Osteonecrosis is a degenerative bone condition characterized by death of cellular components of bone secondary to an interruption of the subchondral blood supply. Also known as avascular necrosis, it typically affects the epiphysis of long bones at weight-bearing joints. Advanced disease may result in subchondral collapse which threatens the viability of the joint involved. Therefore, early recognition and treatment of osteonecrosis are essential. This review article discusses the etiology and pathogenesis of the disease, presentation and treatment options of the most common forms of osteonecrosis.
The widely accepted view in the literature is that a reduction in subchondral blood supply is responsible for osteonecrosis. However, there are numerous risk factors and theories on the development of this vascular impairment. Shah et al. succinctly categorizes these into six groups:
In a small percentage of cases mutations in the COL2A1 gene which codes for type 2 collagen production has demonstrated autosomal dominant inheritance patterns. However, in many cases, a cause cannot be identified, and these patients receive the designation of idiopathic osteonecrosis.
Osteonecrosis is most common in the hip, but also seen in the humerus, knee, and talus and more rarely seen in the smaller bones of the wrist such as the lunate. While it is also documented to affect the jaw this review chooses to focus on common forms presenting to an orthopedic surgeon.
A reduction in subchondral blood supply induces a state of hypoxia leading to loss of integrity of cell membranes and necrosis of cells. The pathological appearances of necrosis marked by the appearance of neutrophils and macrophages will predominate. Macroscopically this induces subchondral collapse and subsequent joint degeneration.
Non-traumatic cases will typically present with mechanical pain of variable onset and severity and often difficult to localize. In early disease, the physical examination is often normal which inevitably causes a delay in diagnosis.
Initial evaluation with plain radiographic films demonstrating two orthogonal views is the initial diagnostic standard, although in the early course of the disease they often appear normal. Magnetic resonance imaging is the recommendation for detection of earlier stages of the disease due to its high sensitivity in detecting bone edema.
Osteonecrosis of the Hip
Femoral head osteonecrosis falls into two classes: traumatic or atraumatic. Of the atraumatic cases, up to 70% may be bilateral. Common classifications that map the phases of osteonecrosis of the hip include the Ficat and Arlet classification and the Steinberg classification. Ficat and Arlet describe the four stages of disease progression based on clinical and radiographic findings. Stage 1 is the initiation of the disease without radiological findings. Stage IV is the end stage with femoral head collapse, flattening and narrowing of the joint space. The Steinberg classification incorporates the use of MRI to detect a pre-clinical lesion and also to assess the size of the lesion.
Osteonecrosis of the Knee
Spontaneous osteonecrosis of the knee (SONK) is the most common type. Secondary osteonecrosis is commoner in a younger population and often associated with a number of risk factors common to all kinds of osteonecrosis as previously discussed. The third and rarest type is called post arthroscopic osteonecrosis and has been seen in 4% of patients having undergone an arthroscopic meniscectomy. SONK typically presents in the sixth decade of life and is more common in the female population. Classically it affects the medial femoral condyle, and subsequent cadaveric studies have demonstrated a watershed area of the medial femoral condyle. The overriding symptom is that of medial knee pain often mimicking a torn meniscus. The Koshino classification describes the four stages of disease progression. Stage 1 describes clinical disease without radiologically apparent disease. Stage 4 is the degenerative phase with osteosclerosis and osteophyte formation around the condyles.
Osteonecrosis of the Shoulder
Osteonecrosis of the shoulder most frequently results from trauma however it can arise from the causes outlined above, for instance, prolonged high-dose corticosteroid usage. Hertel et al. showed that specific fracture plane combinations had associations with impaired head perfusion and that additional elements such as length of the posteromedial metaphyseal head extension and the integrity of the medial hinge were the key elements for the occurrence of osteonecrosis. Most of those fracture patterns with an increased risk of avascular necrosis had an anatomic neck component. Interestingly fracture dislocations, and degree of displacement of the fragments do not predict an increased incidence of avascular necrosis of the humeral head although contradictory evidence does exist. Classification is the Cruess classification and uses five categories. Stage 1 describes normal x-ray findings with pathology only recognized on MRI scans. Stage four demonstrates flattening of the humeral head with collapse. Stage five is the end stage with degenerative changes that extend to the glenoid.
Osteonecrosis of the Talus
Most commonly caused by trauma resulting in displaced fractures to the neck of the talus. The incidence of avascular necrosis increases with co-existing dislocation at the ankle joint or subtalar joint. The Hawkins classification best describes this relationship. If osteonecrosis is to occur the pathognomonic subchondral lucency known as Hawkins sign will be absent on plain radiographs at 6-8 weeks.
Osteonecrosis of the Lunate
More commonly known as Keinbock’s disease involves a collapse of the lunate due to vascular insufficiency and osteonecrosis. A history of repetitive trauma, biomechanical factors related to ulna variance and anatomic factors such as the presence of both dorsal and palmar blood supply may contribute to the risk of avascular necrosis. The Lichtman staging of Keinbock’s disease uses four stages. The first radiographic feature becomes apparent in stage 2 disease, represented by sclerosis of the lunate. Lunate collapse and palmar scaphoid rotation is the radiologic feature in stage 3 disease. Intercarpal joint degeneration is the dominant feature of end stage disease.
Osteonecrosis of the Hip
Many patients will ultimately need a total hip arthroplasty however joint salvaging procedures such as core decompression report with varying results. Core decompression is most effective in the early stages of osteonecrosis and when the lesions only involve a small amount of the weight bearing surface of the femoral head. The procedure may use vascularised bone grafts or biologic agents that promote bone repair. Interestingly Zhao et al. used perfusion studies to show core decompression is more effective in femoral heads with venous congestion that those with arterial compromise.
