Understanding Rubber Jaw Syndrome (Fibrous Osteodystrophy) in Pets

Rubber jaw syndrome, also known as fibrous osteodystrophy, is a disorder characterized by the replacement of calcium in bones with softer connective tissue. This condition arises when the parathyroid gland produces excess parathyroid hormone (PTH), leading to a state known as hyperparathyroidism.

The Parathyroid Gland

The parathyroid glands in dogs, like in other mammals, are small endocrine glands located behind the thyroid gland in the neck. Dogs typically have two pairs of parathyroid glands, making them four in total. These glands play a crucial role in regulating calcium and phosphorus levels in the dog’s body, which are essential for various physiological processes.

The Parathyroid Hormone

The parathyroid glands produce a hormone called parathyroid hormone (PTH), which helps maintain the balance of calcium in the bloodstream. When blood calcium levels drop too low, the parathyroid glands release PTH. PTH acts on the bones, kidneys, and intestines to increase the absorption of calcium from the diet, reabsorb calcium in the kidneys, and release calcium from the bones.

Maintaining the right balance of calcium is vital for a dog’s overall health because calcium is essential for muscle contraction, nerve function, blood clotting, and the development and maintenance of strong bones and teeth. Issues with the parathyroid glands, such as overproduction or underproduction of PTH, can lead to imbalances in calcium levels, which can result in various health problems for dogs. Hyperparathyroidism, for example, is a condition where the parathyroid glands produce too much PTH, leading to elevated blood calcium levels.

This hormone plays a key role in regulating calcium and phosphorus metabolism in the body. Primary hyperparathyroidism, caused by a malformed parathyroid gland, or secondary hyperparathyroidism, stemming from low blood calcium levels, can both lead to an overproduction of this hormone. Over time, excessive release of parathyroid hormone causes the skeleton, especially the skull and jaw bones, to lose minerals like calcium and become infiltrated with immature fibrous connective tissue. This syndrome not only affects the skeletal structure but can also significantly impact an individual’s or animal’s quality of life.

How does the parathyroid hormone control calcium and phosphorus levels?

Parathyroid hormone (PTH) initially triggers cells in the renal tubules to excrete phosphorus while retaining calcium. Over time, sustained high levels of PTH lead to increased bone breakdown through enhanced osteocytic and osteoclastic activity.

Osteocytic bone resorption:

Osteocytes, which are fully developed bone cells integrated into the mineralized bone matrix, play a crucial role in bone remodeling. This process, known as osteocytic resorption, involves osteocytes detecting mechanical strains or minor damage within the bone. In response, they start the localized breakdown of bone tissue by releasing signaling molecules like cytokines or osteoclast-activating factors (OAFs). These factors activate osteoclasts, the cells tasked with bone resorption, to target and break down bone in the necessary areas.

Osteoclastic bone resorption:

Osteoclasts, originating from hematopoietic stem cells, are sizable, multinucleated entities primarily tasked with bone breakdown. Their resorption activity is direct and intense, involving the attachment of these cells to the bone surface and the secretion of enzymes and acids that dissolve the mineralized bone matrix. This process liberates calcium and phosphate ions into the bloodstream, playing a crucial role in regulating and stabilizing blood calcium levels. Osteoclastic resorption is vital during bone development, repair, and remodeling. It facilitates the removal of aged or damaged bone, paving the way for the creation of new bone by osteoblasts.

Mineral content is extracted from the skeleton and substituted with undeveloped fibrous connective tissue. This condition, known as fibrous osteodystrophy, affects the entire skeleton with pronounced effects in specific areas like the skull’s cancellous bone. Elevated parathyroid hormone (PTH) levels also reduce phosphorus reabsorption in the renal tubules. As PTH activates osteoclasts, leading to phosphorus release from the bone, the concentration of phosphorus in the blood remains mildly reduced or sometimes normal.

Primary Hyperparathyroidism

Normal parathyroid glands compared with parathyroid adenoma

Normal parathyroid glands compared with parathyroid adenoma

In primary hyperparathyroidism, an overproduction of parathyroid hormone (PTH) occurs, often due to a benign, active tumor or a self-sufficient functional lesion in one or more of the parathyroid glands. The tumor in the parathyroid gland in dogs is usually an adenoma, occasionally a carcinoma, composed of active chief cells. Usually, adenomas are single, light brown-red, and located in the cervical region near the thyroid gland. This condition disrupts the normal feedback mechanisms that regulate PTH release in response to blood ionized calcium levels. As a result, the parathyroid glands continue to secrete excessive PTH even when blood calcium levels are high. This condition is relatively rare in older dogs and is not typically a consequence of renal secondary hyperparathyroidism.

Is there a breed predisposition to fibrous osteodystrophy (Rubber Jaw Syndrome)?

While this condition can affect dogs of various breeds, it is more commonly reported in certain breeds and is believed to have a genetic predisposition, inherited as an autosomal recessive gene.

The condition has been described alot in German Shepherd puppies, associated with hypercalcemia, hypophosphatemia, increased immunoreactive PTH, and increased fractional excretion of inorganic phosphorus in the urine.

Breeds that are more commonly associated with a predisposition to fibrous osteodystrophy include Keeshond, German Shepherd, Irish Setter, Standard Poodle, Labrador Retriever, Golden Retriever, Boxer, Great Dane, Old English Sheepdog and Dachshund

It’s important to note that while these breeds may have a higher reported incidence of fibrous osteodystrophy, the condition can occur in other breeds and mixed-breed dogs as well.

What are the Clinical Signs of Primary Hyperparathyroidism?

An illustration of a dog with thickened jaw bones due to severe fibrous osteodystrophy

An illustration of a dog with thickened jaw bones due to severe fibrous osteodystrophy

The increase in parathyroid hormone can lead to weakened bones, resulting in bone pain and lameness besides a tendency for bones to fracture easily after minor physical trauma. This condition can also lead to the facial bones becoming denser. Damage to the nasal cavities and loosening of teeth are common effects. Affected animals may struggle to close their mouths correctly and suffer from gum sores that heal slowly.

The jaw bones often thicken coarsely, while the skull bones become markedly thinner due to the increased bone resorption and have a characteristic “moth-eaten” appearance radiographically.

increased bone resorption and have a characteristic “moth-eaten” appearance radiographically.

An x-ray of a dog that was attended at the clinic suffering from severe rubber jaw syndrome showing increased bone resorption and the characteristic “moth-eaten” appearance of the skull bones.

A video of a dog attended at the clinic suffering from rubber jaw syndrome showing how the jaw easily twists when manipulated.

In severe cases of fibrous osteodystrophy, known as “rubber jaw” syndrome, the jaw is so deteriorated that it can be gently twisted without resistance. Fibrous osteodystrophy can also lead to a variety of clinical signs

associated with high calcium levels in the blood, such as increased thirst and urination. Other clinical signs include stunted growth, weakness, polyuria, polydipsia, and a diffuse reduction in bone density.

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