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CASE REPORT Table of Contents   
Year : 2005  |  Volume : 39  |  Issue : 4  |  Page : 257-259
Transient osteoporosis of hip-A case report


Department Of Orthopaedics and Obstetrics and Gynaecology, Himalayan Institute of Medical Sciences, Dehradun, India

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How to cite this article:
Gupta P, Sharma S, Gupta V, Singh D, Agarwal A, Chauhan V. Transient osteoporosis of hip-A case report. Indian J Orthop 2005;39:257-9

How to cite this URL:
Gupta P, Sharma S, Gupta V, Singh D, Agarwal A, Chauhan V. Transient osteoporosis of hip-A case report. Indian J Orthop [serial online] 2005 [cited 2019 Sep 20];39:257-9. Available from: http://www.ijoonline.com/text.asp?2005/39/4/257/36622

   Introduction Top


Transient osteoporosis of hip (TOH) is a self limiting, reversible condition of unknown etiology characterized by rapidly developing osteoporosis of hip in absence of trauma, infection or immobilization etc [1],[2] . MRI findings showing bone marrow edema are diagnostic of the disease [3] . We present a case of 28 years old female who came two months after delivery with complaint of pain in right hip. She was diagnosed as a case of TOH and treated accordingly. The disease is self-limiting and complete cure can be achieved by assurance, observation and conservative treatment.


   Case report Top


A 28 years female was referred from Obstetrics & Gynaecology department, two months after delivery with complaint of pain in right hip for last five months. Pain was initially mild in intensity but progressively increased so much so that she was not able to put weight on her right lower limb. There was no pain during rest. No history of trauma, fever or other joint involvement was present. On examination, local temperature was normal with fullness in Scarpa's triangle and diffuse tenderness around right hip. Though no fixed deformity was present but active as well as passive movements were grossly restricted in all directions due to pain. Hip telescopic test was negative. Apparent lengthening of one cm without real limb length discrepancy was noted. Tuberculin test was negative. Her blood investigations revealed Hb 12.2 gm, TLC 8450/cumm, DLC P78 L22, ESR 28mm, serum calcium 8.7mg/dl, serum phosphorus 4.5mg/dl and serum alkaline phosphatase 96IU/L which were within normal laboratory reference range. Normal appearing synovial fluid, 7ml in amount was aspirated from the right hip. It was negative for gram staining and acid fast bacilli and sterile on culture and sensitivity. In wet mount of synovial fluid 5-8 RBC/HPF, 3-4 Pus cell/HPF, TLC7500cells/cubicmm (N-<300/ cubicmm), DLC 60%Mononuclear cells (N-<70%) and 40%Polymorphonuclear cells (N-<25%) were present. In biochemical analysis of synovial fluid, protein-8100mg/dl (N­<3000mg/dl) and glucose-37mg/dl (N-equal to serum) was present. Though some of the synovial fluid values were abnormal they did not indicate any specific pathology [4],[5].

Skiagram of pelvis with both hips and right hip lateral view revealed diffuse periarticular osteoporosis around hip involving acetabulum, head, neck and trochanteric area of femur, increased joint space without any evidence of articular cartilage destruction or pathological fracture [Figure - 1]a,b. MRI right hip showed decreased signal intensity of bone marrow on T1 images and increased signal intensity relative to the intensity of normal marrow on T2 images with evidence of joint effusion [Figure - 2]a,b.

Bilateral skin traction was given for six weeks along with symptomatic and supportive treatment. Alendronate 70 mg per week was given to her in first three months. She was followed up at 6 weeks, 3 months, 6 months and one year period. At 6 months follow up, she had 80% symptomatic relief and at one year follow up, she was completely asymptomatic.


   Discussion Top


Transient osteoporosis is a rare well recognized clinical syndrome that presents a diagnostic challenge. In 1959 Curtiss and Kincaid described a peculiar pattern of regional osteoporosis of the hip occurring in women in the third trimester of pregnancy [6] . According to the literature the most appropriate term for transient osteoporosis is Bone Marrow Edema Syndrome. This term is based on the early magnetic resonance imaging findings. Osteopenia appears as a late finding on plain skiagram, usually 4-6 weeks after the onset of symptoms. Bone marrow edema is confirmed by bone biopsy that reveals marrow edema without evidence of ischemic changes [7] .

