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).