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Enamel is considered the hardest tissue in the body, being of epithelial origin it acts as a protective covering for the teeth. The cells responsible for the formation are lost as the tooth erupts into the oral cavity. So the regenerating properties of enamel are almost none. To compensate for this inert limitation, enamel has acquired a very high degree of mineralization rendered possible by the almost total absence of organic matrix in its mature state. All these characteristics reflect the unusual life cycle of enamel forming ameloblasts and the unique physiochemical characteristics of the matrix proteins that regulate the formation of its long crystals.
Enamel specifically evolved to serve as an abrasion resistant, protective coating for blocks of dentine projecting into the oral cavity as crowns of teeth. This specified purpose may also explain the unique gross structure and chemical composition of the tooth. It also explains that why there are no live processes and cells present at the end when the maturation finishes making it the only tissue which can not repair it self.
The structure of tooth has always been a topic of interest for the dental professionals. The latest clinical practice of dentistry inclines us towards the preservation of the tooth. It involves the promotion of enamel remineralization, the restoration of carious enamel where the mineralization of the tooth can not be restores, the bleaching of discolored teeth, the diagnosis and treatment of developmental enamel malformations, which can be caused by environmental or genetic factors.
Dental surgeons' everyday makes decisions about the diagnosis and treatment plans influenced by their understanding of the structure of the tooth and their clinical competence. A systemic disease such as a high fever can produce a pattern of enamel defects in the dentition. The knowledge of the diagnostician about the sequence and timing of teeth eruption can influence the clinical out come of the teeth. The process of enamel maturation continues after the eruption of the teeth so that erupted teeth can become less susceptible to decay over time.
Enamel Structure :
Tooth enamel is a very unique tissue because of its high mineral content. Enamel is made of tightly packed crystallites that make up for 87 percent of its volume and 95 percent of its weight. As compared to other mineralized tissues which are about 20 percent organic in nature the enamel has less than 1 percent organic matter. Enamel crystallites contain more than one thousand times the volume of corresponding crystals in bone, dentine and cementum. Enamel crystals are extremely long relative to their thickness and are highly oriented. They extend from the underlying dentine towards the surface of the tooth and are organized into bundles, called prism. The organization and mineralization give dental enamel its unique physical properties, making it the hardest tissue in the body. Despite the hard structure the tooth can be easily destroyed by the carious process.
The mineral process taking place in the enamel is closely related to that of calcium hydro apatite [Ca10 (PO4)6(OH) 2], but contains many impurities, such as carbonates substitute for phosphate in the crystal lattice. Calcium hydoxapatite can be prepared in the lab as well but it is always different from those of dental enamel.
Stages of Enamel Formation :
Enamel formation or amelogenesis occurs in stages in a well delineated extracellular compartment. Dentine and enamel formation take place simultaneously, and both processes start along a line that will become the dentino enamel junction, or DEJ. On the side of the enamel, the crystals enlarge into long thin ribbons. The ribbons are evenly spaced, oriented parallel to each other, and extend from the DEJ to the mineralization front just outside the membrane of ameloblasts. As the enamel proteins are secreted, the crystallites continue to grow in length but very little in width and thickness. The final length of enamel is determined by how long the ameloblasts continue to add the enamel proteins, which also determines the final thickness of the enamel layer as a whole. Any disturbance in this process can affect the thickness or length of the enamel formed at the end.
After the secretion according to genetic programming the ameloblasts undergo massive change that reduces their secretion of enamel proteins. Instead of the structural proteins, proteinases are secreted, and the organic matrix is degraded and disappears from the extracellular compartment. These changes cause the growth of enamel crystallites to stop specially in length and cause acceleration in the growth of thickness and width. Crystal elongation is arrested by curbing the secretion of enamel matrix constituents such as amelogenin, ameloblastin, and enamelin.
Mineral deposition on the sides of the crystallites increases, in part, because of the degradation and removal of growth- inhibiting enamel protein cleavage products. In humans, the maturation stage, during which the crystallites grow in thickness, takes about 3 to 4 years to complete. This process is really important to complete the hardness of the enamel. Fluoride is incorporated in to the enamel during the maturation process. Any disturbance during this process leads to massive changes in the thickness of enamel leading to the pathologically soft enamel (hypo mineralized enamel).
