, Muhammad Alaa Terkawi 1,2, Yoichi M Ito 1,2, Norimasa Iwasaki 1,2
PMCID: PMC6437563  PMID: 29698301

Abstract

Background

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?

Methods

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.

Results

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).

Conclusions

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.

Clinical Relevance

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.

Introduction

In developmental dysplasia of the hip (DDH), the contact area of the articular surface is diminished [38], and the characteristic shallow acetabulum leads to increased mechanical stress on the cartilage [19]. This abnormal stress distribution pattern results in osteoarthritis (OA). Several preservative procedures have been approved for treating severe DDH and preventing OA progression, including periacetabular osteotomy (PAO) such as rotational acetabular osteotomy (RAO) [30], eccentric RAO (ERAO) [16], and Bernese PAO [3]. To date, no consensus has been reached regarding the treatment of borderline-to-mild dysplasia [6, 39].

Although several investigations using cadaveric techniques [1, 7] and finite element methods [13, 15, 35] have suggested that underlying structural abnormalities of the dysplastic hip lead to accelerated joint degradation, direct in vivo measurements of contact stress pressure and stress distribution patterns of the dysplastic hip are extremely difficult. However, it has been assumed that subchondral bone density distribution reflects the stress pattern of a joint under long-term physiological conditions [27]. CT-osteoabsorptiometry (OAM) was developed by Müller-Gerbl and colleagues [26] to predict the physiologic biomechanical conditions of joints by evaluating subchondral bone density. Thus, CT-OAM is used to assess long-term stress distributions in individual joints [18, 22, 25, 31-33, 36].

Although numerous attempts have been made to evaluate and compare hip mechanical stress between severely dysplastic and normal hips, little has been reported on stress distribution patterns of the borderline to mildly dysplastic hip [2], and few comparative evaluations according to dysplasia severity including borderline-to-mild dysplasia have been reported. The natural course of the borderline to mildly dysplastic hip has not been well clarified and much remains unclear regarding whether there is an association between borderline-to-mild dysplasia and the pathogenesis of OA. Although hip arthroscopy has advanced the treatment of symptomatic labral tears [21, 44], the indications and outcomes in borderline-to-mild dysplasia have remained controversial [6, 40]. A more comprehensive understanding of the etiology of hip OA and clarification of any possible association between borderline-to-mild dysplasia and the pathogenesis of OA are essential for making decisions about conservative treatment or surgical interventions such as PAO and arthroscopic treatment.

In the current study, we examined whether (1) the distribution of acetabular subchondral bone density increases according to dysplasia severity using CT-OAM; and (2) whether there is an association between borderline-to-mild dysplasia and the pathogenesis of OA.

Patients and Methods

Institutional review board approval was obtained before the study (approval ID: 016-0149). We evaluated bilateral hips of patients with DDH who underwent ERAO between January 2013 and August 2016 at our institution for inclusion in the dysplasia group. Exclusion criteria were (1) age < 15 years old or > 50 years old; (2) lateral center-edge angle (LCEA) [42] ≥ 25°; (3) prior ipsilateral hip surgery or trauma; (4) ipsilateral hip subluxation; (5) aspherical femoral head; (6) presence of an ipsilateral cam deformity defined as an α angle > 55° [9]; or (7) radiographic OA (Kellgren-Lawrence Grade 1, 2, 3, or 4). ERAO was performed in 46 patients during this time and all patients underwent bilateral hip CT scans for preoperative examinations. Two patients were excluded for reasons of age < 15 years old or > 50 years old. Among the remaining 44 patients (88 hips), two hips had undergone prior ipsilateral hip surgery, four hips had subluxation, three hips had aspherical femoral heads, eight hips had cam deformity, and 16 hips had radiographic OA. Those 33 hips were excluded (Fig. 1). For the control group, we evaluated the contralateral hips of patients with unilateral idiopathic osteonecrosis of the femoral head (ONFH) who underwent curved intertrochanteric varus osteotomy during the same period at our institution. Inclusion and exclusion criteria were the same as for the dysplasia groups with the additional exclusion criteria of bilateral ONFH and LCEA < 25° or ≥ 35°. Curved intertrochanteric varus osteotomy (CVO) was performed in 32 patients during this time and all patients underwent bilateral hip CT scans for preoperative examinations. Three patients were excluded for reasons of age < 15 years old or > 50 years old. Among the remaining 29 contralateral hips, eight hips had bilateral ONFH, three hips had LCEA < 25° or ≥ 35°, two hips had cam deformity, and one hip had radiographic OA. A total number of 17 hips were excluded (Fig. 1). Finally, we evaluated 55 hips as dysplastic hips and 15 hips as controls.

Fig. 1.

Fig. 1

The flowchart shows the selection of hips to be evaluated and the actual number of hips in each group.

First, we calculated the delta using data from our previously reported pilot study [10, 31, 33]. Furthermore, we calculated the power for various possible deltas using 15 cases per group by using the standardized effect size delta multiplied by the SD of each group to convert to expected group differences. A delta of 1.3 gave a power of 93.1%. Because delta was calculated to be 1.9, a sample size of at least 15 cases in each group provides > 90% power. Therefore, we considered the sample size of at least 15 hips in each group sufficient for the current study.

