Osteitis fibrosa cystica is the result of unchecked hyperparathyroidism, or the overactivity of the parathyroid glands, which results in an overproduction of parathyroid hormone (PTH).
PTH causes the release of calcium from the bones into the blood, and the reabsorption of calcium in the kidney.
Thus, excess PTH in hyperparathyroidism causes elevated blood calcium levels, or hypercalcemia.

There are four major causes of primary hyperparathyroidism that result in OFC:
Parathyroid adenoma
The vast majority of cases of hyperparathyroidism are the result of the random formation of benign, but metabolically active, parathyroid adenoma swellings.
These instances comprise approximately 80–85% of all documented cases of hyperparathyroidism.

Hereditary factors
Approximately 1 in 10 documented cases of hyperparathyroidism are a result of hereditary factors.
Disorders such as familial hyperparathyroidism, multiple endocrine neoplasia type 1 (MEN Type 1) and hyperparathyroidism-jaw tumor syndrome can, if left unchecked, result in OFC.
MEN Type 1 is an autosomal dominant disorder and the most common hereditary form of hyperparathyroidism, affecting about 95% of genetic cases of OFC, and also tends to affect younger patients than other forms.
Major mutations which can lead to hyperparathyroidism generally involve the parathyroid hormone receptor, G proteins, or adenylate cyclase.
 Certain genetic mutations have been linked to a higher rate of parathyroid carcinoma occurrence, specifically mutations to the gene HRPT2, which codes for the protein parafibromin.

Parathyroid carcinoma
Parathyroid carcinoma (cancer of the parathyroid gland) is the rarest cause of OFC, accounting for about 0.5% of all cases of hyperparathyroidism.
OFC onset by parathyroid carcinoma is difficult to diagnose.

Renal complications
OFC is a common presentation of renal osteodystrophy, which is a term used to refer to the skeletal complications of  end stage renal disease (ESRD).
OFC occurs in approximately 50% of patients with ESRD.
 ESRD occurs when the kidneys fail to produce calcitriol, a form of Vitamin D, which assists in the absorption of calcium into the bones.
When calcitriol levels decrease, parathyroid hormone levels increase, halting the storage of calcium, and instead triggering its removal from the bones.
The concept of renal osteodystrophy is currently included into the broader term chronic kidney disease-mineral and bone disorder (CKD-MBD).

Fluoride intoxication
OFC was noticed in the early years of community fluoridation to be at higher risk when water supplies were fluoridated.
Indeed, death rates which in some cases were gruesomely dramatic during dialysis quickly brought attention to the fact that fluoride in water during dialysis was a health hazard.
Modern dialysis takes pains to de-fluoridate water in order to minimize bone disease including OFC.
The 2006 National Research Council confirmed kidney patients are a sub-population particularly susceptible to ill effects from fluoride exposure which manifest in bones.
  
fanconi syndrome, : decrease aminoacids, phosphate, glucose, bicarbonate and potasum salts.
Osteitis fibrosa cystica is the result of unchecked hyperparathyroidism, or the overactivity of the parathyroid glands, which results in an overproduction of parathyroid hormone (PTH). PTH causes the release of calcium from the bones into the blood, and the reabsorption of calcium in the kidney. Thus, excess PTH in hyperparathyroidism causes elevated blood calcium levels, or hypercalcemia.
There are four major causes of primary hyperparathyroidism that result in OFC:
Parathyroid adenoma
The vast majority of cases of hyperparathyroidism are the result of the random formation of benign, but metabolically active, parathyroid adenoma swellings. These instances comprise approximately 80–85% of all documented cases of hyperparathyroidism.
Hereditary factors
Approximately 1 in 10 documented cases of hyperparathyroidism are a result of hereditary factors. Disorders such as familial hyperparathyroidism, multiple endocrine neoplasia type 1 (MEN Type 1) and hyperparathyroidism-jaw tumor syndrome can, if left unchecked, result in OFC. MEN Type 1 is an autosomal dominant disorder and the most common hereditary form of hyperparathyroidism, affecting about 95% of genetic cases of OFC, and also tends to affect younger patients than other forms. Major mutations which can lead to hyperparathyroidism generally involve the parathyroid hormone receptor, G proteins, or adenylate cyclase.  Certain genetic mutations have been linked to a higher rate of parathyroid carcinoma occurrence, specifically mutations to the gene HRPT2, which codes for the protein parafibromin.
Parathyroid carcinoma
Parathyroid carcinoma (cancer of the parathyroid gland) is the rarest cause of OFC, accounting for about 0.5% of all cases of hyperparathyroidism. OFC onset by parathyroid carcinoma is difficult to diagnose.
Renal complications
OFC is a common presentation of renal osteodystrophy, which is a term used to refer to the skeletal complications of  end stage renal disease (ESRD). OFC occurs in approximately 50% of patients with ESRD.  ESRD occurs when the kidneys fail to produce calcitriol, a form of Vitamin D, which assists in the absorption of calcium into the bones. When calcitriol levels decrease, parathyroid hormone levels increase, halting the storage of calcium, and instead triggering its removal from the bones. The concept of renal osteodystrophy is currently included into the broader term chronic kidney disease-mineral and bone disorder (CKD-MBD).
Fluoride intoxication
OFC was noticed in the early years of community fluoridation to be at higher risk when water supplies were fluoridated. Indeed, death rates which in some cases were gruesomely dramatic during dialysis quickly brought attention to the fact that fluoride in water during dialysis was a health hazard. Modern dialysis takes pains to de-fluoridate water in order to minimize bone disease including OFC. The 2006 National Research Council confirmed kidney patients are a sub-population particularly susceptible to ill effects from fluoride exposure which manifest in bones.   
fanconi syndrome, : decrease aminoacids, phosphate, glucose, bicarbonate and potasum salts.
Osteitis fibrosa cystica