SEMINAR ON

DENTINDEVELOPMENT ANDAGE CHANGES

Submitted by:Aditi Chandra MDS- 2012 Department of conservative dentistry and endodontics

CONTENTSIntroductionDevelopment (Dentinogenesis)Age and functional changesClinical implications Developmental anomalies Conclusion References

INTRODUCTIONDentine is a hard connective tissue located between pulp and external surface of tooth. It is about 70% inorganic hydroxyapatite crystals; the remaining 30% is primarily organic composed of collagen and mucopolysaccride ground substance, as well as water. In the crown it is covered by enamel and in the root by cementum.The combination of enamel and dentin provide a rigid hard structure suitable for tearing and chewing that resists both abrasion and fracture resistance. The cementum covering the dentin of the root anchors the tooth to the bone of the socket via the periodontal ligament.Dentin forms the bulk and general form of tooth. It is characterized as a hard tissue with tubules throughout its thickness. It begins to form slightly before the enamel and determines the shape of crown, including the cusp, ridges and number, size of root.Dentine is similar to bone (physically and chemically) and cementum (origin similar to mesenchyme). Difference between bone and dentine lies in the location of osteoblasts (within bony matrix) and odontoblasts (external to dentinal matrix).

Pattern of dentine formationDentin formation begins at the bell stage. It spreads down the cusp slopes as far as the cervical loop. Unlike amelogenesis, which has a well defined end point, dentinogenesis will continue throughout life.

Dentinogenesis can be subdivided into the following stages1) Differentiation of the dentin forming cells (odontoblasts).2) Deposition of the organic matrix (pre-dentin).3) Mineralization of the matrix.Odontoblast Differentiation

Odontoblasts differentiate from the ectomesenchymal cells of the dental papilla and are of neural crest origin. Thus the dental papilla is the formative organ of the dentin. The differentiation of odontoblasts from the dental papilla is brought about by the expression of genes, signaling molecules and growth factors responsible for production of the unique dentin matrix proteins and also those responsible for the morphology of the completed tooth. Fibronectin, decorin, laminin and chondroitin sulphate may be involved in odontoblast differentiation.The dental papilla cells are small and undifferentiated and exhibit a central nucleus and few organelles. They are separated from the inner enamel epithelium by an acellular zone that contains fine collagen fibrils. Almost immediately after the cells of the inner enamel epithelium reverse polarity the ectomesenchymal cells adjoining the acellular zone rapidly enlarge and elongate to become preodontoblasts first and then odontoblasts as their cytoplasm increases in volume. Factors like TGF, IGF and BMP are released from the inner enamel epithelium and taken up by the preodontoblasts. The acellular zone between the dental papilla and the inner enamel epithelium is gradually eliminated as the odontoblasts differentiate and increase in size. As the odontoblasts increase in size, they change from an ovoid to columnar shape and their nuclei become basally oriented. Length of the odontoblast increase to approx. 40um.Deposition of organic matrixFormation of mantle dentinAfter the differentiation of odontoblasts the next step in the production of dentin is the formation of its organic matrix. The matrix consists primarily of type 1 collagen fibrils; DDP is the 2nd most abundant constituent. The 1st sign of dentin formation is the appearance of distinct large diameter collagen fibrils (0.1 0.2um) called von korffs fibers. These fibers consist of collagen type 3 with fibronectin. They originate deep within the odontoblasts, extend towards the inner enamel epithelium and fan out in the structureless ground substance. As the odontoblast continues to increase in size, they also produce smaller collagen type 1 fibrils that orient themselves parallel to the future DEJ. Coincident with this deposition of collagen, the Plasma membrane of odontoblasts adjacent to the inner dental epithelium gives rise to stubby processes called as enamel spindles. Odontoblasts may give rise to small membrane bound vesicles called matrix vesicles. These matrix vesicles are present near basal lamina and act as mineralization front. As they grow they rupture and lead to release of crystallites. These crystallites, fuse with each other to form layer of mineralized matrix. Non collageneous matrix proteins are formed by odontoblasts which regulate mineralization. Hence coronal mantle dentine (15 to 20um thick) is formed over which circumpulpal dentine is formed.Formation of circumpulpal dentinOnce the initial mantle dentin formation is completed the bulk of primary circumpulpal dentin is laid down. The odontoblasts eliminate the extracellular compartment between them to form tightly packed layer of cells. The matrix of dentin is produced exclusively by odontoblasts. Elaboration of this matrix involves the secretion of collagen fibrils that are smaller in dimensions than those in the mantle dentin and noncollagenous ground substance. The odontoblasts move pulpally as the matrix is secreted. The intertubular dentin matrix comprises the bulk of the circumpulpal dentin. As this matrix forms, peritubular dentin matrix is secreted around the tubule perimeter. Peritubular dentin is more highly mineralized than the intertubular dentin matrix. It contains few collagen fibrils and is rich in non collagenous matrix components.

