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Treating the Subchondral Environment and Avascular Necrosis
Introduction
Although cartilage research has grown exponentially, basic science and clinical studies focusing on its foundation, namely the subchondral bone, have not received the same attention. The subchondral bone provides mechanical and biological support for the overlying articular cartilage, and it undergoes constant adaptation in response to changes in the biomechanical environment of the joint. It is noticeably involved in several chondral entities such as osteochondritis dissecans, osteoarthritis, and focal chondral defects.
Consequently, subchondral bone lesions are commonly associated with cartilage lesions. To better understand the pathology of the subchondral bone, a thorough understanding of the anatomy, morphology, and physiology of the subchondral bone and its function is required. The articular cartilage consists of 5 different zones, which can be distinguished based on the morphology and orientation of collagen fibrils. In the superficial zone, the collagen fibers are tangentially oriented into tightly packed parallel laminae that radiate vertically from the calcified zone. Zone two, or intermediate zone, contains randomly oriented collagen fibrils. Zone three, which is also referred to as the radial zone, is the thickest layer with the highest amount of proteoglycans and water. The tidemark serves as the junction between the calcified and uncalcified cartilage matrix (zone 4). Finally, the zone of calcification (zone 5) serves as an anchor to a complex network of collagen fibrils ( Fig. 12.1 ).
The definition of subchondral bone is still a subject of debate. The most accepted definition is that the subchondral plate is as a zone that divides the articular cartilage from the marrow cavity. It comprises two parts: (1) the calcified region of the articular cartilage and (2) a layer of lamellar bone. The subchondral bone is located deep to the calcified layer and includes an arterial plexus that has branches to the calcified layer ( Fig. 12.2 ). The blood flow in this zone is 3–10 times higher than that in cancellous bone. Likewise, the venous systems contain a plexus of vessels that are vulnerable to compressive and shear forces. The cortical endplate contains perforations that form channels to allow communication with the basal cartilage. These channels are dynamic and change in response to compressive forces that act on the cartilage and subchondral bone.
The purpose of this chapter is to review the different pathologic entities originating from the subchondral bone; define the characteristics of each; and discuss treatment indications, outcomes, and complications of different approaches for the treatment of each subchondral bone pathology.
Osteonecrosis
Spontaneous osteonecrosis of the knee (SPONK) was first described by Ahlback in 1968, in 40 patients with severe sudden onset of pain. It is defined as a disease of the subchondral bone that leads to focal ischemia, with subsequent necrosis, and possible structural collapse if not addressed properly. Although the etiology is not always clearly defined (idiopathic in most of the cases), patient features as well as underlying risk factors can help classify the type of osteonecrosis (ON) and therefore guide treatment. In this regard, ON of the knee can be divided into three categories: (1) primary or SPONK, (2) secondary ON (SON), and (3) postarthroscopic ON. Irrespective of the type of ON, the treatment goals for this disease are to stop further progression and delay the onset of end-stage arthritis of the knee. Once considerable joint surface collapse has occurred or advanced osteoarthritis has developed, arthroplasty is often the most appropriate treatment option.
Spontaneous ON of the knee
SPONK classically presents in the older population with a reported incidence of 9.4% in patients older than 55 years. It affects females three to five times more than males and typically presents in the medial femoral condyle. The medial femoral condyle is typically affected in 94% of the times. This can be caused because of a relatively diminished extraosseous and intraosseous blood supply to the medial femoral condyle, with apparent watershed areas making it more vulnerable to a vascular insult. Despite the varying blood supply, the lateral condyle, tibial condyles, as well as the patella can also be affected. Though the true incidence is not well established, it may be more prevalent than SON.
Although the precise etiology of spontaneous ON remains tenuous, various etiologies have been proposed. In ON of the hip, it is widely accepted that a vascular insult precipitates bone death. However, this has not been demonstrated in the knee as of yet. Several authors have reported that a traumatic event leads to microfractures in a debilitated subchondral bone (osteopenic) resulting in accumulated fluid in the space created by the subchondral microfractures. The fluid accumulation results in increased intraosseous pressure and bone marrow edema, decreased blood perfusion, and eventual focal osseous ischemia. Although a traumatic etiology has been implicated, only a minority of patients can specifically recall an injury. However, given the demographics of the affected patients and the high incidence of insufficiency fractures among postmenopausal women, associating an insidious precipitating event with the onset of knee pain can be challenging ( Fig. 12.3 ).
Tears involving the medial meniscus, specifically the posterior meniscal root, have been proposed as a potential etiologic factor for SPONK. Robertson et al. identified 30 consecutive patients with spontaneous ON of the medial femoral condyle. The radiographs and magnetic resonance imaging (MRI) were reviewed, and 80% of the patients were found to have a medial meniscal root tear. The authors suggested that the loss of hoop stress results in an increased load in the compartment (similar to a total meniscectomized state), inducing a subchondral insufficiency fracture. Moreover, early detection of these lesions is crucial because knee biomechanics can be restored to a near-native state if this lesion is properly diagnosed and treated in a timely fashion, and the progression to ON and ultimately to osteoarthritis can be significantly slowed. This theory is supported by a study demonstrating that there was a positive association between low bone mineral density and the incidence of SPONK in women older than 60 years.
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