Rapidly Progressive Osteoarthritis of the Hip

    The authors describe a uniquely aggressive case of rapidly destructive osteoarthritis of the left hip in a 91-year-old female patient. An infectious etiology was suspected but ultimately ruled out.


    Andrew Fleischman, MD, and Antonia F. Chen, MD, MBA


    The authors have no disclosures relevant to this article.


    Rapidly destructive osteoarthritis (RDOA) is an uncommon form of degenerative hip disease distinct from osteonecrosis. [1] By definition, RDOA involves loss of joint space at a rate greater than 2 mm per year or 50% in 1 year. [2]

    The mean time to radiographic joint destruction has been reported to be 14 months. However, several cases with a more rapidly progressive pattern of destruction, within a 6-month period, have been reported. [3-5]

    Patients with RDOA, who are often older females, present with worsening radiographic evidence of “hatchet-like” femoral head destruction and an atrophic response resulting in few osteophytes. [6] One author has pointed to subchondral insufficiency fracture as a key underlying element in association with this pathology. [7]

    It is important to rule out septic arthritis, osteonecrosis, inflammatory arthritis, and neuropathic arthropathy to arrive at an accurate diagnosis and to minimize morbidity associated with inappropriate interventions.In exceedingly rare instances in which destruction is especially rapid and pronounced, an infectious etiology may be chiefly suspected, even in the presence of a negative initial workup. [8]

    It is our experience that RDOA can mimic the destructive capacity of even the worst cases of septic arthropathy. In the following report, we present such a case that demonstrates how this uncommon phenomenon can represent a diagnostic challenge, which may lead to indecision as to the appropriate therapeutic intervention.

    Case Report

    Patient Presentation

    A 91-year-old female patient was referred to our service 6 weeks after onset of moderate but increasing left groin pain. She had been seen in an outside orthopedic clinic 12 weeks earlier and had a cortisone injection that provided little relief.

    Thirteen years earlier, the patient had undergone total hip arthroplasty of the right hip at our institution to treat osteoarthritis that had followed the typical pattern. She had no history of inflammatory arthropathy, systemic steroid use, alcohol abuse, or trauma.

    The patient presented with moderate pain, limited range of motion, and functional impairment. She was scheduled for total hip arthroplasty of the left hip 4 weeks later.

    On the day of surgery, the patient presented with severe, unrelenting pain, and she could no longer ambulate. Imaging showed complete femoral head disintegration possibly representative of septic arthritis.


    A radiograph of the left hip taken on presentation to our service (6 weeks after symptom onset) showed severe degenerative disease, with slight flattening and irregularity of the femoral head (Figure 1).

    Figure 1. Preoperative radiographs 6 weeks after symptom onset.

    A radiograph of the left hip taken on the day of surgery (10 weeks after symptom onset) shows complete disintegration of the femoral head, essentially resulting in a spontaneous Girdlestone (Figure 2).

    Figure 2. Preoperative radiographs 10 weeks after symptom onset.

    Magnetic resonance imaging (MRI) performed the day of surgery showed significant marrow edema in the femoral neck and increased T2 signal in the joint space and acetabulum.

    Differential Diagnosis

    • Rapidly destructive osteoarthritis
    • Septic arthritis
    • Avascular necrosis

    Diagnostic Testing


    • Leukocyte count of 5.1 x 109/L
    • Erythrocyte sedimentation rate (ESR) of 10 mm/hr
    • C-reactive protein (CRP) of 0.6 mg/dL
    • “Dry” tap on fluoroscopic-guided aspiration
    • No culture growth of the biopsy specimen


    • No pus, but abundant adhesions
    • Leukocyte esterase negative
    • Alpha-defensin negative
    • Synovial fluid CRP of 3.4 mg/L
    • Negative cultures with 5 tissue biopsies


    • Focal, scattered necrotic bone fragments (Figure 3)
    • Mild chronic inflammation; no acute or granulomatous inflammation
    • Increased fibrosis and vascular proliferation
    • Degenerative changes of the adjacent articular cartilage
    • No crystals

    Figure 3. Pathology specimen showing degenerative cartilage changes and underlying focal necrosis.


    Intraoperative testing suggested infection was unlikely, so the surgeon made the decision to proceed with total hip arthroplasty as definitive treatment.

    • Other treatment options considered:
    • Staged total hip arthroplasty with placement of an antibiotic spacer
    • Interposition arthroplasty (Girdlestone)


    RDOA is a rare and poorly understood disease of the hip. To our knowledge, this case represents a dramatic example of the rapidly destructive potential of this unusual entity in a previously asymptomatic patient.

