On the contrary, Toiler suggested that the breakdown of proliferating cells of the follicle after impeded eruption is likely to be the origin of the dentigerous cyst. The breakdown products may result in increased osmotic tension, resulting in cyst formation. The exact histogenesis of dentigerous cysts remains unknown, but most authors favor a developmental origin from the tooth follicle. In 1928, Bloch-Jorgensen suggested that the overlying necrotic deciduous tooth is the origin of all dentigerous cysts. The resultant periapical inflammation might spread to involve the follicle of the unerupted permanent successor, an inflammatory exudate ensued with resultant dentigerous cyst formation. He reported 22 cases of follicular cysts and stated that in each case a deciduous tooth or the remnants thereof was found in direct contact with the cyst cavity and that the related deciduous tooth always was diseased. Azaz and Shteyer similarly suggested that the persistent and prolonged periapical inflammation caused chronic irritation to the follicle of the successors. This may trigger and hasten the formation of a dentigerous cyst developing around the permanent teeth. They reported five cases of dentigerous cysts which involved the second mandibular premolar in four children aged 8 to 11 years old. These children were referred for extraction of carious, nonvital primary molars with swelling of the surrounding soft tissue. Occlusal radiographs showed buccal expansion of bone at the affected site. The primary teeth were not in direct contact with the underlying dentigerous cyst. It has been suggested that dentigerous cysts may be either extrafollicular or intrafollicular in origin.
Sarcosinemia (SAR), also called hypersarcosinemia and SARDH deficiency, is a rare autosomal recessive metabolic disorder characterized by an increased concentration of sarcosine in blood plasma and urine ("sarcosinuria"). It can result from an inborn error of sarcosine metabolism, or from severe folate deficiency related to the folate requirement for the conversion of sarcosine to glycine. It is thought to be a relatively benign condition. Cause
Sarcosinemia is thought to be caused by a mutation in the sarcosine dehydrogenase (SARDH) gene, which is located at human chromosome 9q34.The disease is inherited in an autosomal recessive manner, which means the defective gene responsible for the disorder is located on an autosome (chromosome 9 is an autosome), and two copies of the defective gene (one inherited from each parent) are required in order to be born with the disorder. The parents of an individual with an autosomal recessive disorder both carry one copy of the defective gene, but usually do not experience any signs or symptoms of the disorder. Diagnosis
Treatment
See also
Inborn errors of metabolism

References
External links
Sarcosinemia at NIHs Office of Rare Diseases