Mineralization of dentinAlthough several hypotheses have been put forward to explain the mineralization of dentin, the key element in initiating and controlling mineralization is the odontoblast. It controls the release and transport of calcium ions, determines the distribution and presence of the matrix components and initiate and modulate the process. How mineral ions reach mineralization site?The junction between odontoblasts are palisade and incomplete and thus leaky. Simple percolation of tissue fluid supersaturated with calcium and phosphorous ions could take place. It occurs mainly through L shaped channels at basal plasma membrane. The presence of alkaline phosphatase activity and calcium adenosine tri phosphatase activity in the distal end of the cell also has an implication in the transport and release of mineral ions into the forming dentin.

Pattern of mineralizationHistologically two patterns of mineralization can be observed:1. Globular calcification2. Linear calcification

Globular calcificationInvolves the deposition of crystals in several discreet areas of matrix due to heterogeneous capture in collagen. With continuous crystal growth, globular masses are formed that enlarge and fuse to form a single calcified mass. This pattern is best seen in the mantle dentin. Linear mineralizationWhen rate of mineralization slows down, mineralization front appears to be uniform. The size of the globules depends on the rate of dentin formation. Largest globules occur where rate of dentin deposition is fastest. Seen in circumpulpal dentin.

Formation of root dentinRoot dentin is formed in a similar manner as coronal dentin but some differences have been reported. The epithelial cells of hertwigs root sheath initiate the differentiation of odontoblasts that form root dentin.Coronal dentin is structurally different from root dentin in the following: Different orientation of collagen fibers occur in mantle dentine. Phosphoryn content of root dentine is lesser as compared to coronal dentine. Rate of deposition of root dentine is slower and lesser. Larger interodontoblastic bundles in root dentine (more organic matrix present)

Secondary and tertiary dentinogenesisSecondary dentin is deposited after root formation is completed. It is formed by the same odontoblasts that form the primary dentin and is laid down as a continuation of the primary dentin. It is formed at a much slower pace than primary dentin and can be differentiated from primary dentine by demarcation lines, sparse and irregular dentinal tubules. Tertiary dentine is formed at specific sites in response to damaged odontoblasts and cells recruited from damaged pulp. The rate of deposition depends on the degree of injury. During formation of tertiary dentine, formation of collagen, DSP and DMP1 (decreases) and Bone sialoprotein and Osteopontin (increases).

AGE CHANGES IN DENTINLike all body tissues, dentino pulpal complex undergo changes:1. There is decrease in volume of pulp chamber due to secondary dentine formation.2. Cells decrease in number, collagen may increase (collagen bundles). 3. Cells reduced to half from 20 years to 70years.4. Irregular areas of dystrophic calcification in central pulp.5. Continuous deposition of intratubular dentine, resulting in sclerosis.

VITALITY OF DENTIN If vitality is considered to be the capacity of the tissue to react to physiologic and pathologic stimuli, dentin must be considered a vital tissue. Dentin is laid down throughout life although after teeth have erupted and have been functioning for a short time, dentinogenesis slows and further dentin formation is at a much slower rate. Pathologic effects of dental caries, abrasion, attrition or cutting of dentin by operative procedures cause changes in dentin such as dead tracts, sclerosis & addition of reparative dentin.

REPARATIVE DENTINOdontoblastic processes may be cut or exposed due to extensive abrasion, erosion, caries or operative procedure. Depending on the intensity of injury the odontoblast dies or survives. If the odontoblasts survive then the dentin that is formed is called as reactionary or regenerated dentin. Odontoblasts that die are replaced by migration of undifferentiated cells which deposit reparative dentin. The origin of the new odontoblasts is from the cells in the cells in the cell rich zone or from the undifferentiated perivascular cells deeper in the pulp. This action to seal of the zone of injury occurs as a healing process initiated in the pulp resulting in resolution of the inflammatory process and removal of dead cells.Reparative dentin is characterized by fewer & more twisted tubules than normal dentin.

DEAD TRACTSLoss of odontoblast process may occur in teeth as a result of caries, attrition, abrasion, cavity preparation and erosion. This degeneration is often observed in areas of narrow pulp horns because of crowding of odontoblasts. Dentinal tubules fill with fluid or gaseous substances. Such group of tubules in ground sections may entrap air and appear black in transmitted and white in reflected light. Dentin areas characterized by degenerated odontoblast processes give rise to dead tracts. These areas demonstrate decreased sensitivity and appear to a greater extent in older teeth. Dead tracts are the initial step in formation of sclerotic dentin.