Hip dysplasia severity was measured based on LCEA, then classified into borderline-to-mild dysplasia (15° ≤ LCEA < 25°), moderate dysplasia (5° ≤ LCEA < 15°), or severe dysplasia (LCEA < 5°) [19, 28]. In the borderline-mild group, 18 hips were from female patients, and one hip was from a male patient. Sixteen hips were from patients with bilateral dysplasia. In the moderate group, 18 hips were from female patients, and two hips were from male patients. Eighteen hips were from patients with bilateral dysplasia. In the severe group, 13 hips were from female patients, and three hips were from male patients. Fourteen hips were from patients with bilateral dysplasia. In the control group, 10 hips were from female patients, and five hips were from male patients. All hips were unilateral. Clinical evaluations were performed using the Harris hip score (HHS) preoperatively for ERAO or CVO. No differences were noted among the four groups in age, sex, body weight, body mass index (BMI), or HHS with the numbers available. However, there were differences in the intragroup ratios of both the preoperative side versus contralateral side and bilateral versus unilateral (Table 1; Fig. 1).

Table 1.

Patient demographics in each group according to severity of hip dysplasia versus control group

graphic file with name abjs-476-1455-g002.jpg

Supine AP pelvic radiographs were taken preoperatively using Siebenrock’s standardized technique [37]. HHS, AP pelvic radiographs, and CT images were obtained within 7 days for each patient. A break in the Shenton line on AP radiographs of > 5 mm was defined as joint subluxation [19]. We also evaluated OA, LCEA, and acetabular roof obliquity (ARO) [23]. We performed all digital measurements and calculations using Centricity™ Web-J 3.0 HD software (GE Healthcare Japan, Tokyo, Japan).

We used a high-resolution (pixel matrix, 512 × 512) helical CT scanner (CT High Speed Advantage; GE Medical Systems, Milwaukee, WI, USA) to obtain axial images of bilateral hips. Slice thickness and interval were set at 1 mm each, and table speed was set at 1 mm/s. Imaging data were analyzed using an Aquilion One image analysis system (Toshiba Medical Systems, Tokyo, Japan), and a three-dimensional bone model was generated from the axial image stack. Thereafter, coronal views based on the anterior pelvic plane at 1-mm intervals were reconstructed from the multiplanar reconstruction model. We defined the acetabular anteversion angle in the axial plane using Fujii’s technique [8].

To evaluate subchondral bone density, we used noncommercial software developed in our institution (OsteoDens 4.0). The target area was the subchondral bone region of the weightbearing acetabular surface. First, the AP range was determined to be the area in all coronal images between lines drawn 5 mm posterior to the anterior border and 5 mm anterior to the posterior border of the femoral head (Fig. 2A). Second, the width of the weightbearing surface, which extends from the medial margin bordering the fossa acetabuli to the lateral margin of the subchondral sclerotic line, was measured in the midcoronal image (Fig. 2B). Next, the subchondral bone region of the weightbearing acetabular surface was automatically identified using the OsteoDens 4.0 software. We took measurements parallel to the ARO for each joint. In each slice, x-ray attenuation (in Hounsfield units [HU]), whereby water is 0 HU and compact bone is 1000 HU of the identified subchondral bone region, was measured at each coordinate in 1-mm intervals. For each patient, we divided the range of HU values into nine equal grades, and we created a surface mapping image with a nine-grade color scale (Fig. 2C) using previously described CT-OAM methods [10, 31, 33].

Fig. 2 A-C.

Fig. 2 A-C

(A) The image shows how we established the AP range of measurement. (B) The image shows how we established the width of the weightbearing surface. (C) The image shows the surface mapping image with a nine-grade color scale of the acetabular surface using CT-OAM methods. *Line from anterosuperior iliac spine to pubic tubercle; tangential line of the anterior border of the femoral head and parallel line 5 mm posterior; tangential line of the posterior border of the femoral head and parallel line 5 mm anterior; lateral margin of the acetabular subchondral bone; §medial margin of the acetabular subchondral bone bordering on the fovea.

Quantitative analysis of mapping data focused on the location of the area of maximum density across the acetabular articular surface (Fig. 3A). The target area, including the upper 30% of HU values, was defined as the high-density area. The measured target area was divided into six regions: anteromedial, anterolateral, centromedial, centrolateral, posteromedial, and posterolateral (Fig. 3B). We calculated the percentage of the high-density area occupying each region.

Fig. 3 A-B.

Fig. 3 A-B

(A) The image shows segments of bone density for the acetabulum used for quantitative analysis. Lateral margin of acetabular subchondral bone; §medial margin of acetabular subchondral bone bordering on the fossa acetabuli. (B) The image shows maximum bone density mapping data for the acetabulum. Ant-med = anteromedial region; Ant-lat = anterolateral region; Cent-med = centromedial region; Cent-lat = centrolateral region; Post-med = posteromedial region; Post-lat = posterolateral region.

