These vary according to the clinical state of the disease (active or healed), and they have been given a variety of names in the literature, making it difficult to accurately know the number of such reported cases. 1– 3 Less commonly encountered are the facial skeletal changes associated with hyperparathyroidism. 2 Pathognomic radiologic findings include the loss of the dental lamina, thinning of cortical bone in multiple locations (distal phalanges, distal clavicles, distal ulna, inferior margin of femoral neck and pubis, and medial proximal tibia), a coarsened trabecular pattern, and a “salt-and-pepper” appearance of bone, particularly the skull.

The various skeletal changes have been well documented in the literature and include generalized demineralization, subperiosteal resorption, bone cysts, and pathologic fractures. Whether primary, secondary, or tertiary, hyperparathyroidism is usually diagnosed by laboratory tests long before abnormal calcium metabolism results in macroscopic skeletal changes.

Presently, the skeletal sequelae of hyperparathyroidism are considered to be mainly of historic interest. Subsequently, there are 2 major types of metabolic bone disease: 1) high-turnover osteodystrophy (increased bone resorption and formation) and 2) low-turnover or aplastic disease (adynamic bone and osteomalacia). Long-term dialysis also inhibits healthy bone homeostasis, with aluminum deposition that interferes with bone mineralization. Phosphate retention and decreased vitamin D conversion leads to hypocalcemia, which, in turn, stimulates the parathyroid chief cells to produce more parathyroid hormone. Chronic renal failure alters bone metabolism by multiple mechanisms.

Download facial bones