Embryonic Formation Of Enamel:
During the embryonic development, the cells covering the cranial neural crest start its proliferation into the underlying connective tissue and move into the maxillary and mandibular prominences. These cells share the same qualities as the epithelial and connective tissues and are commonly referred to "ectomesenchyme." The deciduous tooth initiation occurs at 20 different sites along the maxillary and mandibular processes. At each site, the oral epithelium thickens as the underling neural crest derived ectomesenchyme condenses beneath it (Chai Y, et al, 2000).
The interaction between these two cells leads to the formation of 2 different and opposite line of columnar cells namely the ameloblasts and odontoblasts. The extracellular space in between these cells is the site for the formation and development of the teeth. Dentine is formed by odontoblasts and the ameloblasts are responsible for the formation of enamel. The cells in these spaces are connected by intercellular junctions. So the development of the cells takes place mainly in the extracellular space created by these cells. The cells lining it also determine the content of this space that is the ameloblasts on one side and the odontoblasts on the other.
Formation Of Dentino Enamel Junction:
Odontoblasts initiate the secretion of an extracellular matrix. Odontoblasts secrete a predentin matrix that contains mostly type I collagen. The collagen molecules assemble into cables that are primary oriented so that they extend outward towards the ameloblasts. An assortment of noncollagenous proteins are also secreted, the most abundant being dentine or DSPP. During the formation of the DEJ, DSPP is secreted by both ameloblasts and odontoblasts (Bronckers AL, et al)
Highly charged, non collagenous proteins are thought to bind collagen and form crystal nucleation centers, while hydrophilic glycosaminoglycans such as decorin and biglycan draw away water molecules, potentially concentrating mineral ions at the nucleation centers. (Boskey AL., Linde A, Goldberg,. 1991)
Prior to the onset of biomineralization, preameloblasts secrete enamel proteins on top of the predentin matrix (Inai T, et al. 1991). Some if the enamel proteins penetrate the predentin and are absorbed by odontoblasts. Immediately following the initial secretion of enamel proteins, the ameloblast basement membrane disappears, and ameloblasts cell processes extend into irregularities on the predentin surface (Ronnholm E 1962).
Enamel crystallites are initiated within these irregularities, in close proximity to both the ameloblast cell membrane and collagen fibres protruding from the predentin. The ameloblastic processes appear to retreat back to the cell body, extending the incipient enamel crystallites as they go. This fills in the irregular surface of dentin with enamel crystallites and converts it into the smooth, undulating surface of aprismatic enamel which is perforated by odontoblastic processes. (Fejerskov O, Thylstrup; 1986).
In the erupted tooth, odontoblastic processes that extend into the enamel layer are known as enamel spindles. These processes presumably act as receptors that detect changes in the enamel layer and potentially covey sensitivity. Dentin and enamel are intimately linked at the dentino-enamel junction. The collagen based organic matrix gives dentin its tensile strength and flexibility, and allows it to cushion the more brittle enamel covering.
Enamel Formation During the Secretory Stage:
Secretory ameloblasts are tall, columnar cells with a proximally polarizes nucleus and proximal and distal cell-cell junctions. After depositing the aprismatic enamel layer, secretory ameloblasts develop a specialized cone shaped Tomes process at their secretory ends.( Reith EJ, Boyd A. ;1978) .Mineral deposition occurs primarily at a mineralization front very near to the ameloblast cell membrane. Enamel crystallites extend in length at extracellular growth sites a short distance away from the secretory faces of the ameloblast cell membrane, in what appears to be a matrix comprised of assemblies of enamel matrix proteins (Ronnholm E.; 1962). Because the mineralization front occurs close to the protruding Tomes process the surface of developing enamel is indented (Fejersjov O, Thylstrup A.; 1986).
The Tomes process organize enamel crystals into rod and interred enamel.(Reith EJ, Boyde A 1973) Enamel crystallites that elongate near the tip of the Tomes process form the rod enamel. Crystallites that lengthen near the intercellular junctions form the interrod enamel is distinct because part of the ameloblast membrane is "nonsecretory" which creates gaps in the mineralization front (Hu C-C et al 1997) The rod enamel and interrod enamel differ solely in the orientation of their crystallites, and the border between these two regions of an enamel prism is indistinguishable where the mineralization front is uninterrupted.
