Cancellous bone is spongy bone in which the matrix forms a lattice of large plates and rods known as the trabecula, partially enclosing many intercommunicating spaces filled with bone marrow. Found in the inner parts of bones.

Osteoclasts are bone resorbing cells. Actively resorbing cells are usually found in cavities on bone surfaces called resorption cavities or Howship’s lacunae.

Osteoblasts are bone-forming cells that synthesize and secrete non-mineralized bone matrix, participate in the calcification and resorption of bone, and regulate the flux of calcium and phosphate in and out of bone. Bone formation occurs in two stages, matrix formation, and mineralization. When osteblasts stop synthesizing matrix and become embedded within bone, they are called ostecytes.

Osteocytes are housed in lacunae. Osteocytes may (1) stabilize bone mineral (2) detect microfractures, and (3) respond to the amount and distribution of strain within bone tissue that influence adaptive modeling and remodeling behavior through cell to cell interaction. Osteocytes play a key role in homestatic, morphogenetic, and restructuring processes that regulate the mineral content and architecture of bone mass.

Bone lining cells are resting osteoblasts. These cells are not completely understood, but they may function like osteocytes, but also may be involved in the hematopoietic process.

Hematopoiesis is the production and development of blood cells, normally in the bone marrow.

Bone remodeling is the process in which bone is resorbed and new bone formed at the same site. A normal rate of adult bone turnover is 20 years for cortical bone and 4 years for cancellous bone. Bone turnover helps to maintain load bearing, to repair microscopic structural damage, and to replace old bone - a dynamic equilibrium.

About 80% of cancellous and cortical bone surfaces are inactive with respect to bone remodeling at any given time. The remodeling cycle, moving from this resting state to resorption, is activated. The initiating factor is unknown but it is believed to occur at random as well as in response to focal structural or biomechanical requirements. The remodeling cycle requires osteoclasts and the means for them to gain access to the bone surface (attraction and attachment). As osteoclasts come in contact with the surface of the bone, they begin to erode the bone, forming cavities (Howship’s lacunae in cancellous bone, resorption cavities in cortical bone). This phase takes about 1 to 3 weeks and is known as resorption. There is a 1 to 2 week interval after this phase until the beginning of formation.

Bone formation occurs in two stages, matrix synthesis followed by extracellular mineralization. Osteoblasts begin to deposit a layer of bone matrix (osteoid seam). Mineralization is approximately 70% completed after about 5 to 10 days. Complete mineralization takes about 3 to 6 months in both cortical and trabecular bone.

The signal for bone remodeling is given by the bone-lining cells (resting osteoblasts), osteoclasts are recruited, attach to the site, demineralize and degrade the matrix. Osteblasts move in, build a new matrix, and mineralize the structure; some osteoblasts become embedded in the calcified bone and become known as an ostecyte. The cycle is in dynamic equilibrium.

Essentially, osteonecrosis in KD, is a process where osteoclastic activity (bone resorption) outpaces osteoblastic activity (bone formation). An insult - arterial insufficiency, venous congestion, hypercoaguability, hypofibrinolysis, microtrauma, trauma, etc breaks the natural cycle. The marrow becomes edematous (marrow can survive 2 to 5 days without oxygen) and cannot function properly, equilibrium is lost. The osteoclasts have cleared a site, ready for new bone. The osteoblasts don’t come, or they are too few. Thus, too little or no new bone is formed. Nearby though, is healthy bone, it reacts to attempt a repair. A zone of granulation tissue (this is not hard bone) develops at the margin between the dead and healthy bone. This tissue contains scattered inflammatory cells. Then, gradually, this reparative tissue moves into the necrotic zone. New osteoblasts deposit seams of bone on the dead trabecular bone. New bone also forms in resorption cavities in the dead bone - known as creeping substitution. The osteoclastic resorption continues at the margin of infarct, but this just further weakens the dead trabeculae, which eventually fractures beneath the subchondral plate. Enough tiny fractures will lead to collapse of the articular surface.

Contributed by Phyllis Walker