We assessed the reproducibility of measurements made using our noncommercial software (OsteoDens 4.0). For this assessment, we randomly selected two hips and measured a total of 12 regions on the contralateral side twice using preoperative and postoperative CT within a 2-week interval. The intraclass correlation coefficient for reproducibility between the two CT measurements was 0.877. In addition, we assessed intra- and interobserver reliability on two randomly selected hips from each group. Two observers (TI, TA) independently measured the percentage of the high-density area in these eight hips; a total of 48 sections were measured twice in a blinded manner with a 1-month interval. The intraclass correlation coefficients for intraobserver reliability were 0.991 (TI) and 0.989 (TA), respectively, and the intraclass correlation coefficient for interobserver reproducibility was 0.981. The chi square test was used to compare categorical parameters among the four groups. Our primary outcome was the percentage of high-density area, which was defined as the upper 30% of HU values in each region. To accommodate for correlations where two hips from one patient were included in the current study, pairwise comparisons among each of the four groups were performed using least square (LS) means difference estimated by the random intercept model as an effect-size metric. We adjusted p values for multiple comparisons using the Tukey–Kramer method for each region. A p value < 0.05 was considered significant. All statistical analyses were performed using JMP Pro 12 software (SAS Institute Japan, Tokyo, Japan).

Results

The mean ARO of the borderline-mild group was larger than the control group (10.2 ± 6.8 [95% confidence interval {CI}, 8.2-12.2] versus 3.0 ± 2.5 [95% CI, 0.7-5.3], p < 0.001) and smaller than the moderate group (10.2 ± 6.8 [95% CI, 8.2-12.2] versus 16.2 ± 3.7 [95% CI, 14.2-18.1], p = 0.004) and severe group (10.2 ± 6.8 [95% CI, 8.2-12.2] versus 23.7 ± 5.1 [95% CI, 21.5-25.9], p < 0.001). Acetabular anteversion angle of the borderline-mild group was not different from the control group with the numbers available (21.5 ± 3.0 [95% CI, 20.0-23.0] versus 18.7 ± 2.6 [95% CI, 17.0-20.4], p = 0.081) or the severe group with the numbers available (21.5 ± 3.0 [95% CI, 20.0-23.0] versus 23.5 ± 3.1 [95% CI, 21.9-25.1], p = 0.195) but was smaller than the moderate group (21.5 ± 3.0 [95% CI, 20.0-23.0] versus 24.2 ± 3.7 [95% CI, 22.7-25.6], p = 0.045) (Table 2; Fig. 4A).

Table 2.

Radiologic parameters in each group

graphic file with name abjs-476-1455-g005.jpg

Fig. 4 A-B.

Fig. 4 A-B

(A) The images show AP pelvic radiographs for each level of severity of hip dysplasia and for the control group. (B) The images show representative distribution patterns of the acetabulum in each group by CT-OAM.

The high-density area in the borderline-mild group was mainly located in the centrolateral and centromedial regions and was not concentrated on the lateral side of the acetabulum, unlike in severe dysplasia (Table 3; Fig. 4B). In all regions, the percentage of high-density area did not differ between the borderline-mild group and the control group with the numbers available (anteromedial, 4.8 ± 4.3 [95% CI, 2.6-7.1] versus 4.1 ± 4.2 [95% CI, 1.6-6.5]; LS means difference 0.7 [95% CI, -3.8 to 5.2], p = 0.975; anterolateral, 16.2 ± 5.6 [95% CI, 13.4-18.9] versus 15.5 ± 5.7 [95% CI, 12.4-18.5]; LS means difference 0.7 [95% CI, -4.7 to 6.2], p = 0.984; centromedial, 24.1 ± 4.7 [95% CI, 21.6-26.7] versus 22.4 ± 3.6 [95% CI, 19.7-25.1]; LS means difference 1.3 [95% CI, -3.6 to 6.3], p = 0.890; centrolateral, 39.1 ± 5.7 [95% CI, 36.4-41.8] versus 39.5 ± 4.7 [95% CI, 36.6-42.5]; LS means difference 0.5 [95% CI, -4.8 to 5.7], p = 0.995; posteromedial, 4.9 ± 2.8 [95% CI, 3.2-6.5] versus 3.4 ± 1.8 [95% CI, 1.7-5.1]; LS means difference 1.5 [95% CI, -1.5 to 4.6], p = 0.549; posterolateral, 10.9 ± 5.2 [95% CI, 8.0-13.8] versus 15.1 ± 6.8 [95% CI, 11.7-18.5]; LS means difference 3.7 [95% CI, -2.5 to 9.9], p = 0.389) (Table 3; Fig. 4B). 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]; LS means difference 11.9 [95% CI, 6.9-17.1], 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]; LS means difference 5.9 [95% CI, 0.5-11.3], p = 0.026). In the centromedial region, a larger percentage of high-density area was observed in the borderline-mild group than in both the moderate group (24.1 ± 4.7 [95% CI, 21.6-26.7] versus 16.1 ± 6.9 [95% CI, 13.6-18.6]; LS means difference 7.8 [95% CI, 3.2-12.4], p = 0.001) and the severe group (24.1 ± 4.7 [95% CI, 21.6-26.7] versus 5.0 ± 3.8 [95% CI, 2.2-7.8]; LS means difference 18.4 [95% CI, 13.5-23.3], p < 0.001). Additionally, a larger percentage of high-density area was observed in the moderate group than in the severe group (16.1 ± 6.9 [95% CI, 13.6-18.6] versus 5.0 ± 3.8 [95% CI, 2.2-7.8]; LS means difference 10.6 [95% CI, 6.1-15.1], p < 0.001). In the posterolateral region, the percentage of high-density area did not differ between the borderline-mild group and the moderate group with the numbers available (10.9 ± 5.2 [95% CI, 8.0-13.8] versus 9.7 ± 6.3 [95% CI, 6.8-12.6]; LS means difference 1.6 [95% CI, -4.3 to 7.5], p = 0.885). However, a smaller percentage of high-density area was observed in the borderline-mild group than in the severe group (10.9 ± 5.2 [95% CI, 8.0-13.8] versus 22.3 ± 7.2 [95% CI, 19.1-25.5]; LS means difference 10.6 [95% CI, 4.2-16.9], p < 0.001). In the anteromedial, centrolateral, and posteromedial regions, the percentage of high-density area did not differ between the borderline-mild group and both the moderate group (anteromedial, 4.8 ± 4.3 [95% CI, 2.6-7.1] versus 3.8 ± 4.7 [95% CI, 1.6-5.9]; LS means difference 1.0 [95% CI, -3.2 to 5.3], p = 0.921; centrolateral, 39.1 ± 5.7 [95% CI, 36.4-41.8] versus 38.7 ± 5.5 [95% CI, 36.0-41.3]; LS means difference 0.4 [95% CI, -4.6 to 5.3], p = 0.997; posteromedial, 4.9 ± 2.8 [95% CI, 3.2-6.5] versus 3.6 ± 3.6 [95% CI, 2.0-5.2]; LS means difference 1.5 [95% CI, -1.4 to 4.3], p = 0.540) and severe group (anteromedial, 4.8 ± 4.3 [95% CI, 2.6-7.1] versus 6.5 ± 5.3 [95% CI, 4.1-9.0]; LS means difference 1.9 [95% CI, -2.6 to 6.5], p = 0.682; centrolateral, 39.1 ± 5.7 [95% CI, 36.4-41.8] versus 39.3 ± 6.1 [95% CI, 36.3-42.2]; LS means difference 0.2 [95% CI, -5.0 to 5.5], p = 0.999; posteromedial, 4.9 ± 2.8 [95% CI, 3.2-6.5] versus 4.7 ± 3.9 [95% CI, 2.9-6.5]; LS means difference 0.2 [95% CI, -2.8 to 3.3], p = 0.997) with the numbers available.