SCLEROTIC OR TRANSPARENT DENTIN In cases of caries, attrition, abrasion, erosion, or cavity preparation, sufficient stimuli are generated to cause collagen fibers and apatite crystals to start appearing in dentinal tubules. Apatite crystals are initially only sporadic in a dentinal tubule but gradually the tubule becomes filled with a fine mesh work of crystals. Gradually the tubule lumen is obliterated with the mineral which appears similar to peritubular dentin. Sclerotic dentin can be observed in the teeth of elderly people, especially in the roots. It may also be found under slowly progressing caries. Sclerosis increases the brittleness of dentin, reduces the permeability of the dentin and helps prolong pulp vitality. Mineral density is greater in this part of the dentin. The hardness of sclerotic is variable; those formed as a result of aging are harder than those found the carious lesion. Sclerotic dentin was harder than normal dentin, its elastic properties were not altered but its fracture toughness was reduced. The crystals present in sclerotic dentin were smaller than those in normal dentin. It appears transparent or light in transmitted light and dark in reflected light.

CLINICAL IMPLICATIONSThese age changes may lead to dentino-pulpal complex resistant to environmental stimuli and vice versa.1) Age increases, spread of caries is slowed down by tubule occlusion. 2) Age changes also accelerate in response to environmental stimuli such as attrition of enamel. The response of complex to gradual attrition is to produce more sclerotic dentin and deposit secondary dentin at an increased rate. 3) If the stimulus is more severe, tertiary dentin formation occurs at the ends of the tubules affected by injury. 4) Age changes also lessen the ability of the pulp dentin complex to repair itself, so traumatic procedures avoided. Dentin must be treated carefully during restorative procedures to minimize damage to the odontoblasts and pulp. Air water spray should be used whenever cutting with high speed hand pieces. The dentin should not be dehydrated with compressed air blasts.

Developmental Anomalies

Dentinogenesis Imperfecta Dentin dysplasia Regional odontodysplasia Dentin hypocalcification

DENTINOGENESIS IMPERFECTA This is an autosomal dominant condition affecting both deciduous and permanent dentition.

Classification:Shields classification: Revised classification (Shafers):Type 1 No substitute in present classification Type 2 Dentinogenesis imperfecta 1Type 3 Dentinogenesis imperfecta 2 (Brandywine dentinogenesis)

DENTINOGENESIS IMPERFECTA - 1Synonyms:Opalescent dentin, dentinogenesis imperfecta without osteogenesis imperfecta, opalescent teeth without dentinogenesis imperfecta, shields type 2, capdepont teeth.Etiology:Dentinogenesis imperfect type 1 is caused by mutation in the DSPP gene (gene map locus 4q21.3) encoding dentin phosphoprotein and dentin sialoprotein.Clinical features:Teeth are blue gray or amber brown and opalescent. Few days after eruption teeth may achieve a normal color, following which they become translucent. The enamel may split readily from the dentin when subject to occlusal stress.Radiographic features:The teeth have bulbous crowns, roots that are narrower than normal, and pulp chambers and root canals that are smaller than normal and completely obliterated.

DENTINOGENESIS IMPERFECTA 2Synonyms:Shields type 3, Brandywine type dentinogenesis imperfectaEtiology:It occurs as a result of mutation in gene that maps for chromosome 4.Clinical features:Crown of the primary and permanent teeth wear rapidly after eruption and multiple pulp exposure may occur. Dentin is amber in colour and smooth. Radiographic features:In primary teeth presence of very large pulp chamber and root canals is seen, although they may become reduced in size with age. Permanent teeth have pulpal spaces that are either smaller than normal or completely obliterated.Dentinogenesis imperfecta type 2 can differ from type 1 by the presence of multiple pulp exposures, normal nonmineralized pulp chambers and canals and a general appearance of shell teeth.Histological features:The appearance of enamel is essentially normal except for its peculiar shade, which is a manifestation of the dentinal disturbance. The dentin is composed of irregular tubules, with large areas of uncalcified matrix. The tubules are larger in diameter and less numerous than normal. In some areas there may be a complete absence of tubules. Pulp chamber is usually completely obliterated by deposition of dentin. The odontoblast seems to degenerate rapidly.

