A person belonging to one of these particular demographics or one who has any of these deformities or syndromes may have a higher risk of having a talon cusp. Mechanism
The exact mechanism of the formation of dens evaginatus and talon cusp is unknown. It has been suggested that the anomaly is caused by an evagination. The formation of the "cusp" is due to excess layering of the internal enamel epithelium and dental papilla into the stellate reticulum. This occurs during the morphological differentiation stage of tooth development. During the developmental stages of tooth formation, certain dental follicle cells were differentiated incorrectly which formed the excess enamel and incorrect morphology of the affected tooth. Talon cusp can progress into severe dental problems if the severity of the cusp affects the persons hygiene and oral functions. Talon cusp may occur on its own or associated with other dental anomalies such as mesiodens, odontome, unerupted or impacted teeth, peg-shaped maxillary incisor, dens invaginatus, cleft lip, bilateral gemination, fusion, and supernumerary teeth. Diagnosis
This anomaly is large enough to be seen with the naked eye. One can see the projection on the incisal edge of a tooth looking into the mouth of the affected person. The structure is described to be "Tshaped" or "X-shaped" however will differ depending on its shape, size, structure, location and site of origin. X-rays and radiographs can also show evidence of the abnormality.
Glucocorticoid deficiency 1  is an adrenocortical failure characterized by low levels of plasma cortisol produced by the adrenal gland despite high levels of plasma ACTH. This is an inherited disorder with several different causes which define the type.FGD type 1 (FGD1 or GCCD1) is caused by mutations in the ACTH receptor (melanocortin 2 receptor; MC2R). FGD type 2 is caused by mutations in the MC2R accessory protein (MRAP). These two types account for 45% of all cases of FGD.Some cases of FGD type 3 are caused by mutations in the steroidogenic acute regulatory protein (StAR), with similarity to the nonclassic form of lipoid congenital adrenal hyperplasia. In this case, a general impairment in not just adrenal steroid production, but gonadal steroid production can affect sexual development and fertility. The causes of other cases of FGD type 3 not due to StAR are currently unknown. References
External links
GCCD1 Online Mendelian Inheritance in Man (OMIM): 202200
GCCD2 Online Mendelian Inheritance in Man (OMIM): 607398
GCCD3 Online Mendelian Inheritance in Man (OMIM): 609197