Table 3.

Mean percentage of the high-density area for each region and least square means difference among the four groups

graphic file with name abjs-476-1455-g007.jpg

Discussion

Although several recent studies have reported the treatment of borderline dysplasia [4, 6, 9, 20], this pathophysiology is a relatively new concept and not fully understood. In patients with borderline-to-mild dysplasia, a more comprehensive understanding of the etiology of OA is essential for making decisions about conservative treatment or surgical interventions such as PAO and arthroscopic treatment. However, the natural course of a borderline-to-mildly dysplastic hip has not been well clarified, and much remains unclear regarding whether there is an association between borderline-to-mild dysplasia and the pathogenesis of OA. In the current study, we examined whether the distribution of acetabular subchondral bone density increases according to dysplasia severity. In the anterolateral region, a smaller percentage of high-density area was observed in the borderline-mild group than in both the moderate group and the severe group. However, in the centromedial region, a larger percentage of high-density area was observed in the borderline-mild group than in both the moderate group and the severe group. We found that the high-density area in the borderline-mild group was mainly located in the centrolateral and centromedial regions and was not concentrated on the lateral side of the acetabulum, unlike in severe dysplasia (Fig. 4B). Furthermore, we found that in all regions, the percentage of high-density area did not differ between the borderline-mild group and the control group with the numbers available.

Several limitations need to be considered with this study. First, we did not directly measure mechanical stresses in each hip, and our results are based on assessment of acetabular bone mineral density with CT-OAM. The theoretical background for CT-OAM is that subchondral bone mineralization functionally adapts to repeated and long-term mechanical stress [26, 33]. We evaluated the acetabular bone mineral density using OsteoDens 4.0 software. Although OsteoDens 4.0 is noncommercial proprietary software, which was developed in our institution, several previous reports using OsteoDens 4.0 have shown it can provide clinically useful information on various joints such as the shoulder, elbow, wrist, knee, and ankle [10, 18, 22, 25, 31, 32, 36] for analyzing individual loading conditions. Second, we evaluated bilateral hips of patients with DDH who underwent ERAO as the dysplasia group and the contralateral hips of patients with unilateral ONFH who underwent CVO as the control group, except when ruled out under the exclusion criteria. All patients who underwent ERAO or CVO at our institution underwent bilateral hip CT scans for preoperative examinations. Because we cannot perform CT scans on healthy subjects for research, we used these CT data for our evaluation. Although we found no differences among the four groups regarding patient characteristics such as age, sex, body weight, BMI, and HHS with the numbers available, there was a difference in the intragroup ratio of bilateral versus unilateral. Our primary outcome was the percentage of high-density area, which was defined as the upper 30% of HU values in each region. To accommodate for correlations where two hips from one patient were included in the current study, pairwise comparisons among each of the four groups were performed using LS means difference estimated by the random intercept model as an effect-size metric. Furthermore, we adjusted p values for multiple comparisons using the Tukey–Kramer method for each region. In our view, this helps to mitigate this limitation, although further research may be needed.

