JordanAng420
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The term, METABOLIC BONE DISEASE is NOT actually a single disease but rather a term used to describe a collection of medical disorders that affect the integrity and function of bones. In an effort to maintain purity in medical description, the terms metabolic bone disease and MBD should NOT be used to describe diseases of reptiles unless accompanied by a qualifier such as "nutritional" or "renal."
To speak quite frankly, i'm tired of seeing this this term being thrown around like it's one big giant disease. There are a COLLECTION of different kinds of metabolic bone diseases. Four of the most common I describe below.
Nutritional Secondary Hyperparathyroidism. (NSHP) (Most Common MBD)
Rubbery limbs and a thin flexible jaw are often the symptoms first shown in animals that have NSHP. This occurs as a result of dietary or husbandry mismanagement. The most common reasons this happens is due to prolonged lack of vitamin d3 or inadequate exposure to UV lights. The main focus on treatment for NSHP is to correct husbandry and nutritional problems, and provide exposure to natural sunlight. However, this often is not enough. In severe cases, treatment goals should include reversing bone loss and promoting new bone production. The overactive parathyroid gland must be reversed. Calcitonin lowers circulating calcium and phosphorus through negative feedback on the gland, thus ceasing the production of parahormone and promoting bone production.
Renal Secondary Hyperparathyroidism (RSHP)
Extremely high phosphate levels are usually associated with RSHP, a consequence of renal disease. The high levels are associated with reduced calcitrol levels, soft tissue calcification, and hypocalcemia. Phosphorus is absorbed from the GI tract and eliminated via the kidneys. In renal failure, decreasing filtration rate leads to phos. retention and high phosphorus levels.
Hypertrophic Osteopathy (HO)
Although not common, HO has been reported in lizards. It is charaterized by lameness, painful limbs, and reluctance to move. In mammals, once HO has been diagnosed HO is usually terminal. The cause is unknown, but theories include chronic lack of oxygen, toxins, and neurologic pathways involving the vagus nerve.
Osteopetrosis
Two forms of this disease exist. One is an autosomal recessive and the other is an autosomal dominant, both cause exvessive thickening of the bones. The bones become radiographically dense, eventually wiping out the entire marrow cavity. The cause is not known, but is believed to be an inabitlity to resorb bone in a normal fashion. Because the narrow cavity is destroyed, patients become anemic. Never sensation in the skull becomes diminished, which leads to blindness and hearing impairments. The bones become brittle and fracture easily.
So, as mentioned, the term MBD is not just a single entity but rather a complex assortment of the pathology that affects the integrity and function of the bones.
To speak quite frankly, i'm tired of seeing this this term being thrown around like it's one big giant disease. There are a COLLECTION of different kinds of metabolic bone diseases. Four of the most common I describe below.
Nutritional Secondary Hyperparathyroidism. (NSHP) (Most Common MBD)
Rubbery limbs and a thin flexible jaw are often the symptoms first shown in animals that have NSHP. This occurs as a result of dietary or husbandry mismanagement. The most common reasons this happens is due to prolonged lack of vitamin d3 or inadequate exposure to UV lights. The main focus on treatment for NSHP is to correct husbandry and nutritional problems, and provide exposure to natural sunlight. However, this often is not enough. In severe cases, treatment goals should include reversing bone loss and promoting new bone production. The overactive parathyroid gland must be reversed. Calcitonin lowers circulating calcium and phosphorus through negative feedback on the gland, thus ceasing the production of parahormone and promoting bone production.
Renal Secondary Hyperparathyroidism (RSHP)
Extremely high phosphate levels are usually associated with RSHP, a consequence of renal disease. The high levels are associated with reduced calcitrol levels, soft tissue calcification, and hypocalcemia. Phosphorus is absorbed from the GI tract and eliminated via the kidneys. In renal failure, decreasing filtration rate leads to phos. retention and high phosphorus levels.
Hypertrophic Osteopathy (HO)
Although not common, HO has been reported in lizards. It is charaterized by lameness, painful limbs, and reluctance to move. In mammals, once HO has been diagnosed HO is usually terminal. The cause is unknown, but theories include chronic lack of oxygen, toxins, and neurologic pathways involving the vagus nerve.
Osteopetrosis
Two forms of this disease exist. One is an autosomal recessive and the other is an autosomal dominant, both cause exvessive thickening of the bones. The bones become radiographically dense, eventually wiping out the entire marrow cavity. The cause is not known, but is believed to be an inabitlity to resorb bone in a normal fashion. Because the narrow cavity is destroyed, patients become anemic. Never sensation in the skull becomes diminished, which leads to blindness and hearing impairments. The bones become brittle and fracture easily.
So, as mentioned, the term MBD is not just a single entity but rather a complex assortment of the pathology that affects the integrity and function of the bones.
