Page 8 - GP Fall 2024

Hyperparathyroidism in Dentistry

Author: Gwen Cohen Brown, DDS, FAAOMP

Anatomically there are four parathyroid Clinical: The characteristic patient with Radiographically, oral lesions may present
glands that are located subjacent to the thy- primary hyperparathyroidism will present as a reduction in cortical bone density which
roid gland. Unless the parathyroid glands are with enlargement of one or more of the four can demonstrate either as a well-defined cys-
enlarged, it can be difficult to find them in a parathyroid glands, tends to be female more tic radiolucency, either unilocular or multi-
typical extra-oral exam using visual evalua- than male, middle-aged, and is often asymp- locular or a ground glass appearance similar
tion and bimanual palpation, and it may be tomatic. Patients may present with kidney to what you would see in a case of fibrous
difficult to find them without the use of ul- stones, or other lith (stone) formation in the dysplasia. Interestingly, there may be a loss
trasound, MRI or CT scan. The parathyroid body due to the excess calcium in the blood. of lamina dura around affected teeth or the
glands consist of two pairs of small glands Blood work will often present with elevat- entire dentition, and the teeth themselves
which secrete parathyroid hormone (PTH or ed serum calcium levels (hypercalcemia) as may present with hypercementosis. Para-
parathormone). The size of each parathyroid well as elevated serum parathormone levels. thormone has a key role in balancing calci-
gland is approximately 0.6 х 0.3 х 0.15 cm. um and phosphorus metabolism and, hence,
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The superior pair is located against the cri- Secondary Hyperparathyroidism occurs has a great influence on bone and teeth min-
coid cartilage and the inferior pair is located when the parathyroid glands are chronically eralization. Osteoporosis is the most com-
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near the pole of the thyroid gland. The para- stimulated to release parathyroid hormone, mon finding after hypocalcemia in patients
thyroid glands help control calcium absorp- by a decrease in circulating calcium. with hyperparathyroidism. The bones which
tion, utilization, and excretion by the body. are affected most often include the ribs, clav-
There are three variants of hyperparathyroid- Etiology of secondary hyperparathyroidism icles, pelvic girdle, and mandible. A patho-
ism; however, primary and secondary are the is multifocal and can be due to chronic renal logic fracture may be the first symptom of
most common by far. Hyperparathyroidism failure, rickets or malabsorption syndromes. the disease (Figures 1-3).
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results from excessive secretion of parathy- These are the most frequent
roid hormone with subsequent osteoclastic conditions leading to sec-
resorption and hypercalcemia. ondary hyperparathyroid-
ism. Kidney disease is a
Primary Hyperparathyroidism result of suppression of the
In primary hyperparathyroidism, one or phosphorus reabsorption
more of the four parathyroid glands devel- in the proximal portions
ops a tumor, typically a benign adenoma or of kidney canaliculus.
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hyperplasia. This results in excess hormone Secondary hyperparathy-
being secreted by the parathyroid regardless roidism often presents in
of the level of calcium in the blood. Normal- children with renal disease.
ly, the parathyroid glands work on a biofeed- Excess calcium makes
back loop regulating calcium, phosphorus, your kidneys work hard-
vitamin D levels and parathyroid hormone er to filter urine. This can
secretion. The etiology of either parathyroid lead to excessive thirst,
hyperplasia or the development of parathy- frequent urination, and di-
roid adenomas is currently unknown. A non- gestive system complaints.
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cancerous growth (adenoma) on a gland is Hypercalcemia (too much
the most common cause. Enlargement (hy- calcium in the blood) can Figure 1. Loss of lamina dura. Figure 2. Hyperparathyroidism.
perplasia) of two or more parathyroid glands also lead to stomach upset,
accounts for most other cases. It is rare for a nausea, vomiting and con-
cancerous tumor to be present, however it is stipation.
quite common for the patient to present with
one to three parathyroid adenomas. Oral Manifestations of
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Primary Hyperparathy-
Typical symptoms are often described as roidism
“moans, groans, stones, and bones”. There can also be increased
mobility in the teeth which
The most common symptoms of hyperpara- correlates with loss of bone
thyroidism are chronic fatigue, body aches, and an increase in calculus
difficulty sleeping, bone pain, memory loss, as calcium is secreted into Figure 3. Multilocular radioluscent lesion consistent with a
poor concentration, depression, and head- the oral cavity at a higher Brown tumor of hypothyroidism.
aches. Parathyroid disease frequently leads rate than normal. Other
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to osteoporosis, kidney stones, hypertension, intraoral manifestations include the devel- Microscopically, the bone will demonstrate
cardiac arrhythmias, and kidney failure. 1 opment of pulp stones and obliteration of thinning of the trabeculae and increased os-
The bones become weakened and can lead the canal, delay in tooth eruption (more sec- teoclastic activity. There may be wide zones
to fracture, osteoporosis and osteopenia. ondary hyperparathyroidism than primary), of bone-like material rimmed by active osteo-
The development of symptoms is of gradu- malocclusion, drifting or movement of teeth blasts, multinucleated giant cells (osteoclasts)
al onset, with polydipsia, polyuria, weight with increased spacing, soft tissue calcifica- and fibrous connective tissue stroma. In cases
loss, and bone pain being the most common tions (calculus) and an increase in caries. where there are many osteoclasts this lesion
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symptoms. may be referred to as a Brown tumor of hyper-
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