Introduction
Hyperparathyroidism can present with a variety of oral manifestations. Many of which are only evident on radiographs, such as generalised reduction in bone density, ground glass changes to the trabecular bone pattern and loss of lamina dura around teeth. Brown Tumours can occur in the jaws of patients with hyperparathyroidism(1) and are evident on imaging as well demarcated, radiolucent, often expansile lesions (2). Histologically they are identical to giant cell granulomas which are seen in younger patients who do not have hyperparathyroidism(3) Brown tumours are not frequently seen in developed countries as hyperparathyroidism is usually quickly diagnosed and treated(4).
Hyperparathyroidism occurs when one or more of the four parathyroid glands in the neck, located at the deep surface of the thyroid gland, produce increased levels of parathyroid hormone. Parathyroid hormone regulates calcium metabolism.Hyperparathyroidism can be classified as primary, secondary and tertiary. Primary hyperparathyroidism is associated with elevated serum calcium levels. It is caused by overproduction of parathyroid hormone from either a parathyroid adenoma or hyperplasia of the parathyroid glands. Parathyroid carcinoma also exists but is very rare. Secondary hyperparathyroidism is caused by low serum calcium levels which is often associated with chronic renal failure. This drives a negative feedback mechanism to cause hyperparathyroidism.In this article, a case of tertiary hyperparathyroidism is discussed. Tertiary hyperparathyroidism occurs in cases where longstandingsecondary hyperparathyroidism leads to autonomously functioning parathyroid glands. Therefore, these patients may also have parathyroid adenomas or hyperplastic parathyroid glands(1, 12).Multiple, complimentary imaging modalities are utilised prior to considering a surgical approach to correct a diagnosis of primary or tertiary hyperparathyroidism (3).