Regarding further limitations, we classified hip dysplasia severity based on LCEA only. Furthermore, borderline dysplasia and mild dysplasia were not evaluated independently. We defined moderate dysplasia according to the method of Jessel et al. [19] and this range is 10° (5° ≤ LCEA < 15°). It is reported that LCEA is the most commonly used sign for acetabular coverage, and LCEA > 35° to 40° has been used as a criterion of femoroacetabular impingement (FAI) [34]. To completely exclude both dysplasia and hips with FAI, we defined hips with 25° ≤ LCEA < 35° as controls, and this range is also 10°. Although borderline dysplasia is often defined as 20° ≤ LCEA < 25° [9, 20], this range is 5°. Furthermore, the definitions by Domb et al. [6] and Chaharbakhshi et al. [4] are 18° ≤ LCEA < 25° and this range is 8°. Because the definition of borderline dysplasia remains controversial and we wanted to avoid confusion or intergroup discrepancy, we made borderline dysplasia and mild dysplasia one group (15° ≤ LCEA < 25°). However, mathematical models have shown that peak hip stress changes dramatically at around LCEA 20° [14]. Therefore, the range of our borderline-mild group may imply a theoretical possibility of diversity. Additional inquiry may be needed to evaluate borderline dysplasia independently from mild dysplasia and based on highly detailed classification according to other geometric parameters including ARO, acetabular anteversion angle, and three-dimensional coverage of the femoral head [17], among others.

In the borderline-mild group, a smaller percentage of high-density area in the anterolateral region and a larger percentage of high-density area in the centromedial region were observed than in both the moderate group and the severe group in the current study. Mavcic et al. [24] reported that the peak stress trajectory is displaced closer to the lateral edge of the acetabulum and anteriorly in the case of dysplastic hips. Our results support this report, which was based on mathematical estimation. Furthermore, the distribution of acetabular subchondral bone density in the centromedial region decreased from the borderline-mild group to the severe group, according to dysplasia severity. Our findings suggest that the pathophysiology of borderline-to-mild dysplasia is different from that of moderate to severe dysplasia. Kaya et al. [20] reported that patterns of cartilage damage differed between borderline dysplasia (20° ≤ LCEA < 25°) and acetabular dysplasia (LCEA < 20°) using the arthroscopic geographic zone method. Our results also support this report, which was based on arthroscopic estimation. Therefore, our results suggest that discrimination between borderline-to-mild dysplasia and moderate-to-severe dysplasia is important for effective management and definitive treatment in patients with borderline to mildly dysplastic hips.

In all regions, the percentage of high-density area did not differ between the borderline-mild group and the control group with the numbers available. These results may suggest that there is no association between borderline-to-mild dysplasia and the pathogenesis of OA. However, some patients with borderline to mildly dysplastic hips get premature degenerative joint disease. Cumulative mechanical stress of the acetabulum and instability of the hip have been recognized as a cause of OA in patients with dysplasia [19, 27, 28, 38]. We did not evaluate hip instability and the consequent shear stresses on the cartilage. This is another limitation of the current study. Considering the possibility that OA in patients with borderline-to-mild dysplasia is caused by cumulative mechanical stress concentration and/or instability, and that our results suggest that borderline to mildly dysplastic hips do not cause cumulative mechanical stress concentration, it seems reasonable to suppose that instability and the consequent shear stresses may cause OA in patients with borderline-to-mild dysplasia. Conversely, even a slight variation in acetabular coverage such as that between normal hips and borderline dysplastic hips might influence hip instability but not mechanical stress concentration. Consequently, this instability may cause shear stresses leading to cartilage degeneration or OA. To clarify whether there is an association between borderline-to-mild dysplasia and the pathogenesis of OA, not only evaluating cumulative mechanical stress, but also evaluating instability may be clinically important. Although several indirect indicators of relevant instability have been reported such as the iliocapsularis-to-rectus-femoris ratio [12] and the femoroepiphyseal acetabular roof index [43], the evaluation of hip instability remains challenging. Further studies are needed to clarify the association between borderline-to-mild dysplasia and instability of the hip.

There could be other causes that influence the pathogenesis of OA in patients with borderline-to-mild dysplasia other than cumulative mechanical stress and instability. Ng et al. [29] reported that individuals with cam deformity and varus neck angle may be subjected to elevated mechanical stresses. Although we excluded hips with presence of cam deformity to focus our evaluation on the acetabular side in the current study, Wells et al. [41] reported that cam deformities in DDH are common. Therefore, borderline-to-mild dysplasia with concomitant cam deformity may cause OA. Suitable treatment principles for patients with borderline-to-mild dysplasia remain controversial [6, 40]. Goronzy et al. [11] reported no differences in either outcome scores (WOMAC, EQ-5D) or progression of OA between PAO treatment alone and combined PAO and offset correction for cam deformity. However, according to a recent ANCHOR report [5], PAO is associated with less functional improvement in milder dysplasia (LCEA > 15°) than severe dysplasia. Although establishing suitable treatment principles for patients with borderline-to-mild dysplasia remains challenging, it is essential to consider the presence or absence of cam deformity when making clinical decisions about treatment strategy. Furthermore, Mavcic et al. [24] reported that in addition to the smaller lateral coverage of the femoral head, the larger interhip distance, the wider pelvis, and the medial position of the greater trochanter can also contribute to higher peak stress in dysplastic hips. In the treatment of borderline-to-mild dysplasia, evaluation of other geometric parameters such as these may be important.

