Encyclopedia
Please note this is an old version of this entry, which may differ significantly from the current revision.
Subjects:
Health Care Sciences & Services
Osteonecrosis is a terrible condition that can cause advanced arthritis in a number of joints, including the knee. The three types of osteonecrosis that can affect the knee are secondary, post-arthroscopic, and spontaneous osteonecrosis of the knee (SPONK). Regardless of osteonecrosis classification, treatment for this condition seeks to prevent further development or postpone the onset of knee end-stage arthritis. Joint arthroplasty is the best course of action whenever there is significant joint surface collapse or there are signs of degenerative arthritis. The non-operative options for treatment at the moment include observation, nonsteroidal anti-inflammatory medications (NSAIDs), protective weight bearing, and analgesia if needed. Depending on the severity and type of the condition, operational procedures may include unilateral knee arthroplasty (UKA), total knee arthroplasty (TKA), or joint preservation surgery. Joint preservation techniques, such as arthroscopy, core decompression, osteochondral autograft, and bone grafting, are frequently used in precollapse and some postcollapse lesions, when the articular cartilage is typically unaffected and only the underlying subchondral bone is affected. In contrast, operations that try to save the joint following significant subchondral collapse are rarely successful and joint replacement is required to ease discomfort.
- knee
- spontaneous osteonecrosis of the knee
- SPONK
- osteoarthritis
- bone marrow lesions
1. Introduction
Spontaneous osteonecrosis of the knee (SPONK) is a progressive disease of the subarticular bone that can lead to subchondral collapse [1]. This pathology was first described by Ahlback et al. in 1968 as a medial femoral condyle (MFC) focal lesion, who reported its early stages as often undetected [2]. Patients with SPONK mainly complain of acute onset of pain in the knee and report no previous trauma.
Recent studies have shown an incidence of 3.4% among patients above 50 years of age and 9.4% among patients older than 65 years, with predominant affection of females compared with males by almost three to five times [3].
The clinical importance of this pathology of the knee focuses on structural changes that exert influence on the subchondral bone and articular cartilage [1,3]. Houpt et al. reported, in a review of SPONK, that the most common site of involvement is the MFC, followed by the medial tibial plateau and last, the lateral femoral condyle [4]. However, osteonecrosis (ON) of the knee usually affects a single condyle or plateau and is typically unilateral [1,3,4]. Lateral condyle SPONK is a rare condition and only a few articles have explored it. Aglietti et al. published a review examining 105 knees, reporting only one case of osteonecrosis of the lateral condyle [5].
The most common symptoms are localised tenderness and acute onset of pain [6,7]. Bone marrow oedema (BME) and focal subchondral lesions are cardinal signs for the diagnosis of this disease [6,7]. Yamamoto et al. suggested subchondral insufficiency fractures in the osteopenic bone as the pathogenesis of SPONK, leading to fluid accumulation in the bone marrow. However, the pathogenesis and aetiology of spontaneous knee osteonecrosis are yet to be fully understood; therefore, its management is still up for discussion [8].
Different publications have reclassified SPONK, previously considered a single entity, into three conditions: spontaneous ON of the knee; secondary ON (when the condition has a known cause); and post-arthroscopy ON [6,7].
2. Demographics and Classification
SPONK presents itself in patients older than 55 years of age [9]. Studies report this condition’s incidence to be 3.4% and 9.4% in persons older than 50 and 65, respectively [1]. There is no known risk factor associated with SPONK, contrary to secondary ON, to which persons younger than 50 years of age and with a history of alcohol and corticosteroid use are at risk. This disease is more prominent in women than in men [6,7]. Akamatsu et al. demonstrated a positive association between low bone mineral density and the incidence of SPONK in women over 60 years of age [10]. The male-to-female incidence is 1:5, according to Pape [11]. Al-Rowaih et al. demonstrated that the MFC was affected 94% of the time [12]. Spontaneous ON usually involves a single condyle, most often the MFC [1,3].
Koshino classified SPONK into four stages: symptoms with normal X-ray, subchondral radiolucency and osteosclerosis, subchondral collapse, and osteoarthritis (OA) [13]. This condition can also be categorised based on the size of the lesion upon X-ray examination to achieve a prognostic factor. Lesions of <3.5 cm tend to regress with no surgery, lesions of size 3.5–5 cm may or may not regress, and lesions of >5 cm lead to collapse.
The lesion can also be categorised using the Ficat classification, which describes four stages based on chondral collapse and joint space.
3. SPONK Aetiology
SPONK’s real aetiology is still unknown. Even though the real incidence of this disorder is not completely known, it is said to be more prevalent than secondary osteonecrosis of the knee. In contrast with SPONK, secondary ON has many known conditions and risk factors, such as sickle cell disease, myeloproliferative disorders, tobacco use and obesity, but the two most common among them are corticosteroid and alcohol abuse (>90%) [14].
Spontaneous ON is more prominent in women than in men [1,6,7]. A positive association with SPONK in women over 60 years of age and low bone mineral density supported this in a recent study by Akamatsu et al. [15].
Many publications indicate that SPONK mainly affects the medial condyle. Al-Rowaih et al., in a study of 109 patients diagnosed with spontaneous ON, identified that the medial femoral condyle was affected in 94% of the cases (102 out 109) [12].
Out of the many theories suggesting the pathogenesis for this disorder, two are the most advanced. One theory proposes a vascular affection from interference with microcirculation that produces oedema in the bone marrow, increasing pressure and further diminishing circulation until ischaemia [16]. Uchio et al. reported higher intraosseous pressure on the medial femoral condyle in SPONK patients on both femoral condyles in OA patients [17]. Reddy and Fredericks reported limited blood supply to the medial femoral condyle as opposed to the lateral femoral condyle, which has an extraosseous vascular supply [18].