During the secretory stage, enamel crystals do not grow continuously but rather extend in increments. Each increment represents the amount of crystal elongation that occurs in a single day, and is manifested structurally as prism cross- striations. More prominent cross striations occur in a regular period of about every nine days and are known as straie of Retzius or incremental lines (Shelis RP. Dean MC; 1998). The straie of Retzius terminate at the enamel surface at the edge of tiny steps known as perikymata. The amount of enamel deposited in a given day may vary according to systemic factors and can lead to destructive pattern of incremental lines that are faithfully reproduced in the enamel of all the teeth forming at a given time (Boyde A.; 1989).
At birth when the baby is dethatched from the umbilical cord of the mother the infant must establish its own system of diurnal rhythms. At the time of Birth there is a prominent incremental line present on the tooth known as the neonatal line, which may be associated with increased caries susceptibility.
Enamel Formation During the Maturation Stage:
During the maturation stage, in order to replace the lost organic matrix, the enamel crystallites grow in width and thickness, causing the layer to harden. Almost the entire enamel layer is deposited during the maturation stage. The ameloblast incorporate calcium, phosphate and bicarbonate ions into the matrix and remove water. The bicarbonate is responsible for the formation of carbonic anhydrase II, which is expressed by ameloblasts, starting in the transition stage. During the maturation stage the PH of the fluid around the enamel crystals fluctuates from less than 6 to 7.2. These changes are similar to those experienced naturally, after eruption in the oral cavity. The developing enamel crystals are not homogenous. Those crystals which are more susceptible to acid dissolution are selectively removed during the low ph cycle. So during this stage the low resistant mineral is replaced by highly resistant apatite. This process also takes place in the oral cavity after the eruption, so the enamel becomes more caries resistant over time.
In some dental procedures, the crown becomes exposed in the oral cavity before time. This happens, for instance, when an unerupted third molar with open root apices is transplanted into the socket of an extracted first molar. Such a tooth due to the incomplete state of enamel maturation, and should be treated with fluoride and sealant as soon as possible after the transplantation procedure. At the end of the maturation stage, about 90 percent of the enamel volume is mineral, which contains less than 1 percent residual protein. Vital bleaching is a popular esthetic treatment that uses high concentrations of peroxide to remove extrinsic stains (Mokhlis GR, et al. 2000) and which may also remove residual organic material from superficial enamel. Despite this, vital bleaching has not been associated with the development of structural weaknesses in the enamel. This shows that the degradation product retained in the finished enamel do not contribute significantly to enamel's structural properties.
Ameloblasts continuously secrete enamel proteins, starting just before the onset of dentin biomineralization and continue until the end of the secretory stage. The three major structural proteins are amelogenin (80-90 percent of enamel protein), ameloblastin (5- 10 percent), and enamelin (1-5 percent). These proteins are secreted at the mineralization front where they appear to form assemblies responsible for incremental increases in the lengths of existing crystallites.
Effect of Clinical Practice On Enamel Surface:
As enamel is the outer most layer of the tooth and is contact with the oral cavity, itââ‚¬â„¢s the first layer which is directly affected by any procedure done on it whether it is cavity preparation, bleaching, scaling or any orthodontic treatment. The layer of enamel is very brittle but it is affected. This should be kept in mind while performing any procedure. The strength and hardness is greatly affected.
Effect of Etching, Micro abrasion and Bleaching on Enamel:
Some enamel defects, such as opacities' and discolorations can adversely effect the color and translucency of enamel. These defects are mostly intrinsic in nature, resulting from incorporation of pigmented materials into the dental tissues (Eisenberg and Bernick, 1975).
The ingestion of tetracycline during the mineralization phase of odontogenesis can result in its deposition at the mineralizing front and lead to a yellow or grayish-brown discoloration of the tooth (Beckelman and Gingold, 1964; Bevelander and Nakahara, 1966; Mello, 1967; Arens et al., 1972). Fluorosis, which occurs when excessive amounts of fluoride are ingested during amelogenesis (Black and McKay, 1916), is a common cause of opacities in enamel. A high concentration of fluoride is believed to cause a disturbance in the metabolism of the ameloblasts, which results in either a defective matrix or an impairment of the maturation process. Fluorosed enamel, depending upon the severity, exhibits a brown pigmentation, white opaque spots, or pitting.
