Patients who have recurrent intra-articular bodies or in whom the entire synovial lining is metaplastic require total synovectomy. References
Further reading
FletcherCDM, UnniKK, MertensF, editors. Pathology and genetics of tumours of soft tissue and bone. World Health Organization classification of tumours. Lyon: IARC Press, 2002. Bianchi S, Martinoli C (July 1999). "Detection of loose bodies in joints". Radiol. Clin. North Am. 37 (4): 679–90. doi:10.1016/S0033-8389(05)70123-8. PMID 10442075. Coles MJ, Tara HH (January 1997). "Synovial chondromatosis: a case study and brief review". Am. J. Orthop. 26 (1): 37–40. PMID 9021034. Crotty JM, Monu JU, Pope TL (March 1996). "Synovial osteochondromatosis". Radiol. Clin. North Am. 34 (2): 327–42, xi. PMID 8633119. Maurice H, Crone M, Watt I (1 November 1988). "Synovial chondromatosis". J Bone Joint Surg Br. 70 (5): 807–11. doi:10.1302/0301-620X.70B5.3192585. PMID 3192585. Milgram JW, Gilden JJ, Gilula LA (January 1996). "Multiple loose bodies: formation, revascularization, and resorption. A 29-year followup study". Clin. Orthop. Relat. Res. (322): 152–7. doi:10.1097/00003086-199601000-00019. PMID 8542691. S2CID 25265519. == External links ==
Familial hypocalciuric hypercalcemia (FHH) is an inherited condition that can cause hypercalcemia, a serum calcium level typically above 10.2 mg/dL; although uncommon. It is also known as familial benign hypocalciuric hypercalcemia (FBHH) where there is usually a family history of hypercalcemia which is mild, a urine calcium to creatinine ratio <0.01, and urine calcium <200 mg/day. Signs and symptoms
Most cases of familial hypocalciuric hypercalcemia are asymptomatic. Laboratory signs of FHH include:
High blood levels of calcium (hypercalcemia)
A low amount of calcium excreted in the urine (Ca excretion rate < 0.02 mmol/L)
High blood levels of magnesium (hypermagnesemia)
High normal to mildly elevated parathyroid hormone

Causes
Types include:

Pathogenesis
Most cases of FHH are associated with loss of function mutations in the calcium-sensing receptor (CaSR) gene, expressed in parathyroid and kidney tissue. These mutations decrease the receptors sensitivity to calcium, resulting in reduced receptor stimulation at normal serum calcium levels. As a result, inhibition of parathyroid hormone release does not occur until higher serum calcium levels are attained, creating a new equilibrium. This is the opposite of what happens with the CaSR sensitizer, cinacalcet. Functionally, parathyroid hormone (PTH) increases calcium resorption from the bone and increases phosphate excretion from the kidney which increases serum calcium and decreases serum phosphate. Individuals with FHH, however, typically have normal PTH levels, as normal calcium homeostasis is maintained, albeit at a higher equilibrium set point. As a consequence, these individuals are not at increased risk of the complications of hyperparathyroidism.Another form has been associated with chromosome 3q.