“Osteonecrosis” means death (“necrosis”) of bone (“osteo”). Osteonecrosis is often caused by overt interruption of the bone’s blood supply, which is often caused by dislocation or fracture (hence the older, still in use term, “avascular necrosis,” or AVN). Interruption of the blood supply is the key step to the development of osteonecrosis, as this causes ischemia (and, in turn, loss of perfusion) of bones, though the interruption may be subtle. For example, sickled red blood cells may clog flow in small spaces without any frank arterial occlusion.
This ischemia can lead to the development of arthritis. Here’s why:
- Ischemia → cell death
- Cell death → less bone remodeling
- Less bone remodeling → poorer structural properties of bone
- Poorer structural properties of bone → increased chance to collapse with load
- Collapse of subchondral bone → irregularities of the joint surface above that bone
- Irregularities of the joint surface on one side of the joint plus motion → damage to the other side of the joint
- Damage to the other side of the joint plus motion → more irregularities on the other side
- Cycle of irregularities of one side inflicting damaging the other side → arthritis!
Osteonecrosis can be caused by trauma, excess use of alcohol, and some medications, such as steroids. Disorders commonly associated with osteonecrosis include hemoglobinopathies (interfering with blood flow), systemic lupus erythematosus, Gaucher disease, and antiphospholipid antibody syndrome.
Many cases of osteonecrosis are also idiopathic: a fancy saying of “we don’t know what caused it.” Osteonecrosis typically affects the hip and shoulder but can also affect the knee (femoral condyle), ankle (talus), or wrist (scaphoid).
Patients suffering from osteonecrosis will often present with a complaint of pain that is exacerbated by activity or even present during rest and at night. Imaging is required to make the diagnosis of osteonecrosis. X-rays can often show characteristic changes in bone structure, but MRI (Figure 1) is most specific.
Contribution of osteonecrosis to end-stage arthrosis
The biological steps implicated in osteonecrosis follow a logical series of events that ultimately leads to compromised bone and are listed below:
- Loss of blood supply to bone results in ischemia and tissue death. In particular, the osteoclasts and osteoblasts will die.
- Loss of osteoclasts preclude the clearance of damaged/old bone; loss of osteoclasts and osteoblasts interferes with the creation of new bone.
- When bone does not remodel, there is an accumulation of damaged tissue. This compromises the bone’s structural properties, particularly its compliance, which contributes to stiffness of the bone.
- Compliance is technically defined as the property of a material to undergo deformation when subjected to an applied force. In layman’s terms, greater compliance refers to the propensity of a tissue to break rather than bend. (You may be familiar with the concept from pulmonology. Pulmonary compliance measures the extent to which the lungs will expand with increases in pressure). Simply put, a non-compliant lung or a non-compliant bone is stiff.
- Stiffness is bad for bones. There exists a load, L, that would bend a healthy bone but break a non-compliant one. When load L is applied, the stiff bone will crack below the surface.
- Cracks below the surface lead to collapse, and a loss of smoothness at the articular surface (Figure 2). Remember: the cartilage surface is supported from below-it’s not like a drumhead held taut above empty space.
- A loss of smoothness on the articular surface is like sandpaper for the other side; thus, the cycle is self-perpetuating.
Note that the blood supply to bone primarily serves to maintain the tissue. With this in mind, histologic examination of bone that lost its blood supply just hours ago will often not reveal acute histological changes, whereas dead muscle would show such changes. This is clinically significant: the symptoms from bone breakdown can appear far after the insulting event.
You may have noticed that the introduction to this answer and the recapitulation are awfully similar. Indeed they are: this is an important cascade to master!. (If you are going to study the coagulation cascade and know, for instance, that heparin binds to and increases the activity of antithrombin III by inducing a conformational change to some factor or another, you can memorize master this one too.) So here it is a third time: ischemia → cell death → decreased remodeling → decreased compliance → collapse → irregularities of the joint surface → damage to the other side of the joint → more → more→ arthritis. Know this!