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Relation between ectopic ossification after total hip arthroplasty and activity of general inflammation in patients with ankylosing spondylitis
  1. YOSHITAKA TANI,
  2. JUNICHI NISHIOKA,
  3. KOJI INOUE,
  4. SINSUKE HUKUDA
  1. Department of Orthopaedic Surgery, Shiga University of Medical Science, Shiga, Japan
  2. Department of Rheumatology, Osaka Rosai Hospital, Osaka, Japan
  1. Dr Y Tani, Department of Orthopaedic Surgery, Shiga University of Medical Science, Tsukinowa-cho, Seta, Otsu, Shiga, 520–21, Japan.
  1. MASAKI TSUJIMOTO
  1. Department of Orthopaedic Surgery, Shiga University of Medical Science, Shiga, Japan
  2. Department of Rheumatology, Osaka Rosai Hospital, Osaka, Japan
  1. Dr Y Tani, Department of Orthopaedic Surgery, Shiga University of Medical Science, Tsukinowa-cho, Seta, Otsu, Shiga, 520–21, Japan.

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Ectopic ossification (EO) is a well known complication after total hip arthroplasty (THA). Some previous studies have considered ankylosing spondylitis (AS) a risk factor of EO, however other studies have refuted this association.1 The reported incidence of EO varies widely in different series.2

We retrospectively studied a total of 20 primary THAs in 16 Japanese patients with definite AS. The age of the patients at surgery ranged from 30 to 64 years (mean 45). All THAs apart from three cases were performed using bone cement. Surgical exposure was achieved by the posterolateral approach. The length of follow up averaged 93 months (range 29 to 148). Compared with the incidence of EO in AS patients, we investigated 126 primary THAs (92 osteoarthritis (OA), 26 rheumatoid arthritis (RA) and eight aseptic necrosis of the femoral head (ANF)) in 107 patients (15 male/92 female, mean age 61 years; range 32 to 85, mean follow up period 63 months; range 28 to 128). Bone cement was used in 118 of these 126 cases of THA. We evaluated supine anteroposterior roentgenographic findings of the hips. EO was graded according to Brooker’s classification.3

Six of 20 THA cases showed evident radiographic EO after THA in AS patients (Class I: 2 THAs, Class II: 3 THAs, Class III: 1 THA). The incidence of EO was 30.0%. In the control group, the incidence of EO was 32.5% (OA; 38.0%, RA; 15.4%, ANF; 25.0%), and there was no significant difference in the incidence of EO between the AS group and the control group using the χ2 test (χ2=0.051, p>0.01, NS). Mean age of the ossification group in AS patients (6 THAs) was 42 years, and mean age of the non-ossification group in AS patients (14 THAs) was 46 years. Mean (SEM) erythrocyte sedimentation rate (ESR) was 33.0 (7.7) mm 1st h and mean (SEM) C reactive protein (CRP) was 43.0 (8.9) mg/l in the ossification group, while mean ESR was 19.8 (4.1) mm 1st h and mean CRP was 10.8 (2.7) mg/l in the non-ossification group. There was a significant correlation between CRP values and the formation of EO using the Mann-Whitney U test (p<0.005). However, there was no correlation between ESR and EO (p=0.08, NS), as previously reported.4 In patients with RA, no relation between the formation of EO and acute phase reactants was found.

Although the results of different series are difficult to compare simply because there were other risk factors and different criteria of EO were used, our study did not recognise a high incidence of EO in AS patients compared with that in the controls. Based on this result, we did not conclude that AS is a risk factor of EO. However, we found a significant correlation between the formation of EO and preoperative serum CRP values in AS patients. Recently, significant increases in serum anti-collagen (type I, II, III and IV) antibody concentrations, especially in the IgA class, have been reported in AS patients.5 6 Type I collagen is present predominantly in bones, tendons, and joint capsules. After THA, type I collagen was found in the residue of excised joint capsules and bone fragments around hip joints. A significant correlation between the serum IgA concentration and CRP has been reported in AS patients.7Therefore, this periarticular residue may trigger local inflammations and induce the formation of EO in active general inflammatory phases and at high serum CRP concentrations.

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