The degree to which bleaching techniques are successful in the treatment of different types of discoloration is dependent upon a number of inter-related variables, such as the severity (Bailey and Christen, 1968; Colon, 1971; Jordan and Boksman, 1984), location (Arens et al., 1972; Jordan and Boksman, 1984), color (Bailey and Christen, 1968; Colon, 1971; Arens et al., 1972; Christensen, 1978; Jordan and Boksman, 1984; Seale and Thrash, 1985), and depth (Bailey and Christen, 1968; Christensen, 1978; Seale and Thrash, 1985) of the discoloration, the number and duration of bleaching sessions (Bailey and Christen, 1968; Seale and Thrash, 1985), and the age of the subject (Seale and Thrash, 1985).
The conservative techniques to improve the appearance of discolored teeth have become popular in the past decade. These include in office bleaching with 30% hydrogen peroxide, home bleaching with a mild form of peroxide such as carbamide 10 % and enamel micro abrasion with 18% hydrochloric acid. There is a severe loss of enamel when these procedures are being conducted on the enamel surface causing massive decrease in the strength and hardness of the enamel. According to the test conducted on the extracted teeth the teeth treated with 37% phosphoric acid showed a loss of enamel of 5.7 plus minus 1.8 Um. Those with 30 % hydrogen peroxide showed loss of 5.3 plus minus 1.6 um. A direct application of hydrochloride for 100 seconds causes a loss of 100 plus minus 47 um.
According to the tests done by LSM. Tong et al. on extracted teeth with all the acids and bleaching agents there was evidence of enamel loss after the treatment. The different measurements of enamel loss have been recorded and have been given in the table.
Amount of Enamel Loss After Treatment With Different Acids & Bleaching Agents:
5 sec 18% HCL Pumice Abrasion(10 times)
160 plus minus 33
5 sec 18% HCL Pumice Abrasion (20 times)
360 plus minus 130
100 sec Direct 18% HCL
100 plus minus 47
30 sec Etching with 37% Phosphoric Acid
5.7 plus minus 1.8
30 min Direct Application 30% Hydrogen Per oxide under bleaching light
30 sec Etching 37% Phosphoric Acid Direct App of 30 % Hydrogen per oxide under bleaching light
5.3 plus minus 1.6
Effect of Bracket Bonding and Debonding on Enamel Surface :
When orthodontic treatment is being conducted on a patient a major concern is to avoid cohesive failures in the enamel during debonding brackets and at the same time obtain tooth surface without the adhesive. The bonding and removal of brackets from the tooth surface causes severe damage to the surface in form of cracks, scarring, scratches, or loss of enamel. The problem in adhesion of orthodontic brackets is that it should be strong enough to prevent failure during all treatment but at the same time should also be low enough so as to cause minimum damage to the enamel surface during bracket removal.
Debonding forces can be influenced by many factors
Type of enamel conditioning agents (Phosphoric acid, Self etching primers, Poly acrylic) (Shinya et al; 2008)
Bracket base architecture(Ireland AJ et al ;2005)(Ozcan M et al; 1993)
Usually when there is an increase in the debonding force there is an increase in the risk of enamel damage (Ostman-Anderson E et al; 1993). Depending upon the thickness of the enamel surface the loss of enamel is variable depending upon the type of tooth. When we remove the remnants of adhesive material from the enamel surface there is further loss of enamel from the tooth because of use of pliers. Although there is no concrete evidence but the best method used to remove the bracket is with carbide bur. There is a loss of calcium from the surface causing dental erosion, which is a loss of dental hard tissue.
The irregularities are caused on the enamel surface by use of these burs and drills. An estimated measurement of 10.7 to 30 um of enamel loss has been observed. This causes large amount of plaque accumulation causing increase risk of dental caries or gingivitis depending upon the location. There are several tests done on the enamel surface and effects on the surface due to the bracket bonding. The conclusions extracted from the tests done by Huib Berghauser Pont , Mutlu Ozcan, Bora Bagis and Yijin Ren ( Huib et al: American dental Journal ) on the enamel surface and its effects on the enamel surface the following conclusions were made
With the adhesive materials and bonding protocol used, after debonding metal brackets, mainly adhesive failures between the adhesive resin and bracket bases were observed (Score of 3which means the surface was all rough and deep pits and coarse scratches were found and no perkiymata) and they were more frequently in the maxillary anterior teeth.
