Discussion
The earliest reported case of hyperparathyroidism was documented in 1930 (2) and since then the further classification into primary, secondary and tertiary forms has helped to directappropriate treatment.In the United Kingdom, it is suggested approximately one to four people per thousand have a diagnosis of hyperparathyroidism (8). Brown tumoursoccur more commonly in cases of primary than secondary hyperparathyroidism. However, most cases clinicians see are with secondary hyperparathyroidism as it is more prevalent in the general population (7).
The clinical manifestations of hyperparathyroidism are bone pain, insufficiency fractures and renal colic. Dental clinical findings can include drifting teeth and delayed dental development (1). There are also associated radiographic changes. An increased production of parathyroid hormone results in increased osteoclastic activity and bone resorption. On radiographs there is often cortical thinning and generalised bony changes which can range from osteopenia to a granular or ground glass appearance to the bone of the skeleton and jaws (10).Loss of lamina dura in patients with hyperparathyroid disease is a well-recognised consequence but it isactually only evident in about 10% of cases (8). There are also a range of other characteristic bony changes that can occur such as a ‘pepper –pot’ skull (10).Brown tumours can arise when the hyperparathyroid status is prolonged and the most common sites are the mandible, clavicles, ribs, pelvis and femur. Brown tumours can be single or multiple.Osteitis fibrosa cystica describes a more severe skeletal manifestationwith multiple cyst-like Brown tumours affecting the bone (10,11). Soft tissue calcifications may also be evident on imaging.
The panoramic radiograph identified multiple radiolucent lesions in the jaws. A range of differential diagnoses were considered to explain the multiple radiolucent lesions: