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Excess PTH causes cortical bone loss via RANKL-mediated osteoclast activation; classic radiology: subperiosteal resorption, salt‑and‑pepper skull, brown tumors. Primary (adenoma), secondary (CKD/vit D deficiency), tertiary (autonomous) forms dictate biochemistry and treatment. DEXA: cortical loss at one‑third radius; labs—↑PTH, ↑ALP; Ca high in primary/tertiary, low‑normal in secondary; phosphate low in primary, high in CKD. Orthopaedic issues: fragility fractures, brown tumors, tendon ruptures; treat endocrine cause first, then stabilize fractures as per principles. Parathyroidectomy is definitive for symptomatic primary disease; watch for hungry bone syndrome post‑op.
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Hyperparathyroidism is an endocrine disorder characterized by excessive secretion of parathyroid hormone (PTH), leading to disturbances in calcium and phosphate metabolism. The skeletal system is one of the most significantly affected organs because PTH plays a major role in regulating bone remodeling.
Increased PTH levels stimulate osteoclastic bone resorption, resulting in progressive loss of bone mineral density. Chronic elevation of PTH can lead to skeletal manifestations such as osteitis fibrosa cystica, subperiosteal bone resorption, pathological fractures, and generalized osteoporosis.
From an orthopaedic perspective, hyperparathyroidism is important because it can predispose patients to fragility fractures, bone deformities, and impaired fracture healing.
Parathyroid hormone is secreted by the parathyroid glands in response to low serum calcium levels. The primary function of PTH is to increase serum calcium concentration through actions on bone, kidneys, and the gastrointestinal tract.
| Organ | Effect |
|---|---|
| Bone | Increases bone resorption |
| Kidney | Increases calcium reabsorption |
| Kidney | Decreases phosphate reabsorption |
| Intestine | Increases calcium absorption via vitamin D activation |
These combined effects result in increased circulating calcium levels while reducing serum phosphate levels.
Hyperparathyroidism is classified into three main types based on the underlying cause.
| Type | Cause | Example |
|---|---|---|
| Primary | Autonomous PTH secretion | Parathyroid adenoma |
| Secondary | Response to chronic hypocalcemia | Chronic kidney disease |
| Tertiary | Long-standing secondary hyperparathyroidism | Autonomous gland hyperplasia |
Excessive parathyroid hormone stimulates osteoclastic bone resorption. Over time this leads to progressive weakening of the skeleton.
The cortical bone is particularly affected, which explains why subperiosteal resorption is most commonly seen in the phalanges of the hand.
Osteitis fibrosa cystica represents the severe skeletal form of hyperparathyroidism. It is characterized by increased osteoclastic activity leading to bone resorption and replacement of bone with fibrous tissue.
This process results in the formation of cystic bone lesions known as brown tumors. These lesions are not true neoplasms but represent areas of hemorrhage and fibrous tissue proliferation within bone.
Radiographic findings in hyperparathyroidism are often characteristic and help establish the diagnosis.
| Radiographic Feature | Description |
|---|---|
| Subperiosteal resorption | Most commonly along radial aspect of middle phalanges |
| Salt and pepper skull | Granular skull appearance |
| Brown tumors | Expansile lytic lesions |
| Diffuse osteopenia | Generalized reduction in bone density |
Biochemical investigations play a crucial role in confirming the diagnosis of hyperparathyroidism.
| Test | Typical Finding |
|---|---|
| Serum calcium | Elevated |
| Serum phosphate | Low |
| Parathyroid hormone | Elevated |
| Alkaline phosphatase | Elevated |
Treatment depends on the underlying cause of hyperparathyroidism. Primary hyperparathyroidism is usually treated with surgical removal of the abnormal parathyroid gland.
Orthopaedic treatment may be required for pathological fractures or severe skeletal deformities resulting from prolonged disease.
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