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A 52-year-old male with secondary hyperparathyroidism resulting from polycystic kidney disease, undergoing dialysis for 18 years, is documented. The case showed radiographic mandibular bilateral osteolytic lesions with ground glass appearance, diminished lamina dura, maxillary horizontal bone loss, but no maxillofacial expansion. Additionally, cases of hyperparathyroidism are reviewed to associate oral radiographic features with disease severity. The review suggests that in secondary hyperparathyroidism: 1) jaw demineralization, lamina dura loss, and osteolytic lesions occur with varying consistency depending on disease stage; 2) there is no gender predilection of oral manifestation occurrence; and 3) with advancing age, lamina dura changes may occur with increasing frequency.
CPD/Clinical Relevance: This article discusses the oral radiographic signs and symptoms that present in patients with secondary hyperparathyroidism.
Article
Clinical and radiographic examination of the oral cavity can reveal many findings indicative of systemic diseases. One such systemic condition is elevated parathyroid hormone (PTH) in which its oral manifestations have been described in both early and recent oral pathology and radiology textbooks.1,2,3,4
Parathyroid hormone, a hormone released by the parathyroid gland, holds a vital role in calcium homeostasis. PTH is secreted during low blood calcium levels and encourages calcium release from the bones. Despite tight calcium control, homeostatic irregularities leading to an increase in PTH level can occur in a variety of circumstances, such as:
In primary hyperparathyroidism, an adenoma or ectopic parathyroid gland secretes excess PTH into the blood. In secondary hyperparathyroidism, abnormal calcium regulation (from chronic kidney diseases such as a polycystic kidney or vitamin D deficiency) stimulates greater production and release of PTH. Tertiary hyperparathyroidism is also possible, where excessive PTH is released as a result of persistent secondary hyperparathyroidism.5
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