Another proposed theory cites microfractures as a cause of ON. Recent evidence has demonstrated that subchondral insufficiency fractures in osteopenic bone could cause this disorder. Microfractures weaken the subchondral plate and allow joint fluid to flow from the cracked articular cartilage into the subchondral bone [19]. This may lead to the accumulation of fluid in the bone marrow, oedema with focal ischaemia, and eventual necrosis [8]. The increase in pressure may cause pain at rest or at night [19].
A published review of 14 patients who underwent knee surgery for SPONK by Tamamoto and Bullough evaluated the morphology of lesions, both gross and histological, and concluded that subchondral insufficiency fractures represented the primary event leading to SPONK [8]. Based on this observation, many authors consider the term SPONK as misused and suggest it be redefined as “unstable fracture resulting in bone death of the displaced fracture fragment” [14].
Post-arthroscopic osteonecrosis is considered a different category of ON, distinct from SPONK and secondary ON. Brahme et al. specifically considered arthroscopic meniscectomy as an associated cause of SPONK [20].
A systematic review of suspected aetiology found the occurrence of meniscal injuries in 50–100% of patients and suggested a strong correlation between meniscal lesions and SPONK [21].
Postmeniscectomy ON could result from subchondral bone fractures according to Higuchi et al., due to articular signal changes in bone marrow [22].
Five studies associated tears of the posterior root of the medial meniscus with SPONK [22,23,24,25,26,27]. LaPrade attributes this to the less inherent mobility of the medial meniscus because of its robust attachment to the tibia [27]. The increased femoro–tibial contact after an arthroscopic meniscectomy could cause the aforementioned subchondral insufficiency fractures due to altered lad transmission [21].
Using preoperative MRI and X-rays from 45 patients with SPONK, Yamagami et al. reported that 62.2% of SPONK patients had medial meniscus posterior root tears [28], and Robertson et al. found them in 80% of SPONK patients, assuming that ON was caused by femoral overload after meniscectomy [24].
4. SPONK Histology
Histology findings on SPONK were reported in a few cases in the literature, showing similar patterns: a loss of the superficial zone, vertical fissures and chondrocyte proliferation were observed in the cartilage layer. In the subchondral bone layer, articular bone plate fractures were found in addition to endochondral ossification, reactive cartilage formation and the proliferation of fibrous tissue at a depth of 3 mm from the articular surface (range: 2–5 mm). In some cases, osteonecrosis was observed in the subchondral bone of disconnected osteochondral lesions or in a thin subchondral bone attached to free cartilaginous fragments. While the deeper subchondral bone led to abnormalities, including woven bone formation and congested medullary sinuses, in some cases, no evidence of osteonecrosis was observed in this layer [29,30].
Takeda et al. reported different characteristics based on the stage of SPONK. In stage one, there is no evidence of osteonecrosis. Fibrous tissue is present around the fracture line, but the osteoid formation is not active, suggesting an early reparative reaction. In stage two, there is no evidence of antecedent osteonecrosis. However, a reparative reaction is noted, mainly consisting of osteoids and the formation of immature bone. In stage three, it is possible to see an osteonecrotic lesion confined to the area distal to the fracture line. In this case, there is inadequate repair tissue on the articular cartilage side of the fracture line, which is interpreted as a delayed union. In stage four, there are empty lacunae and necrotic debris confined to the area distal to the gap that was interpreted as showing nonunion [29].
5. Clinical Presentations
In primary SPONK, pain is the most common presenting feature for patients. This pain is usually localised on the affected side of the knee. The majority of patients describe the onset of the pain as spontaneous, while the pain builds up gradually in a few of them. Most patients associate it with minor knee trauma and they do recollect the exact duration of their pain [31]. Activities involving weight-bearing aggravate the pain. Progressively in the natural course of the disease, patients resort to using walking aids, and if untreated, they may end up with night pain and resting pain requiring varying doses of analgesia [32].
Knee effusion is present during the initial clinical visit and patella ballottement can be performed. The most common area with localised tenderness is over the medial femoral condyle (MFC). In the context of simultaneous involvement of both the femur and tibia, tenderness is observed in both the affected areas and gives a clue to the underlying pathology [6,7,31]. Joint range of motion (ROM) is fairly preserved apart from terminal restriction, which is painful. On valgus and varus stress, there is no evidence of instability or ligament laxity in the early stages. However, in the later stages, there is progression to most likely varus deformity and a manifestation of gait abnormalities, characterised by limp and lateral thrust. The progression to either varus or valgus deformity depends on the affected femoral condyle. MFC is the most common area and varus deformities are seen commonly in this type of patient [32].
In contrast, patients with secondary ON typically report pain that is gradual in onset and associated with risk factors related to primary aetiology. Associations with systemic lupus erythematosus and the use of corticosteroids were found to be the most common [14]. Due to the effects of multiple joints, patients usually complain of polyarthralgia, which can pose a diagnostic challenge [14].
In the context of osteonecrosis in the postoperative knee (ONKP), patients present with acute onset or exacerbation of knee pain and recent history (4–8 weeks) of arthroscopy knee surgery. As knee surgery is performed mostly for knee pain, it is usually reported by patients with concerns about the failure of knee surgery or repair damage [33]. On clinical examination, they will demonstrate a tender joint line along with effusion. However, this can be a transient normal finding in the postoperative course, and a clinician should bear this in mind for further evaluations and patient counselling [7,32,33].
This entry is adapted from the peer-reviewed paper 10.3390/jcm11236943
This entry is offline, you can click here to edit this entry!
