Increased parathyroid hormone secretion results in diffuse bone resorption and dimineralization, most apparent at areas of greatest surface area.
- Periostitis: More commonly seen in secondary hyperparathyroidism. In children periostitis and extensive bone resorption may mimic syphilis or leukemia.
- Subperiosteal resorption: Classically at the distal phalangeal tufts (acroosteolysis, pink arrows) and along the radial margins of the second and third middle phalanges (blue arrows). Can also be seen along the medial aspect of the humerus, femur, and tibia, the superior and inferior aspects of the ribs and the lamina dura of the teeth (white arrow).
- Intracortical resorption: Intracortical linear striations (cortical tunneling) can be seen, classically at the index finger metacarpal.
- Endosteal resorption: Well-seen in the hands. Endosteal scalloping can mimic the endosteal erosions seen in multiple myeloma, and endosteal thinning can mimic cortical thinning seen in osteoporosis.
- Trabecular resorption: Resorption within medullary bone gives bone a granular appearance, with loss of distinct trabecular detail. In the skull, the diploic space is replaced by connective tissue, leading to a speckled appearance ("salt and pepper" skull).
- Subchondral resorption: Can mimic inflammatory arthropathy, especially in the sacroiliac (lower 2/3 is articular), acromioclavicular, sternoclavicular, and temperomandibular joints, and at the pubic symphysis (cartilaginous joint).
- Subligamentous resorption: Most commonly seen at the trochanters, ischial tuberosities, sacroiliac joints (upper 1/3 is syndesmotic), the inferior surface of the calcaneus, the inferior surface of the distal clavicle, and at the elbow.
- Calcium pyrophosphate dihydrate deposition disease: More commonly seen in primary hyperparathyroidism (up to 40%).
- Brown tumors (black arrow): Accumulations of osteoclasts and fibrous tissue. Tend to heal after treatment of the underlying disorder. Eccentric/intracortical, lytic, and often expansile. Incidence is greater in primary hyperparathyroidism, but more commonly seen with secondary hyperparathyroidism due to the higher prevalence.
- Soft tissue calcifications: More commonly seen in secondary hyperpararthyroidism.
- Bone sclerosis: More commonly seen in secondary hyperpararthyroidism. Can be seen in the metaphyses of long bones, the skull, or the vertebral body endplates (rugger jersey spine). Progressive hypertrophy of the facial and cranial hones can produce "leontiasis ossea" (lion face), and can mimic Paget disease and fibrous dysplasia.
- Gisler DG. Chapter 4: Metabolic bone diseases. in Musculoskeletal Radiology: The Requisites (3rd ed). Mosby (2002): pp 401-404.
- Resnick D. Chapter 52: Parathyroid Disorders and Renal Osteodystrophy. in Diagnosis of Bone and Joint Disorders (4th ed). Saunders (2002): pp 2043-2111.