I learned some interesting points about bone metabolism that I would like to share with you. When assessing bone volume abnormalities, it is important to differentiate between cortical and cancellous bone. The cortical bone, as the name implies, forms the cortex (outer shell) of most bones, being harder, stiffer and stronger than cancellous bone. It is responsible mainly for the mechanical function of the bones. On the other hand, the cancellous bone typically occurs at the ends of long bones, it has many trabeculations and is highly vascularized. Due to its high surface area, it is the predominant place of metabolic activity of the bone (e.g. exchange of calcium ions).
Now comes the interesting part. Loss of cortical bone occurs mainly in patients with high turnover bone disease, while loss of cancellous bone is often seen in patients with low bone turnover. The clinical outcome of decreased bone strength is fracture, while abnormal metabolic activity results in the inability to maintain mineral homeostasis, which is associated with vascular and soft tissue calcifications. Following these lines, adynamic bone is typically asymptomatic but it is strongly associated with hypercalcemia, cardiovascular calcifications and mortality.
What are the risk factors for adynamic bone disease?High calcium load, low PTH and vitamin D over-treatment. Older patients, DM and peritoneal dialysis are additional associated factors.
Can we predict the type of bone disease in a dyalisis patient with PTH levels?No, but it could give you some direction:
Bone specific alkaline phosphatase levels could also be an adjunctive marker (below 7 ng/mL low bone turnover, above 20 high bone turnover). Radiographic examination of bone can provide important information regarding the presence of hyperparathyroidism (such as subperiosteal resorption). However, radiographic findings are less sensitive than PTH levels and will not establish the type of bone disease. The gold standard is bone bx.
When should you perform a bone bx?Controversial topic but a bx could be considered in the setting of unexplained fractures, unexplained hypercalcemia, and/or unexplained hypophosphatemia; persistent bone pain; possible aluminum toxicity; and before therapy with bisphosphonates.
How should adynamic bone be treated? Lower PTH levels should be achieved by decreasing the doses of calcium-based phosphate binders, vitamin D, a low dialysate calcium concentration, and perhaps by the use of non-calcium-based phosphate binders ( though no data yet supporting this ).
My feeling is that we should be cautious in the administration of vitamin D and adjust with small increments based on PTH levels, especially due to the metabolic complications of adynamic bone and difficulty to reverse it. Adynamic bone disease is a relative new entity and long-term complications have not been fully determined yet. I must confess that since PTH does not truly predict the type of bone disease, it is a hell of an empirical area...