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Transient Osteoporosis of the Hip

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Other Names

  • Transient osteoporosis of the hip (TOH)
  • Primary bone marrow edema syndrome (BMES)
  • Primary TOH
  • Secondary TOH
  • Transitory Demineralization of the Hip
  • Transient Marrow Edema Syndrome
  • Bone Marrow Edema (BME)
  • Transient Regional Osteoporosis
  • Regional Osteoporosis
  • Algodystrophy
  • Regional migratory osteoporosis

Background

  • This page describes Transient osteoporosis of the hip (TOH), an idiopathic and temporary clinical condition that affects the femoral head
    • Overall this phenomenon is poorly described in the literature and there is a paucity of data surrounding it

History

  • First described by Curtiss in 1958[1]
  • Termed transient osteoporosis of the hip by Hunder and Kelly in 1967[2]

Epidemiology

  • More common in men than women (need citation)
  • Mean age is 40 years of age (range 20 to 80)[3]

Pathophysiology

  • General
    • Typically considered to be benign and self limiting
    • In women, typically seen in the last trimester of pregnancy
  • Some type of insult initiates the process, typically idiopathic
    • Leads to leading to an increase in bone turnover, venous hypertension, and/or microfracture causing edema[4]
  • 3 stage hypothesis[5]
    • Stage 1: acute onset hip pain is due to edema (insult often unknown)
    • Stage 2: involves increased resorption and demineralization of the bone
    • Stage 3: resolution of the process clinically and by radiograph
  • The cause of hip pain is not always clear, proposed etiologies include[4]
    • Increased intraosseous pressure
    • Venous hypertension
    • Increased focal bone turnover
    • Microfracture
    • Periosteal irritation
  • Uncommon, can progress to ischemic injury to the femoral head and Avascular Necrosis
    • Distinguishing between TOH and early AVN is challenging clinically and radiographically
    • Also unclear if TOH represents early AVN or is a separate clinical entity
    • Some authors suggest TOH represents an abortive syndrome of the AVN pathway[6]

Etiology

  • Most commonly idiopathic
    • May be primary vs secondary, challenging to distinguish
    • Proposed insults leading to TOH include trauma, infection, inflammation, degenerative process, ischemic injury, neoplasia, surgery, drugs, metabolic, and neurologic disorders
    • Compression of the Obturator Nerve

Associated Conditions

Risk Factors

Differential Diagnosis

Clinical Features

  • History
    • Pain of TOH usually starts spontaneously
    • Pain presentation may vary from insidious vague pain with antalgic gait
    • Less commonly, may result in more severe progressive pain leading to immobility and hospitalization
  • Physical Exam: Physical Exam Hip
  • Special Tests

Evaluation

Radiographs

  • Standard Radiographs Hip
    • Screening tool
  • Early Findings (first 3-6 weeks from symptom onset)
    • Typically normal
  • Later findings (after the first 3-6 weeks)
    • Eventually will see diffuse osteopenia of the femoral head, sometimes bilateral
    • Periarticular demineralization
    • Absence of subchondral changes

MRI

  • Preferred imaging modality for suspected TOH
    • Sensitive enough to detect TOH up to 48 hours after onset[10]
  • Findings
    • Intermediate signal sequences on T1-weighted image
    • High signal intensity on T2-weighted images
    • Hyper intensity on contrast enhanced images
    • Delayed peak enhancement of edematous marrow is particularly characteristic of TOH
  • Characteristic of TOH[11]
    • Homogenous pattern of enhancement with no clear border
    • Diffuse pattern of edema with no focal defect, typically located at femoral head, sometimes neck
    • The presence of an irregular band of low signal intensity due to stress fracture
    • Absence of subchondral changes
    • Findings are often accompanied by joint effusion

Bone Scintography

  • Radionucleotide uptake occurs in all 3 phases of TOH
    • Lasts for up to 4 weeks after resolution of symptoms[12]

Classification

  • N/A

Management

Prognosis

  • Typically resolves in 6 months (range 2-12 months) with conservative therapy[13]
  • Core decompression therapy vs conservative therapy
    • Does not appear to improve outcomes compared to medical therapy[3]
    • Note that data is limited to case reports
  • Progression to Avascular Necrosis of the Hip
    • Limited data does makes prognostication challenging