Bone marrow edema syndrome can present in variable pattern like Transient osteoporosis of hip, Regional migratory transient osteoporosis where features migrate from one joint to other and partial transient osteoporosis in which a portion of foot or portion of knee joint is involved [2] .

Etiology of TOH is unknown. Initial reports of its occurrence in pregnancy suggested several possible factors that might be important in the pathogenesis of this condition such as increased demand for protein and minerals in pregnant woman, endocrine dysfunction during pregnancy and local compression of vessels and nerves by enlarging foetus. Presence of TOH in early pregnancy, nonpregnant woman, man and involvement of other joints made most of these factors questionable [2] .

Clinically presenting symptom is abrupt onset of pain in the hip joint. Pain is exacerbarated by weight bearing and relieved by taking rest. Disease course has been described into three phases. In first phase, there is rapid aggravation of pain and functional disability lasting approximately 1-2 months. Second phase is characterized by pain reaching a plateau of intensity and lasting 4-6 months. In third phase, symptoms regress and hip joint resumes normal condition. This phase lasts for another 6-9 months. The mean interval from the onset of symptoms until complete clinical resolution ranges from 4-24 months [9] . In our case clinical features were similar as described in literature.

In the early phase, plain skiagram reveals no significant finding. However, MRI confirms the diagnosis. A delay between the onset of symptoms and finding of osteopenia in plain skiagram is the rule. Second phase skiagram reveals variable focal loss of bone density and blurring of trabecular structure with poorly defined cortical borders, sometimes with complete effacement of the subchondral cortex. Femoral head and neck and often intertrochanteric region is affected and occasionally acetabulum is also involved. In all cases, normal joint space is preserved and osseous erosion or subchondral collapse never occurs [10] . Computed tomography shows features similar to plain skiagram. Radionuclide bone scanning is sensitive but not specific. It helps in early detection and occasionally reveals simultaneous asymptomatic areas. Koshi et al (1997) reported three cases in which effusion was detected by ultrasonography and related it to TOH [11] .

Magnetic resonance imaging is the modality of choice for early detection of TOH. T1 weighted images reveal low signal intensity while T2 weighted images reveal matching high signal intensity in bone marrow [12],[13],[14] .

Histopathological examination done in core decompression cases revealed features consistent with marrow edema without any evidence of ischaemic changes [7] . Though biopsy gives conclusive diagnosis of TOH, this invasive procedure was deferred in present case as the patient started responding to conservative treatment.

Differential diagnosis of TOH includes exclusion of infective arthritis of hip, rheumatoid arthritis and monoarticular conditions like pigmented villonodular synovitis and idiopathic osteochondromatosis. It should also be differentiated from reflex sympathetic dystrophy and avascular necrosis of femoral head. Koo et al (1999) suggested that TOH is not an early stage of AVN of femoral head instead these are two different entities with different outcome [15] .

Treatment of TOH, as most authors believe, is observation, assurance and symptomatic. It is a self-limiting disease that needs no intervention. Conservative treatment in the form of protected weight bearing, analgesics and anti­inflammatory drugs and traction is required. Patient is to be assured of complete recovery. In our case, excellent result was achieved by conservative and symptomatic treatment. Alendronate, an antiresorptive biphosphosnate agent has been used. It provides early relief in pain but does not change natural course of the disease[16] . Miltner et al also reported the mechanism of action of Alendronate in reducing the pain during treatment of TOH [17] .

Attempts to hasten recovery with vasoregulatory drug, intra-articular or systemic corticosteroid administration, calcitonin or sympathetic blocking agents have failed in changing the natural history of TOH [18] . Core decompression in cases refractory to conservative treatment also give pain relief but do not alter disease course[10].