The majority of cases resolve following a trial of protected weight bearing and physiotherapy. As SONK is more common in the older person a unicompartmental knee replacement provides a good functional outcome with a relatively short rehabilitation time. However, a total knee replacement may be more appropriate in larger lesions. Smaller lesions following intraosseous decompression have achieved good operative results.
Osteonecrosis of the Shoulder
Operative management is classified according to staging. For early disease, core decompression is the preferred treatment option. Humeral head resurfacing or hemiarthroplasty is recommended for moderate disease, reserving a total shoulder replacement in advanced disease.
Osteonecrosis of the Talus
The incidence of osteonecrosis of the talus in talar neck fractures is reduced utilizing a procedure to achieve operative anatomic reduction and stable fixation.
Treatment in the early stage disease aims to revascularize the lunate either directly using bone grafts or indirectly utilizing procedures aiming to offload the lunate. Surgical options aiming to address the carpal collapse are reserved for stage 3 disease whereas advanced disease may warrant joint sacrificing procedures such as wrist arthrodesis.
Mont et al. reported that 59% of asymptomatic lesions progressed to symptoms or collapse. Therefore once the patient faces the onset of osteonecrosis, there is a high probability that it will continue to advance.
There are several identified risk factors for osteonecrosis, but the exact pathogenesis remains unestablished. More likely a combination of different factors and conditions leads to the destruction of bone cells.
Intervention depends on the phase of disease progression and varies from preservation procedures to more definitive salvage operations.
Treatment of early-stage disease reports better results although this may be difficult to achieve as osteonecrosis is often asymptomatic in its early stages.
Osteonecrosis frequently poses a diagnostic dilemma to orthopedic surgeons. There are several risk factors outlined in the literature yet the exact pathophysiology is not fully understood. Diagnostic difficulty frequently results in delayed presentation of advanced cases of the disease, which often prevents the joint from being salvaged and increases patient morbidity. While an orthopedic surgeon is almost always involved in the care of patients with osteonecrosis, it is important to educate healthcare professionals who encounter these patients at the hospital front door such as general practitioners, emergency department physicians, nurses, and physiotherapists.
|||Shah KN,Racine J,Jones LC,Aaron RK, Pathophysiology and risk factors for osteonecrosis. Current reviews in musculoskeletal medicine. 2015 Sep [PubMed PMID: 26142896]|
|||Mont MA,Zywiel MG,Marker DR,McGrath MS,Delanois RE, The natural history of untreated asymptomatic osteonecrosis of the femoral head: a systematic literature review. The Journal of bone and joint surgery. American volume. 2010 Sep 15 [PubMed PMID: 20844158]|
|||Liu YF,Chen WM,Lin YF,Yang RC,Lin MW,Li LH,Chang YH,Jou YS,Lin PY,Su JS,Huang SF,Hsiao KJ,Fann CS,Hwang HW,Chen YT,Tsai SF, Type II collagen gene variants and inherited osteonecrosis of the femoral head. The New England journal of medicine. 2005 Jun 2 [PubMed PMID: 15930420]|
|||Kaushik AP,Das A,Cui Q, Osteonecrosis of the femoral head: An update in year 2012. World journal of orthopedics. 2012 May 18 [PubMed PMID: 22655222]|
|||Jawad MU,Haleem AA,Scully SP, In brief: Ficat classification: avascular necrosis of the femoral head. Clinical orthopaedics and related research. 2012 Sep [PubMed PMID: 22760600]|
|||Steinberg ME,Hayken GD,Steinberg DR, A quantitative system for staging avascular necrosis. The Journal of bone and joint surgery. British volume. 1995 Jan [PubMed PMID: 7822393]|
|||Karim AR,Cherian JJ,Jauregui JJ,Pierce T,Mont MA, Osteonecrosis of the knee: review. Annals of translational medicine. 2015 Jan [PubMed PMID: 25705638]|
|||Koshino T, The treatment of spontaneous osteonecrosis of the knee by high tibial osteotomy with and without bone-grafting or drilling of the lesion. The Journal of bone and joint surgery. American volume. 1982 Jan [PubMed PMID: 7033231]|
|||Hertel R,Hempfing A,Stiehler M,Leunig M, Predictors of humeral head ischemia after intracapsular fracture of the proximal humerus. Journal of shoulder and elbow surgery. 2004 Jul-Aug [PubMed PMID: 15220884]|
|||Cruess RL, Experience with steroid-induced avascular necrosis of the shoulder and etiologic considerations regarding osteonecrosis of the hip. Clinical orthopaedics and related research. 1978 Jan-Feb [PubMed PMID: 639411]|
|||Allan CH,Joshi A,Lichtman DM, Kienbock's disease: diagnosis and treatment. The Journal of the American Academy of Orthopaedic Surgeons. 2001 Mar-Apr [PubMed PMID: 11281636]|
|||Stubbs AJ,Atilla HA, The Hip Restoration Algorithm. Muscles, ligaments and tendons journal. 2016 Jul-Sep [PubMed PMID: 28066734]|
|||Zhao DW,Yu XB, Core decompression treatment of early-stage osteonecrosis of femoral head resulted from venous stasis or artery blood supply insufficiency. The Journal of surgical research. 2015 Apr [PubMed PMID: 25582883]|