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Enamel spindles are "short, linear defects, found at the dentinoenamel junction (DEJ) and extend into the enamel, often being more prevalent at the cusp tips." [ 1 ] The DEJ is the interface of the enamel and the underlying dentin .
Enamel tufts are small branching defects that are found only at the DEJ, and so differ from lamellae which can be facing either direction and are strictly linear. Enamel spindles are also linear defects, but they too can be found only at the DEJ, because they are formed by entrapment of odontoblast processes between ameloblasts prior to and ...
Enamel tufts should also not be confused with the similar enamel spindles. Enamel spindles are also linear defects, similar to lamellae, but they too can be found only at the dentinoenamel junction, similar to enamel tufts. This is because they are formed by entrapment of odontoblast processes between ameloblasts prior to and during amelogenesis.
Enamel hypocalcification is a defect of tooth enamel in which normal amounts of enamel are produced but are hypomineralized. [ 1 ] [ 2 ] In this defect the enamel is softer than normal. Some areas in enamel are hypocalcified: enamel spindles, enamel tufts, and enamel lamellae.
Metal can scratch or damage the enamel finish, leading to more damage. Soft silicone is always better for scraping stuck-on food; you won’t risk damaging the finish.
Produced during the second stage of enamel calcification, also known as the maturation stage, ameloblasts produce matrix and enamel at the rate of 4 micrometers per day; however every fourth day there is a change in development. Brownish lines, the striae of Retzius, develop as a result of a change in the growth process.
The dentinoenamel junction or dentin-enamel junction (DEJ) [1] is the boundary between the enamel and the underlying dentin that form the solid architecture of a tooth. It is also known as the amelo - dentinal junction, [ 2 ] or ADJ.
In primates enamel spindles were observed where the odontoblast process reaches until the border between dentin and enamel. With the discovery of TRPC5 as cold transducer the odontoblast transduction theory has become a likely explanation of dentinal hypersensivity [ 6 ]
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