ALCOHOL‐RELATED SKELETAL DISORDERS

Throughout life, the skeleton is constantly remodeling. Somewhere bone is being torn down by osteoclasts, only t o be rebuilt again by osteoblasts. The sequence of events is repeated again and again throughout the skeleton, starting with division of progenitor cells giving rise t o daughter cells and the daughter cells giving rise t o osteoclasts which resorb bone. The osteoclasts die off in about 1 month, and osteoblasts now appear formed from the same daughter cells that had originally given rise t o osteoclasts. The osteoblasts lay down bone matrix in the resorption cavities or o n bone surfaces, and the matrix is 80% calcified within 48 hours, the remaining 20% calcification occurring more slowly. Now the osteoblasts die off within 2 months while a few of them become trapped by mineralized bone, and they become osteocytes in their lacunae. Osteocytes can, under some conditions, effect the release of calcium from their immediate vicinity. There are various factors, such as trauma, which will “turn on” progenitor cells t o start off the intense cycle of bone resorption and new bone formation. Even a crack of the lateral malleolus at the ankle will stimulate intense bone activity, not only in the fibula but in the tibia, the femur, and even the iliac bone on the same side. Parathyroid hormone stimulates production of new osteoclasts and, in addition, stimulates osteoclasts to greater activity, thus resorbing and releasing bone mineral. Alcohol may interact with these complex homeostatic relations in a variety of ways. In 1963, Kalbfleish observed that 30 ml of ethanol given t o controls and t o alcoholics had a similar effect; within 20 minutes there was very nearly 100% increase in urinary calcium excretion and a 167% increase in magnesium excretion, lasting for about 2 hours.’ This calcium diuresis tends t o lower serum calcium, thus stimulating parathyroid hormone release, which in turn stimulates osteoclasts and osteocytes t o resorb calcium from the skeleton. Persistently increased parathyroid hormone stimulates progenitor cells t o produce extra osteoclasts. In the absence of a n adequate calcium dietary intake or in the presence of intestinal disease o r lack of vitamin D , bone resorption predominates and the skeleton wo-lld be expected t o become less dense. In the presence of a high calcium diet and a healthy intestinal mucosa, increased calcium absorption should compensate for the increased urinary excretion.