RA is a cause of secondary osteoprosis (low bone mass and density) increasing fracture risk. Factors in RA patients contributing to osteoporosis are: low body mass, decreased physical activity and muscle power, proinflamatory cytokines ( tumoral necrosis factor, interleukine, etc) and medication (metotrexate, corticosteroids).
if younger patients with both, symptoms for RA and Osteoporosis, it might be useful to determine the alkaline phosphatase level. If it is low (below 35U/l) hypophosphatasia should be taken into consideration.
Younger women with RA had an increased risk for fractures because of early development of generalized osteoporosis for two reasons: first, RA leads to reduced physical activity and second, one of the adverse effects of corticosteroids on bone metabolism is osteoporosis. As compared to men, these effects are less expressed.
Testosteron plays an important role in the maintenance of bone metabolism. It restricts the increased osteoclast activity , and therefore reduces the extent of osteoporosis in men with RA as compared to women.
RA is a cause of secondary osteoporosis. Firstly, because of disease nature and secondarily, due to drugs like corticosteroids dispensed to patients. In addition, immobility and muscle wasting leads to more falling risk and bad body response to trauma.
RA is affecting the collagen. Also is causing osteoporosis. There are areas of "normal" bone and "abnormal" bone due to the "collagenous disease" creating the risk of fracture in the areas on tension (for example subtrochanderic region). Similar "failure" of the bone but for different reasons is observed in the long term treatment of osteoporosis with biphosphonates. Women have usually less bone mass than the men and so the male bones are "stronger" and can resist the loading
Dr. Zafiropoulos, I allow me to express a different opinion at 2 points in your answer: First, subtrochanteric region is not a predilection place for osteoporotic fractures at all in comparison with femoral neck for example, and second, when prescribing biphophonates we are trying to increase bone mass density through blocking the osteoclast activity and reduce fracture risk.
Anyway, the question here is different and obviously is not well studied. Probably, the estrogen levels in young women with RA are lowered more than testosteron in young men with RA under corticosteroid medication ?
Dear Panayot, thank you for the comments. I agree that this is a different question and the example given with the biphosphonates is just for some stimulus, and to gine some parallelity to what maybe happening. Long treatment (for many years) with biphosphonates can create islands of very dense and brittle bone next to very osteoporotic one. This creates stress rising within the bone resulting to pathological fractures. I agree about the possible explanations for the chemistry that influences the bone but I tried to approach the problem from a mechanical point of view based on the potential structure of the bone. I hope that this made things clearer.
Thank you, George, in fact things are clear before this discussion. One more question, you do not use any biphosphonates any more in the treatment of osteoporosis, do you ?
As Orthopaedic Surgeon following the BOA guidelines I used Aledronate blindly (I had used also Calcitonine in the past with Calcium and Vut D combinations). But there is a great loop-hole, as I have seen complications as mandibular softening and also stress pathological fractures. The loop hole is that it is mentioned in the report that, the indicated specialists to treat osteoporosis are the Rheumatologists or Endocrinologists. I liked this so much as it was a relief from un-necessary headaches.
You are right. Obviously, the treatment of osteoporosis is an interdisciplinary domain. In cases of osteoporotic fractures orthopaedic surgeons are more active than internists. So we prescribe anti-osteoprotic medicaments given that the osteodensitometry objectivizes the need for medication treatment. Furthermore, we have some experience with postoperative administring of biphosphonates in patients with THR with the belief that this tactics may strengthen the connection between prosthesis and bone.