Nonoperative

  • First line treatment
    • Goal: Prevent microfractures, relieve pain
  • Minimizing weight-bearing activities and relative rest
  • Using Crutches or Wheelchair if needed
  • Hot packs
  • Ultrasound therapy
  • Bisphosphonates
    • IV pamidronate showed an average clinical recovery of 2 months, compared to a historical control recovery of 6 months[14]
    • However, alendronate oral therapy in 8 cases shows an average clinical recovery of 6 months
  • Calcitonin
    • In 6 cases shows a shortened mean clinical recovery of 4.7 months
  • Teriparatide
    • Case reports of benefit[15]
  • Combination therapy
    • Combination of calcitonin and bisphosphonate therapy, zoledronate, or teriparatide in different reports shows almost a 1 month recovery time[16][17]
  • Corticosteroids including Prednisolone, Deflazacort have been used
  • Special Population: Pregnant women
    • Many of the above drugs are not safe or approved in pregnancy or in women who are breastfeeding
    • Consider Calcium, Vitamin D supplements in these patients

Operative

  • Indications
    • Progression to AVN
  • Technique
    • Core Decompression +/- bone grafting
    • Total Hip Arthroplasty
    • Rotational Osteotomy
    • Curettage and Bone Grafting
    • Vascularized Free-fibula Transfer
    • Total Hip Resurfacing
    • Hip Arthrodesis

Rehab and Return to Play

Rehabilitation

  • Needs to be updated

Return to Play

  • Needs to be updated

Complications

See Also

References

  1. ↑ Curtiss PH Jr, Kincaid WE (1959) Transitory demineralization of the hip in pregnancy. A report of three cases. Am J Orthop 41-A: 1327–1333
  2. ↑ Hunder GG, Kelly PJ. Transient osteoporosis of the hip: a clinical syndrome? Arthritis Rheum 1967; 10: 285.
  3. ↑ 3.0 3.1 Asadipooya, K., L. Graves, and L. W. Greene. "Transient osteoporosis of the hip: review of the literature." Osteoporosis International 28.6 (2017): 1805-1816.
  4. ↑ 4.0 4.1 Patel S (2014) Primary bone marrow oedema syndromes. Rheumatology (Oxford) 53(5):785–792
  5. ↑ Cano-Marquina A, Tarín JJ, García-Pérez MÁ, Cano A (2014) Transient regional osteoporosis. Maturitas 77(4):324–329
  6. ↑ Korompilias AV, Karantanas AH, Lykissas MG, Beris AE. Bone marrow edema syndrome. Skeletal Radiol 2009; 38: 425-36.
  7. ↑ Young SD 3rd, Nelson CL, Steinberg ME (2008) Transient osteoporosis of the hip in association with osteogenesis imperfecta: two cases, one complicated by a femoral neck fracture. Am J Orthop (Belle Mead NJ) 37(2):88–91
  8. ↑ Mepani JB, Findling JW (2009) Reversible bone marrow edema of the hip due to severe hypothyroidism. J Clin EndocrinolMetab 94(4):1068
  9. ↑ Whyte MP, Wenkert D, McAlister WH, Mughal MZ, Freemont AJ, Whitehouse R, Baildam EM, Coburn SP, Ryan LM,Mumm S (2009) Chronic recurrent multifocal osteomyelitis mimicked in childhood hypophosphatasia. J Bone Miner Res 24(8):1493–1505
  10. ↑ Szwedowski D, Nitek Z,Walecki J (2014) Evaluation of transient osteoporosis of the hip in magnetic resonance imaging. Pol J Radiol 79:36–38
  11. ↑ Malizos KN, Zibis AH, Dailiana Z, Hantes M, Karachalios T, Karantanas AH (2004) MR imaging findings in transient osteoporosis of the hip. Eur J Radiol 50(3):238–244
  12. ↑ Korompilias AV, Karantanas AH, Lykissas MG, Beris AE (2009) Bone marrow edema syndrome. Skelet Radiol 38(5):425–436
  13. ↑ Bijl M, van Leeuwen MA, van Rijswijk MH. Transient osteoporosis of the hip: presentation of (a)typical cases and a review of the literature. Clin Exp Rheumatol 1999; 17: 601-4.
  14. ↑ Varenna M, Zucchi F, Binelli L, Failoni S, Gallazzi M, Sinigaglia L (2002) Intravenous pamidronate in the treatment of transient osteoporosis of the hip. Bone 31(1):96–101
  15. ↑ Fabbriciani, Gianluigi, et al. "Transient osteoporosis of the hip: successful treatment with teriparatide." Rheumatology international 32.5 (2012): 1367-1370.
  16. ↑ Fabbriciani G, Pirro M, Manfredelli MR, Bianchi M, Sivolella S, Scarponi AM, Mannarino E (2012) Transient osteoporosis of the hip: successful treatment with teriparatide. Rheumatol Int 32(5): 1367–1370
  17. ↑ Seok H, Kim YT, Kim SH, Cha JG (2011) Treatment of transient osteoporosis of the hip with intravenous zoledronate—a case report. Ann Rehabil Med 35(3):432–435
Created by:
John Kiel on 21 September 2020 11:25:27
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Last edited:
5 October 2022 13:06:20
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