The subchondral bone is the dense layer of bone tissue situated immediately beneath the articular cartilage within a joint. This structure, along with the cartilage it supports, forms the osteochondral unit. While joint health was once viewed primarily through the lens of cartilage, current understanding recognizes the subchondral bone as an active player in maintaining joint function. It acts as a dynamic interface, constantly adapting to mechanical stresses and influencing the metabolic state of the overlying cartilage. The condition of this underlying bone is intrinsically linked to the initiation and progression of joint diseases.
Structure and Location
Subchondral bone is positioned deep to the calcified cartilage layer, anchoring the softer, avascular articular cartilage to the rest of the skeleton. This region is structurally organized into two distinct layers. The outermost layer is the subchondral bone plate, a thin, compact sheet of cortical bone that lies directly under the calcified cartilage.
Beneath this dense plate lies the subchondral trabecular bone, a more porous, spongy network. This trabecular layer is highly metabolically active and contains bone marrow, blood vessels, and sensory nerves. This structural arrangement creates a unique transition zone, as the cartilage above is entirely avascular and aneural.
Primary Physiological Role
The healthy subchondral bone performs a dual function, providing mechanical support and metabolic regulation for the joint. Mechanically, it acts as a shock absorber, distributing forces generated during movement across the joint surface. The dense subchondral plate offers firm structural support, while the more elastic, spongy trabecular bone deforms slightly under load to dissipate energy and protect the overlying articular cartilage.
The second primary role involves continuous, dynamic communication with the cartilage above, often termed “crosstalk.” Since articular cartilage is avascular, it relies on the underlying bone for nourishment. The highly vascularized subchondral bone contains terminal vessels that facilitate the exchange of nutrients, oxygen, and waste products with the cartilage. This metabolic exchange maintains the health of the avascular cartilage tissue, and the bone also releases signaling molecules that influence cartilage cell activity.
Subchondral Bone in Joint Disease
Changes within the subchondral bone are now recognized as active components that often precede or drive the development of joint diseases, particularly Osteoarthritis (OA). One common pathological change is subchondral sclerosis, where the bone increases in density and becomes harder, appearing bright or dense on imaging. This hardening reduces the bone’s normal elasticity, causing it to transmit increased mechanical loads directly to the overlying cartilage.
The resulting heightened stress can accelerate the breakdown and degeneration of the articular cartilage. Another significant finding in joint disease is the formation of Bone Marrow Lesions (BMLs), which are areas of abnormal signal intensity observed on Magnetic Resonance Imaging (MRI) scans. BMLs are linked to microscopic bone microdamage, increased vascularity, and inflammation within the subchondral bone.
These lesions are strongly associated with joint pain and an increased risk of cartilage loss and disease progression. The pain experienced in joint disease is often directly attributable to the subchondral bone pathology. Unlike cartilage, the subchondral bone is richly innervated with sensory nerve fibers.
In the progression of OA, the density of these sensory nerves increases, and they may show aberrant sprouting, which contributes to the perception of pain. Abnormal bone remodeling can lead to the formation of subchondral cysts, which are fluid-filled cavities that represent a local failure in the bone structure. These pathological changes confirm that OA is a disorder affecting the entire osteochondral unit, with the subchondral bone playing a central role in its onset and severity.
Assessment and Intervention Strategies
Clinical assessment of subchondral bone health relies on various imaging modalities that capture the distinct pathological changes within the tissue. Standard X-rays are routinely used to detect subchondral sclerosis, which appears as increased bone density and thickness. Magnetic Resonance Imaging (MRI) is particularly valuable because it can visualize the soft tissue changes and the presence of Bone Marrow Lesions, which appear as hyperintense signals on fluid-sensitive sequences.
Treatment strategies aimed at correcting subchondral bone defects are becoming increasingly targeted to manage pain and slow disease progression. One minimally invasive procedure is microfracture, which involves creating small perforations in the subchondral bone plate. This technique allows mesenchymal progenitor cells and growth factors from the bone marrow to enter the joint defect, stimulating the formation of new repair tissue.
A newer intervention for BMLs is subchondroplasty, a procedure that targets the unstable bone. This technique involves injecting a flowable, osteoconductive bone substitute material, such as calcium phosphate, directly into the area of the BML. The injected material stabilizes the microfractures and mechanical insufficiency in the bone, and it is gradually resorbed and replaced by the body’s own healthy bone over time. These direct interventions underscore the shift in focusing on the subchondral bone as a primary therapeutic target. Ongoing research continues to explore the dynamic interplay between bone and cartilage, which will lead to further therapies designed to preserve this foundational tissue and improve long-term joint function.