Measurements of contact stress pressure and stress distribution patterns in the living dysplastic hip are extremely difficult. The theoretical background for CT-OAM is that subchondral bone mineralization functionally adapts to repeated and long-term mechanical stress under live loading conditions [33]. In the case of the finite element method and cadaveric techniques, analyses are generally undertaken using only one or two static loading conditions [13, 15, 35]. The mechanical stress of the dysplastic hip during gait or activities of daily living thus cannot practically be evaluated [15]. Cumulative mechanical stress likewise cannot practically be assessed. However, CT-OAM allows the evaluation of alterations in characteristic stress distribution patterns under live loading conditions through measuring subchondral bone mineralization [10, 33]. This is a strength of the present study.

In conclusion, in the borderline-mild group, a smaller percentage of high-density area in the anterolateral region of the acetabulum and a larger percentage of high-density area in the centromedial region were observed than in both the moderate group and the severe group. Additionally, our results show that the percentage of high-density area in all regions of the acetabulum did not differ between the borderline-mild group and the control group with the numbers available. 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 in 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. Our findings may contribute to clarifying the natural course of the borderline to mildly dysplastic hip and understanding the etiology of hip OA more comprehensively. However, to clarify whether there is an association between borderline-to-mild dysplasia and the pathogenesis of OA with more precision, further studies are needed to evaluate any association between borderline-to-mild dysplasia and instability of the hip.

Footnotes

Each author certifies that neither he, nor any member of his immediate family, has funding or commercial associations (consultancies, stock ownership, equity interest, patent/licensing arrangements, etc) that might pose a conflict of interest in connection with the submitted article.

All ICMJE Conflict of Interest Forms for authors and Clinical Orthopaedics and Related Research® editors and board members are on file with the publication and can be viewed on request.

Clinical Orthopaedics and Related Research® neither advocates nor endorses the use of any treatment, drug, or device. Readers are encouraged to always seek additional information, including FDA approval status, of any drug or device before clinical use.

Each author certifies that his institution approved the human protocol for this investigation, that all investigations were conducted in conformity with ethical principles of research, and that informed consent for participation in the study was obtained.