The highest surface damage and loss of enamel was observed at the score 3 in the central incisors with the lowest percentage of score 0 in the first molars.
The maxillary teeth show more calcium loss as compared to the mandibular teeth.
Effect of Scaling on the Enamel Surface:
The scaling also presents as a procedure which causes effect on the surface of enamel. Both types of scaling the manual and the ultrasonic cause its negative effect on the surface of enamel. There is a loss of enamel surface when the scaling is performed that is why the patients can feel sensitivity in their teeth , because the dentinal tubules have been exposed after the surface layer is removed by the procedure. Thus causing damage to the enamel surface.
Effect of Cavity preparation on the Enamel Surface:
The process of cavity preparation is a lengthy process, removing all the effected enamel surface and dentine as well depending upon the extent of the caries in to the tooth surface. It causes the loss of enamel structure on a massive scale. The dentist should be well equipped and have a good knowledge about the structure of the tooth and enamel in order to understand the concept of preservation and extension of the cavity in order to save the tooth under examination.
The instrumentation and method used to make the cavity preparation causes the formation of a specific pattern of enamel loss. The significance of these features is that all the forms of surface roughness predispose towards the retention of bacterial plaque on the tooth surface and may therefore have some effect on the occurrence of dental caries and marginal gingivitis. Even developmental surface irregularities found in the troughs of the perikymata on human permanent teeth may accumulate hundreds of carcinogenic streptococci and are beyond the reach of routine tooth cleaning methods.
Cut Enamel Surfaces :
There are different observations made upon the examination of enamel in the newly prepared cavities done by Boyde and Knight in 1969 in which they discussed the orientation of enamel structure and the effect of cavity preparation by using different types of burs. They also discussed the smearing caused after the preparation of cavity. In which they concluded that the irregularities of the enamel caused by the drilling facilitate the retention of bacterial plaque and consequently the likelihood of the formation of dental calculus or dental caries.
It was found out in the studies that the enamel fractures along its prism boundaries on the exit side embrasure walls, along chiseled margins, and its incremental lines. These circumstances should be kept in mind by the clinicians while preparing the cavity and avoid it if possible. The use of diamond other coarse abrasive instruments such as sand paper discs and strips for enamel surface finishing procedures is to be strongly deprecated. (Boyde, 1973)
Effect of Laser Etching on Enamel:
Due to the preferential loss of material from the prism core, the classical acid- etched surface appears as honeycomb. The border of acid etching in the enamel is fuzzy. The structure of the enamel exposed by the laser is different and depends on the energy and position of the focus. The energy of 208 mJ produces a drilling effect, so it is possible to observe crater formation in the enamel . The position of the focus (behind the focus, the spot was larger and the energy lower) did not effect crater formation. An irregular loss of enamel was also seen. The energy of 105 mJ can prepare a well-defined roughness of enamel in focus and an irregular undulation of the surface. The indentations lay in straight lines around the cavity edge. In front of the focus where the energy is higher than behind it, no crater formation was found . Behind the focus, (larger spot, lower energy) the enamel structure was smoother, with less prominent indentations.
The studies related with the dye penetration shows quite similar results as compared with the laser etching. When dye penetration was observed, the dye penetrated in only one side of the composite resin restoration. The space in enamel and dentin measured about tenth micrometers. Acid etching has a typical honeycomb appearance due to the preferential loss of material from the prisma core (Hormati et al., 1980). Ferriera et al., (1989) found that CO2 and Nd:YAG irradiation was responsible for reduced enamel porosity.
Generally it can be said that hard dental substances can be removed by pulsed Er:YAG laser radiation. The effect depends on the type of hard dental tissues, i.e., enamel and dentin (Hibst and Keller, 1989). The difference depends on water content (enamel 25%, dentin 13.5%) and inorganic compounds (enamel 96%, dentin 69%) (Hibst and Keller, 1989). For the 2.94 Î¼m Er:YAG laser, the absorption of laser radiation is about twice as high in dentin as compared with enamel (Hibst and Keller, 1989).