In conclusion, the purpose of this case report is to elucidate the diagnosis and therapeutic aspect of TOH as it can mimic conditions like infective arthritis, reflex sympathetic dystrophy and avascular necrosis of femoral neck etc. High level of suspicion of this entity not only makes the diagnosis easier but also avoids unnecessary invasive investigations and interventions.

 
   References Top

1.Arnstein AR. Regional osteoporosis. Orthop Clin North Am. 1972; 3: 585.  Back to cited text no. 1    
2. Resnick D. Osteoporosis. In: Diagnosis of Bone and Joint Disorders. Philadelphia: Saunders, 2002; 1804-1818.  Back to cited text no. 2    
3.Dexter HW. Magnetic Resonance Imaging in Orthopaedics. In: Campbell's Operative Orthopaedics. Philadelphia: Mosby, 1998; 134.  Back to cited text no. 3    
4. David BH, John HS. Arthritis & Musculoskeletal disorders. In: Current Medical Diagnosis & Treatment. Appleton & Lange: McGraw Hill, 2003; 783-838.  Back to cited text no. 4    
5. Daniel JM. Synovial fluid. In: Arthritis and Allied Conditions. Philadel­phia: Lea & Febiger. 1979; 51-69.  Back to cited text no. 5    
6. Curtiss PH, Kincaid WE. Transitory demineralization of the hip in pregnancy. J Bone Joint Surg (Am). 1959; 41: 1327.  Back to cited text no. 6    
7. Plenk H, Hofmann S, Eschberger J et al. Histomorphology and bone morphometry of the bone marrow edema syndrome of the hip. Clin Orthop. 1997; 334: 73-84.  Back to cited text no. 7    
8.Beaulieu J, Razzano CD, Levine RB. Transient osteoporosis of the hip in pregnancy. Clin Orthop. 1976; 115: 165-168.  Back to cited text no. 8    
9. Schapira D. Transient osteoporosis of the hip. Semin Arthritis Rheum. 1992; 22: 98-105.  Back to cited text no. 9    
10. Guerra JJ, Steinberg ME. Distinguishing transient osteoporosis from avascular necrosis of the hip. J Bone Joint Surg (Am). 1995; 77: 616-624.  Back to cited text no. 10    
11. Koshi JM, Mullykangas, Luosujarvi R. Transient Osteoporosis of the Hip with effusion detected by ultrasonography. Clin Rheumatol. 1997; 16(4): 404-408.  Back to cited text no. 11    
12. Bloem JL. Transient osteoporosis of the hip: MR imaging. Radiology. 1988; 167: 753-755.  Back to cited text no. 12    
13. Wilson AJ, Murphy WA, Hardy DC, Totty WG. Transient Osteoporo­sis: transient bone marrow edema? Radiology. 1988; 167: 757-760.  Back to cited text no. 13    
14. Takatori Y, Kokubo T, Ninomiya S, Okutsu I, Kamogawa M. Tran­sient osteoporosis of the hip: magnetic resonance imaging. Clin Orthop. 1991; 27: 190-194.  Back to cited text no. 14    
15. Koo KH, Jeong ST, Jones JP. Borderline necrosis of the femoral head. Clin Orthop. 1999; 358: 158-165.  Back to cited text no. 15    
16. Schapira D, Braun MY, Gutierrez G, Nahir AM. Severe transient osteoporosis of the hip during pregnancy: Successful treatment with intravenous biphosphonates. Clin Exp Rheumatol. 2003; 21(1) : 107­110.  Back to cited text no. 16    
17. Miltner O, Niedhart C, Piroth W, Weber M. Transient osteoporosis of the navicular bone in a runner. Arch Orthop Trauma Surg. 2003; 123: 505-508.  Back to cited text no. 17    
18. Doury P, Delahaye RP, Pattin S, Granier R, Metges PJ. Highly localized transient osteoporosis of the knee. Arthritis Rheum. 1998; 21: 992-993.  Back to cited text no. 18    

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Correspondence Address:
Puneet Gupta
Department Of Orthopaedics, Himalayan Institute of Medical Sciences, Swami Rama Nagar, Doiwala, Dehradun - 248140
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0019-5413.36622

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