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Understanding Rubber Jaw Syndrome (Fibrous Osteodystrophy) in Pets

Updated: Jan 28

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.


How is Primary Hyperparathyroidism Diagnosed?

 

3D illustration of veterinary medical laboratory
3D illustration of veterinary medical laboratory

In animals with primary hyperparathyroidism, tests often reveal significantly elevated blood calcium levels (hypercalcemia), typically due to the rapid release of calcium from bones. Normal blood calcium levels in healthy dogs hover around 10 ± 1 mg/dL, varying with age, diet, and testing methods. However, serum calcium levels exceeding 12 mg/dL are indicative of hypercalcemia. Dogs with primary hyperparathyroidism generally show serum calcium levels between 12 and 20 mg/dL. Concurrently, blood phosphorus levels are usually low or at the lower end of the normal range (≤4 mg/dL). There's often an increased urinary output of phosphorus and sometimes calcium, potentially leading to conditions like nephrocalcinosis and urolithiasis.


Additional tests to measure phosphorus and parathyroid hormone levels can be conducted. Since high blood calcium can be a sign of various diseases, more tests are needed to confirm primary hyperparathyroidism, such as ultrasonography for detecting changes in the parathyroid gland and evaluating bone biomarkers like hydroxyproline. A definitive diagnosis is confirmed by measuring serum or plasma PTH concentration.


Animals with evident bone disease may also show increased serum alkaline phosphatase activity. A definitive diagnosis of primary hyperparathyroidism is supported by finding elevated PTH levels through a species-specific assay in an adult to aged dog with hypercalcemia, hypophosphatemia, and signs of generalized bone disease. Typical PTH circulating levels in most animals are around 20 pg/mL (dogs, 20 ± 5 pg/mL; cats, 17 ± 2 pg/mL), with slightly lower levels in nonhuman primates, though these normal values can vary across different laboratories.


Other causes of hypercalcemia, such as vitamin D intoxication (overdosage)

enzootic calcinosis, malignant neoplasms with osseous metastasis and

humoral hypercalcemia of malignancy should always be ruled out.


How is Primary Hyperparathyroidism Treated?

 

Even though the primary objective of treatment is to stop the overproduction of parathyroid hormone, the management of fibrous osteodystrophy in dogs usually includes both medical intervention and supportive therapy. The exact method of treatment depends on how severe the condition is and the unique requirements of each dog. Always consult with a veterinarian who can evaluate your dog's condition, perform the necessary tests, and recommend the most appropriate treatment plan. Early diagnosis and treatment are essential for the successful management of primary hyperparathyroidism in dogs. The methods of treatment for fibrous osteodystrophy in dogs include:


  1. Underlying Cause Management: If fibrous osteodystrophy is secondary to an underlying condition, such as primary hyperparathyroidism, addressing the primary cause may be necessary. This may involve surgery to remove abnormal parathyroid glands or other treatments.

  2. Medications:

    1. Pain Management: Dogs with fibrous osteodystrophy may experience pain and discomfort. Non-steroidal anti-inflammatory drugs (NSAIDs) or other pain relievers may be prescribed to alleviate these symptoms.

    2. Vitamin and Mineral Supplements: Depending on the underlying cause of the condition, supplements such as calcium and vitamin D may be administered to address imbalances or deficiencies.

    3. Medications: In some cases where surgery is not possible or is not immediately necessary, medical management may be used to control hypercalcemia. Medications like calcitonin and bisphosphonates may be prescribed to lower calcium levels temporarily.

  3. Dietary Management: A low-calcium diet may be recommended to help manage hypercalcemia in dogs with primary hyperparathyroidism. Consult with your veterinarian to determine the most appropriate diet for your dog's specific needs. The best diet for a dog with hyperparathyroidism may depend on the underlying cause and severity of the condition, so it's crucial to consult with a veterinarian for a tailored treatment plan. Some of the dietary considerations that may be relevant include:

    1. Prescription Diet: Your veterinarian may recommend a specific prescription diet formulated to manage hypercalcemia (high blood calcium levels) or hyperparathyroidism. These diets are designed to have controlled levels of calcium and phosphorus to help manage the condition.