References

  • 1.Afoke NY, Byers PD, Hutton WC. Contact pressures in the human hip joint. J Bone Joint Surg Br. 1987;69:536–541. [DOI] [PubMed] [Google Scholar]
  • 2.Akiyama K, Sakai T, Koyanagi J, Yoshikawa H, Sugamoto K. Evaluation of translation in the normal and dysplastic hip using three-dimensional magnetic resonance imaging and voxel-based registration. Osteoarthritis Cartilage. 2011;19:700–710. [DOI] [PubMed] [Google Scholar]
  • 3.Beaulé PE, Dowding C, Parker G, Ryu JJ. What factors predict improvements in outcomes scores and reoperations after the Bernese periacetabular osteotomy? Clin Orthop Relat Res. 2015;473:615–622. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 4.Chaharbakhshi EO, Perets I, Ashberg L, Mu B, Lenkeit C, Domb BG. Do Ligamentum teres tears portend inferior outcomes in patients with borderline dysplasia undergoing hip arthroscopic surgery? A match-controlled study with a minimum 2-year follow-up. Am J Sports Med. 2017;45:2507–2516. [DOI] [PubMed] [Google Scholar]
  • 5.Clohisy JC, Ackerman J, Baca G, Baty J, Beaulé PE, Kim YJ, Millis MB, Podeszwa DA, Schoenecker PL, Sierra RJ, Sink EL, Sucato DJ, Trousdale RT, Zaltz I. Patient-reported outcomes of periacetabular osteotomy from the prospective ANCHOR cohort study. J Bone Joint Surg Am. 2017;99:33–41. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 6.Domb BG, Stake CE, Lindner D, El-Bitar Y, Jackson TJ. Arthroscopic capsular plication and labral preservation in borderline hip dysplasia: two-year clinical outcomes of a surgical approach to a challenging problem. Am J Sports Med. 2013;41:2591–2598. [DOI] [PubMed] [Google Scholar]
  • 7.Eckstein F, von Eisenhart-Rothe R, Landgraf J, Adam C, Loehe F, Müller-Gerbl M, Putz R. Quantitative analysis of incongruity, contact areas and cartilage thickness in the human hip joint. Acta Anat (Basel). 1997;158:192–204. [DOI] [PubMed] [Google Scholar]
  • 8.Fujii M, Nakashima Y, Sato T, Akiyama M, Iwamoto Y. Pelvic deformity influences acetabular version and coverage in hip dysplasia. Clin Orthop Relat Res. 2011;469:1735–1742. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 9.Fukui K, Briggs KK, Trindade CA, Philippon MJ. Outcomes after labral repair in patients with femoroacetabular impingement and borderline dysplasia. Arthroscopy. 2015;31:2371–2379. [DOI] [PubMed] [Google Scholar]
  • 10.Funakoshi T, Furushima K, Momma D, Endo K, Abe Y, Itoh Y, Fujisaki K, Tadano S, Iwasaki N. Alteration of stress distribution patterns in symptomatic valgus instability of the elbow in baseball players: a computed tomography osteoabsorptiometry study. Am J Sports Med. 2016;44:989–994. [DOI] [PubMed] [Google Scholar]
  • 11.Goronzy J, Franken L, Hartmann A, Thielemann F, Postler A, Paulus T, Günther KP. What are the results of surgical treatment of hip dysplasia with concomitant cam deformity? Clin Orthop Relat Res. 2017;475:1128–1137. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 12.Haefeli PC, Steppacher SD, Babst D, Siebenrock KA, Tannast M. An increased iliocapsularis-to-rectus-femoris ratio is suggestive for instability in borderline hips. Clin Orthop Relat Res. 2015;473:3725–3734. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 13.Henak CR, Abraham CL, Anderson AE, Maas SA, Ellis BJ, Peters CL, Weiss JA. Patient-specific analysis of cartilage and labrum mechanics in human hips with acetabular dysplasia. Osteoarthritis Cartilage. 2014;22:210–217. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 14.Iglic A, Iglic VK, Antolic V, Srakar F, Stanic U. Effect of the periacetabular osteotomy on the stress on the human hip joint articular surface. IEEE Trans Rehab Eng. 1993;1:207–212. [Google Scholar]
  • 15.Ike H, Inaba Y, Kobayashi N, Yukizawa Y, Hirata Y, Tomioka M, Saito T. Effects of rotational acetabular osteotomy on the mechanical stress within the hip joint in patients with developmental dysplasia of the hip: a subject-specific finite element analysis. Bone Joint J. 2015;97:492–497. [DOI] [PubMed] [Google Scholar]
  • 16.Irie T, Takahashi D, Asano T, Arai R, Konno T, Onodera T, Kondo E, Iwasaki N. Comparison of femoral head translation following eccentric rotational acetabular osteotomy and rotational acetabular osteotomy. Hip Int. 2017;27:49–54. [DOI] [PubMed] [Google Scholar]
  • 17.Ito H, Matsuno T, Hirayama T, Tanino H, Yamanaka Y, Minami A. Three-dimensional computed tomography analysis of non-osteoarthritic adult acetabular dysplasia. Skeletal Radiol. 2009;38:131–139. [DOI] [PubMed] [Google Scholar]
  • 18.Iwasaki N, Minami A, Miyazawa T, Kaneda K. Force distribution through the wrist joint in patients with different stages of Kienböck’s disease: using computed tomography osteoabsorptiometry. J Hand Surg Am. 2000;25:870–876. [DOI] [PubMed] [Google Scholar]
  • 19.Jessel RH, Zurakowski D, Zilkens C, Burstein D, Gray ML, Kim YJ. Radiographic and patient factors associated with pre-radiographic osteoarthritis in hip dysplasia. J Bone Joint Surg Am. 2009;91:1120–1129. [DOI] [PubMed] [Google Scholar]
  • 20.Kaya M, Suzuki T, Emori M, Yamashita T. Hip morphology influences the pattern of articular cartilage damage. Knee Surg Sports Traumatol Arthrosc. 2016;24:2016–2023. [DOI] [PubMed] [Google Scholar]
  • 21.Larson CM, Ross JR, Stone RM, Samuelson KM, Schelling EF, Giveans MR, Bedi A. Arthroscopic management of dysplastic hip deformities: predictors of success and failures with comparison to an arthroscopic FAI cohort. Am J Sports Med. 2016;44:447–453. [DOI] [PubMed] [Google Scholar]
