Aspirational biopsy of odontogenic keratocysts contains a greasy fluid which is pale in colour and contains keratotic squames. Protein content of cyst fluid below 4g% is diagnostic of odontogenic keratocysts. Smaller and unilocular lesions resembling other types of cysts may require a biopsy to confirm the diagnosis. On a CT scan, the radiodensity of a keratocystic odontogenic tumour is about 30 Hounsfield units, which is about the same as ameloblastomas. However, ameloblastomas show more bone expansion and seldom show high density areas.Radiographs of odontogenic keratocysts show well-defined radiolucent areas with rounded or scalloped margins which are well demarcated. These areas can be multilocular or unilocular. The growth pattern of the lesion is very characteristic from which a diagnosis can be made as there is growth and spread both forward and backward along the medullary cavity with little expansion. No resorption of teeth or inferior dental canal and minimal displacement of teeth is seen. Due to lack of expansion of the odontogenic keratocyst, the lesion can be very large when radiographically discovered. Differential diagnosis
Radiologically

Odontogenic myxoma
Ameloblastoma
Central giant-cell granuloma
Adenomatoid odontogenic tumor
Dentigerous cyst (follicular cyst)Histologically

Orthokeratocyst
Radicular cyst (particularly if the OKC is very inflamed)
Ameloblastoma

Histology
Odontogenic keratocysts have a diagnostic histological appearance. Under the microscope, OKCs vaguely resemble keratinized squamous epithelium; however, they lack rete ridges and often have an artifactual separation from their basement membrane.The fibrous wall of the cyst is usually thin and uninflamed.
Autosomal dominant hypophosphatemic rickets (ADHR) is a rare hereditary disease in which excessive loss of phosphate in the urine leads to poorly formed bones (rickets), bone pain, and tooth abscesses. ADHR is caused by a mutation in the fibroblast growth factor 23 (FGF23). ADHR affects men and women equally; symptoms may become apparent at any point from childhood through early adulthood. Blood tests reveal low levels of phosphate (hypophosphatemia) and inappropriately normal levels of vitamin D. Occasionally, hypophosphatemia may improve over time as urine losses of phosphate partially correct.ADHR may be lumped in with X-linked hypophosphatemia under general terms such as hypophosphatemic rickets. Hypophosphatemic rickets are associated with at least nine other genetic mutations. Clinical management of hypophosphatemic rickets may differ depending on the specific mutations associated with an individual case, but treatments are aimed at raising phosphate levels to promote normal bone formation. References
Further reading
"Hereditary hypophosphatemic rickets". Genetics Home Reference. September 2010. Archived from the original on 17 September 2012. Retrieved 10 October 2012. "Hypophosphatemic Rickets". The Merck Manual Home Health Handbook. Merck Sharp & Dohme Corp. December 2006. Archived from the original on 13 October 2012. Retrieved 10 October 2012. == External links ==