    2. Low-Calcium Diet: In some cases, reducing dietary calcium intake can be beneficial. Commercial dog foods with lower calcium levels may be recommended, but it's essential to consult your vet for guidance on the appropriate calcium levels for your dog's specific needs.

    3. Home-Cooked Diet: In certain situations, a homemade diet prepared under the guidance of a veterinary nutritionist may be recommended. This allows for precise control over the calcium and phosphorus content in the dog's diet.

  4. Surgical Intervention/ Removal (Parathyroidectomy): It's important to note that primary hyperparathyroidism can sometimes be caused by a benign tumor (adenoma) or, less commonly, by a malignant tumor (carcinoma) within the parathyroid gland(s). The surgical approach may vary depending on the specific underlying cause. During the surgery, the veterinarian will locate and remove the enlarged or malfunctioning parathyroid gland(s). In some cases, all four parathyroid glands may need to be examined and evaluated.

    1. Preoperative Stabilization: Before surgery, your veterinarian may focus on stabilizing your dog's condition, especially if severe hypercalcemia is present. This may involve hospitalization, intravenous fluids and medications to correct dehydration and electrolyte imbalances to stabilize your dog's calcium levels and overall health.

    2. Surgery: During the procedure, the veterinarian will locate and remove the enlarged or abnormal parathyroid gland(s). In some cases, all four glands may need to be examined to ensure they are all healthy.

    3. Postoperative Care: After surgery, your dog will require careful monitoring and supportive care. This includes monitoring calcium levels to ensure they normalize after the surgery and the dog may need calcium supplementation or special diets to prevent post-surgical hypocalcemia (low calcium levels).

    4. Long-Term Management:  Following a successful parathyroidectomy, most dogs experience a rapid improvement in calcium levels. However, long-term monitoring is necessary to ensure that calcium levels remain within the normal range. Regular veterinary check-ups and blood tests will be required to assess calcium levels and overall health.

  5. Physical Therapy and Rehabilitation: Physical therapy exercises can help improve muscle strength and joint mobility in affected dogs. This can contribute to better overall mobility and quality of life.

  6. Supportive Care: Providing a comfortable environment for the dog is essential. This includes soft bedding and limiting strenuous activities that could put additional stress on the bones.

  7. Ongoing Monitoring:  Regular monitoring of calcium levels is crucial to assess the effectiveness of treatment and to adjust medications or diet as needed.

  8. Management of Complications: Primary hyperparathyroidism can lead to complications such as kidney stones and urinary tract infections. These complications may need separate treatments.


References

 

Milovancey M, Schmiedt C W (2013) Preoperative factors associated with postoperative hypocalcemia in dogs with primary hyperparathyroidism that underwent parathyroidectomy: 62 cases (2004-2009). JAVMA 242 (4), 507-515 PubMed


Arbaugh M, Smeak D, Monnet E (2012) Evaluation of preoperative serum calcium concentrations of ionized calcium and parathyroid hormone as predictors of hypocalcemia following parathyroidectomy in dogs with primary hyperparathyroidism: 17 cases (2001-2009). JAVMA 241 (2), 233-236 PubMed.


Feldman E C, Hoar B, Pollard R, Nelson R W (2005) Pretreatment clinical and laboratory findings in dogs with primary hyperparathyroidism: 210 cases (1987-2004). JAVMA 227 (5), 756-761 PubMed.


Long C D, Goldstein R E, Hornoff W J, Feldman E C, Nyland T G (1999) Percutaneous ultrasound-guided chemical parathyroid ablation for treatment of primary hyperparathyroidism in dogs. JAVMA 215 (2), 217-221 PubMed.


Torrance A G & Nachreiner R (1989) Human parathyroid assay for use in dog - validation, sample handling studies and parathyroid function testing. Am J Vet Res 50, 1123-1127.


Torrance A G & Nachreiner R (1989) Intact parathyroid assay and total calcium concentration in the diagnosis of disorders of calcium metabolism in dogs. JVIM 3, 86-89.

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