  • 22.Makabe H, Iwasaki N, Kamishima T, Oizumi N, Tadano S, Minami A. Computed tomography osteoabsorptiometry alterations in stress distribution patterns through the wrist after radial shortening osteotomy for Kienböck disease. J Hand Surg Am. 2011;36:1158–1164. [DOI] [PubMed] [Google Scholar]
  • 23.Massie WK, Howorth MB. Congenital dislocation of the hip. Part I. Method of grading results. J Bone Joint Surg Am. 1950;32:519–531. [PubMed] [Google Scholar]
  • 24.Mavcic B, Pompe B, Antolic V, Daniel M, Iglic A, Kralj-Iglic V. Mathematical estimation of stress distribution in normal and dysplastic human hips. J Orthop Res. 2002;20:1025–1030. [DOI] [PubMed] [Google Scholar]
  • 25.Momma D, Iwasaki N, Oizumi N, Nakatsuchi H, Funakoshi T, Kamishima T, Tadano S, Minami A. Long-term stress distribution patterns across the elbow joint in baseball players assessed by computed tomography osteoabsorptiometry. Am J Sports Med. 2011;39:336–341. [DOI] [PubMed] [Google Scholar]
  • 26.Müller-Gerbl M, Putz R, Hodapp N, Schulte E, Wimmer B. Computed tomography-osteoabsorptiometry for assessing the density distribution of subchondral bone as a measure of long-term mechanical adaptation in individual joints. Skeletal Radiol. 1989;18:507–512. [DOI] [PubMed] [Google Scholar]
  • 27.Murphy SB, Ganz R, Müller ME. The prognosis in untreated dysplasia of the hip: a study of radiographic factors that predict the outcome. J Bone Joint Surg Am. 1995;77:985–989. [DOI] [PubMed] [Google Scholar]
  • 28.Nepple JJ, Wells J, Ross JR, Bedi A, Schoenecker PL, Clohisy JC. Three patterns of acetabular deficiency are common in young adult patients with acetabular dysplasia. Clin Orthop Relat Res. 2017;475:1037–1044. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 29.Ng KC, Mantovani G, Lamontagne M, Labrosse MR, Beaulé PE. Increased hip stresses resulting from a cam deformity and decreased femoral neck-shaft angle during level walking. Clin Orthop Relat Res. 2017;475:998–1008. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 30.Ninomiya S. Rotational acetabular osteotomy for the severely dysplastic hip in the adolescent and adult. Clin Orthop Relat Res. 1989;247:127–137. [PubMed] [Google Scholar]
  • 31.Nishida K, Iwasaki N, Fujisaki K, Funakoshi T, Kamishima T, Tadano S, Minami A. Distribution of bone mineral density at osteochondral donor sites in the patellofemoral joint among baseball players and controls. Am J Sports Med. 2012;40:909–914. [DOI] [PubMed] [Google Scholar]
  • 32.Oizumi N, Suenaga N, Minami A, Iwasaki N, Miyazawa T. Stress distribution patterns at the coracoacromial arch in rotator cuff tear measured by computed tomography osteoabsorptiometry. J Orthop Res. 2003;21:393–398. [DOI] [PubMed] [Google Scholar]
  • 33.Onodera T, Majima T, Iwasaki N, Kamishima T, Kasahara Y, Minami A. Long-term stress distribution patterns of the ankle joint in varus knee alignment assessed by computed tomography osteoabsorptiometry. Int Orthop. 2012;36:1871–1876. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 34.Rhee C, Le Francois T, Byrd JWT, Glazebrook M, Wong I. Radiographic diagnosis of pincer-type femoroacetabular impingement: a systematic review. Orthop J Sports Med. 2017;31:5. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 35.Russell ME, Shivanna KH, Grosland NM, Pedersen DR. Cartilage contact pressure elevations in dysplastic hips: a chronic overload model. J Orthop Surg Res. 2006;3:1–6. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 36.Shimizu T, Iwasaki N, Nishida K, Minami A, Funakoshi T. Glenoid stress distribution in baseball players using computed tomography osteoabsorptiometry: a pilot study. Clin Orthop Relat Res. 2012;470:1534–1539. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 37.Siebenrock KA, Schoeniger R, Ganz R. Anterior femoro-acetabular impingement due to acetabular retroversion. Treatment with periacetabular osteotomy. J Bone Joint Surg Am. 2003;85:278–286. [DOI] [PubMed] [Google Scholar]
  • 38.Tönnis D, Heinecke A. Acetabular and femoral anteversion: relationship with osteoarthritis of the hip. J Bone Joint Surg Am. 1999;81:1747–1770. [DOI] [PubMed] [Google Scholar]
  • 39.Tsumura H, Kaku N, Ikeda S, Torisu T. A computer simulation of rotational acetabular osteotomy for dysplastic hip joint: does the optimal transposition of the acetabular fragment exist? J Orthop Sci. 2005;10:145–151. [DOI] [PubMed] [Google Scholar]
  • 40.Uchida S, Utsunomiya H, Mori T, Taketa T, Nishikino S, Nakamura T, Sakai A. Clinical and radiographic predictors for worsened clinical outcomes after hip arthroscopic labral preservation and capsular closure in developmental dysplasia of the hip. Am J Sports Med. 2016;44:28–38. [DOI] [PubMed] [Google Scholar]
  • 41.Wells J, Nepple JJ, Crook K, Ross JR, Bedi A, Schoenecker P, Clohisy JC. Femoral morphology in the dysplastic hip: three-dimensional characterizations with CT. Clin Orthop Relat Res. 2017;475:1045–1054. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 42.Wiberg G. Studies on dysplastic acetabula and congenital subluxation of the hip joint: with special reference to the complication of osteoarthritis. Acta Chir Scand Suppl. 1939;58:7–38. [Google Scholar]
  • 43.Wyatt M, Weidner J, Pfluger D, Beck M. The femoro-epiphyseal acetabular roof (FEAR) index: a new measurement associated with instability in borderline hip dysplasia? Clin Orthop Relat Res. 2017;475:861–869. [DOI] [PMC free article] [PubMed] [Google Scholar]
  • 44.Yeung M, Kowalczuk M, Simunovic N, Ayeni OR. Hip arthroscopy in the setting of hip dysplasia: a systematic review. Bone Joint Res. 2016;5:225–231. [DOI] [PMC free article] [PubMed] [Google Scholar]

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