    Conventionally, the natural history of rapid joint destruction within a period of weeks has been associated with native septic arthritis and osteomyelitis. [9] Even with a negative initial workup for infection, surgeons must maintain vigilance in ruling out an infectious process due to morbidity associated with its long-term sequelae. [8]

    For this case, in which the apparent destructive capacity was beyond what would be expected from previous reports on RDOA, the operating surgeon had to balance the inherent risk for morbidity of untreated osteomyelitis with that of a multiple-stage intervention in an older patient. The ultimate decision to proceed with total hip arthroplasty was not made until the joint was assessed intraoperatively using leukocyte esterase testing on synovial fluid.

    Clinical, radiologic, and microbiologic evaluations should always be considered and, in many cases, provide for a reasonable level of confidence in diagnosing RDOA. Preoperative synovial fluid aspiration analysis and open biopsies can differentiate between septic and non-septic causes of rapid joint destruction. However, examination of pathologic specimens of bone from surgery offers for a more robust diagnosis.

    Pathologic features of RDOA are typically non-specific and overlap with other destructive joint diseases such as avascular necrosis and septic arthritis. However, several distinct histologic patterns are unique to RDOA, including focal and scattered necrosis of subchondral bone with increased vascular proliferation and chronic inflammation. [3,4] In addition, non-specific degeneration typical of osteoarthritis can be seen, such as fissuring, pitting and flaking of cartilage.

    This combination of features is unique compared with other entities in the differential diagnosis:

    • Avascular necrosis typically shows zonal necrosis with a sharp demarcation between the necrotic and viable bone tissue.
    • Septic arthritis involves a much more prominent inflammatory infiltrate, including acute inflammatory cells.
    • Characteristic rhomboid crystals are clearly visible in calcium pyrophosphate dihydrate crystal deposition disease (CPPD).


    Total hip arthroplasty has provided excellent pain relief and improved function for this patient, despite her initial degree of deformity and level of pain.

    Although total hip arthroplasty appears to be the optimal intervention in such cases, surgeons should exhaust all available resources to rule out the possibility of an occult infection before making a therapeutic decision. Staged intervention may be more appropriate in cases in which initial testing for infection is equivocal and the joint appears more grossly synovitic.

    Surgical Pearls

    • Perform a thorough workup for rapid destruction of the femoral head, including aspiration and open biopsy if necessary.
    • Perform a thorough synovectomy.
    • Perform intraoperative leukocyte esterase test to rule out infection.
    • Assess femoral head destruction and place a prophylactic cable if necessary.
    • Plan for a back-up Girdlestone or spacer placement if the hip is found to be infected.

    Author Information

    Andrew Fleischman, MD, is a postdoctoral research fellow at The Rothman Institute, Philadelphia, Pennsylvania. Antonia F. Chen, MD, MBA, specializes in hip and knee replacement surgery at The Rothman Institute, Philadelphia, Pennsylvania.

    Adult Reconstruction Section Editor, Rothman Institute Grand Rounds

    Antonia F. Chen, MD, MBA


    1. Postel M, Kerboull M: Total prosthetic replacement in rapidly destructive arthrosis of the hip joint. Clin Orthop Relat Res 1970;72:138-144.
    2. Lequesne M, Ray G: Rapid idiopathic destructive coxarthrosis. prospective etiologic study of 27 cases. Rev Rhum Mal Osteoartic 1989;56:115-119.
    3. Batra S, Batra M, McMurtrie A, Sinha AK: Rapidly destructive osteoarthritis of the hip joint: A case series. J Orthop Surg Res 2008;3:3-799X-3-3.
    4. Shu J, Ross I, Wehrli B, McCalden RW, Barra L: Rapidly destructive inflammatory arthritis of the hip. Case Rep Rheumatol 2014;2014:160252.
    5. Rosenberg ZS, Shankman S, Steiner GC, Kastenbaum DK, Norman A, Lazansky MG: Rapid destructive osteoarthritis: Clinical, radiographic, and pathologic features. Radiology 1992;182:213-216.
    6. Della Torre P, Picuti G, Di Filippo P: Rapidly progressive osteoarthritis of the hip. Ital J Orthop Traumatol 1987;13:187-200.
    7. Yamamoto T, Bullough PG: Subchondral insufficiency fracture of the femoral head: A differential diagnosis in acute onset of coxarthrosis in the elderly. Arthritis Rheum 1999;42:2719-2723.
    8. Hart G, Fehring TK: Rapidly destructive osteoarthritis can mimic infection. Arthroplasty Today 2016;Epub head of print.
    9. Nair SP, Meghji S, Wilson M, Reddi K, White P, Henderson B: Bacterially induced bone destruction: Mechanisms and misconceptions. Infect Immun 1996;64:2371-2380.