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Hypertrophic osteoarthropathy is a medical condition combining clubbing and periostitis of the small hand joints, especially the distal interphalangeal joints and the metacarpophalangeal joints. Distal expansion of the long bones as well as painful, swollen joints [ 3 ] and synovial villous proliferation are often seen.
A special form of clubbing is hypertrophic pulmonary osteoarthropathy (HPOA), known in continental Europe as Pierre Marie-Bamberger syndrome. This is the combination of clubbing and thickening of periosteum (connective tissue lining of the bones) and synovium (lining of joints), and is often initially diagnosed as arthritis .
Other names are primary hypertrophic osteoarthropathy or Touraine-Solente-Golé syndrome. [2] It is mainly characterized by pachyderma (thickening of the skin), periostosis (excessive bone formation) and finger clubbing (swelling of tissue with loss of normal angle between nail and nail bed). [1] [3] This disease affects more men than women.
Examples of periosteal reactive bone in selected specimens of Triceratops. A periosteal reaction can result from a large number of causes, including injury and chronic irritation due to a medical condition such as hypertrophic osteopathy, bone healing in response to fracture, chronic stress injuries, subperiosteal hematomas, osteomyelitis, and cancer of the bone.
There are many grading systems for degeneration of intervertebral discs and facet joints in the cervical and lumbar vertebrae, of which the following radiographic systems can be recommended in terms of interobserver reliability: [1]
Hypertrophic osteoarthropathy, primary, autosomal recessive, 2; Melorheostosis; Tumoral calcinosis, hyperphosphatemic, familial, 1; Worth disease; Meningioma of the middle third of the sagittal sinus with large hyperostosis
The diffuse pattern of resorption has a widely diverse differential diagnosis which includes: pyknodysostosis, collagen vascular disease and vasculitis, Raynaud's neuropathy, trauma, epidermolysis bullosa, psoriasis, frostbite, sarcoidosis, hypertrophic osteoarthropathy, acromegaly, and advanced leprosy.
Renal osteodystrophy has been classically described to be the result of hyperparathyroidism secondary to hyperphosphatemia combined with hypocalcemia, both of which are due to decreased excretion of phosphate by the damaged kidney.