Talon cusp is a rare dental anomaly resulting in an extra cusp or cusp-like projection on an anterior tooth, located on the inside surface of the affected tooth. Sometimes it can also be found on the facial surface of the anterior tooth.The term talon cusp refers to the same condition as dens evaginatus; however, talon cusp is more specifically the manifestation of dens evaginatus on the anterior teeth. Talon cusp can be simply defined as hyperplasia of the cingulum of an anterior tooth. Although talon cusp may not appear serious, and in some people may be completely benign, it can cause clinical, diagnostic and functional problems, and alters the appearance of a persons teeth. The condition was first described by W.H. Mitchell in 1982 and named by J. Kimball Mellor B.S., D.D.S. and Louis W. Ripa, D.D.S., M.S. due to its similar appearance to an eagles talon. Some sources define a talon cusp as an extra cusp which extends at least half the distance between the cementoenamel junction and the incisal edge of the tooth. Other sources classify all enlarged cingula as talon cusps, and classify them according to the degree of enlargement.The incidence of talon cusp has been found to range from 1% to 6% of the population. Talon cusp tends to occur on permanent teeth only, being very rare in deciduous teeth. In most cases, the involved teeth are the permanent maxillary lateral incisors (55%), followed by maxillary central incisors (33%), mandibular incisors (6%), and maxillary canines (4%).
Risk factors
Many different risk factors play a role in causing a neonatal stroke. Some maternal disorders that may contribute to neonatal strokes include: autoimmune disorders, coagulation disorders, prenatal cocaine exposure, infection, congenital heart disease, diabetes, and trauma. Placental disorders that increase the risk of stroke include placental thrombosis, placental abruption, placental infection, and chorioamnionitis. Other disorders that may increase the risk of a neonatal stroke are blood, homocysteine and lipid disorders, such as polycythemia, disseminated intravascular coagulopathy, prothrombin mutation, lipoprotein (a) deficiency, factor VIII deficiency (hemophilia A), and factor V Leiden mutation. Infectious disorders such as central nervous system (CNS) infection or systemic infection may also contribute.Many infants who have a neonatal stroke also follow an uncomplicated pregnancy and delivery without identifiable risk factors, which exemplifies the necessity for further research on this subject. Mechanism
A neonatal stroke in the developing brain involves excitotoxicity, oxidative stress, and inflammation, which accelerate cell death through necrosis or apoptosis, depending on the region of the brain and severity of stroke. The pathophysiology of neonatal stroke may include thrombosis and thrombolysis, and  vascular reactivity. Apoptosis mechanisms may have a more prominent role in developing an ischemic brain injury in neonatal humans than in adult brain ischemia, as a majority of cells die in the environment where edema developed after a neonatal stroke. There is an increased inflammatory response after hypoxia-ischemia, which corresponds to extensive neuronal apoptosis. Apoptosis involves the mitochondrial release of cytochrome c and apoptosis-inducing factor (AIF), which activate caspase-dependent and –independent execution pathways, respectively.