Treatment: It is directed towards preventing the loss of enamel and subsequent loss of dentin through attrition. Cast metal crowns on posterior teeth and jacket crowns on anterior teeth have been used with success although care must be taken in the preparation of such teeth. These teeth should not be used as abutments because the roots are prone to fracture under stress.

Complex all-ceramic rehabilitation of a young patient with a severely compromised dentition: a case report.

Source:Martin Groten Quintessence Int (Berl) 40(1):19-27 (2009) PMID 19159020

Abstract: A young patient with dentinogenesisimperfecta and a dentition severely compromised by discolorations,abrasion, and breakage of enamel on several teeth was prosthodontically treated with CAD/CAM-manufactured all-ceramic restorations. To reduce treatment risk, preparations were limited paragingivally. Maxillary anterior teeth and premolars were restored with adhesively luted ceramic crowns. All other teeth were treated with zirconia-based restorations luted with a self-etching resin-based material. Considering the deficient pretreatment situation, the use of tooth-colored restoration and luting materials yielded a satisfying functional and good esthetic result. The patient is highly satisfied, even though 3 minor chippings occurred shortly after the completion of treatment.

Fillings are usually not permanent because of softness of the dentin.

Bleaching to an extent lightens the colour.

Successful bleaching of teeth with dentinogenesis imperfectadiscoloration: a case report.Source:Department of Prosthodontics, University of Texas Health Science Center at San Antonio, TX 78229-3900, USA. Abstract:Dentinogenesis imperfecta (DI) is a hereditary condition that can cause discoloration of teeth in addition to other dental abnormalities. Patients often present to the dentist with a main goal of improving their esthetics. A myriad of treatment options have been described for this condition. This clinical report describes the management of a young adult with DI who desired improvement in dental esthetics after orthodontic treatment. As a result of his condition, the patient's dentition exhibited the classic generalized dark amber opalescence. A 14% hydrogen peroxide gel was used for bleaching of the maxillary and mandibular teeth, performed by the patient at home. The patient was followed at different intervals, and the improvement in teeth shade was significant.

Dentin DysplasiaIt is a rare disturbance of dentin formation characterized by normal enamel but atypical dentin formation with abnormal pulp morphology.

Classification:Shields classification:Type 1(dentin dysplasia)Type 2 (anomalous dentin dysplasia)Witkops classification:Type 1 (radicular dentin dysplasia)Type 2 (coronal dentin dysplasia)

Synonyms:Rootless teethEtiology:Dentin dysplasia both type 1 and 2 appear as hereditary disease, transmitted as an autosomal dominant characterstic.

TYPE I (Radicular dentin dysplasia) Clinical features:Both dentitions are affected & crowns appear clinically normal in morphologic appearance and colour. They may sometimes exhibit amber translucency. Teeth generally exhibit a normal eruption pattern. Teeth exhibit extreme mobility & are exfoliated prematurely or after a minor trauma because of their short roots.

Radiographic features:In both dentitions the roots are short, blunt, conical or similarly malformed. In Primary teeth the pulp chambers and root canals are completely obliterated while in the permanent teeth, crescent shaped pulpal remnant is seen. Obliteration in the permanent teeth occurs pre-eruptively.Histological features:Coronal dentin is usually normal. Pulp is obliterated by calcified tubular dentin, osteodentin and fused denticles. Normal dentinal tubule formation is blocked so the new dentin is formed around obstacles and takes the characterstic appearance described as lava flowing around boulders.TYPE II (Coronal dentin dysplasia)Clinical features:Both the dentitions are affected. The primary teeth appear yellow, brown or bluish grey opalescent. Clinical appearance of permanent dentition is normal.Radiographic features:Pulp chambers of primary teeth become obliterated but not before eruption. Permanent teeth show presence of abnormally large pulp chamber in coronal portion of tooth described as thistle-tube in shape. Within such areas radioopaque foci resembling pulp stones may be found.

Histological features:The deciduous teeth exhibit amorphous and atubular dentin in the radicular portion while the coronal dentin is relatively normal.the permanent teeth show normal coronal dentin but the pulp has multiple pulp stones or denticles.Treatment:The most effective treatment is to practice excellent oral hygiene in order to maintain the health of the teeth. Various other treatment modalities are:Implantation Dental implants will become necessary because of tooth loss, generally by the time a patient reaches his 40s. At this time it is common for all remaining teeth to be surgically removed and replaced by a new set of false teeth that are surgically implanted. Some dental surgeons may prefer to implant these one at a time as they are lost, rather than implanting a whole set at a time.Rehabilitation In some cases, dentists may try to replace lost teeth back into the gums, and rehabilitate them there. This will also allow the patient to maintain her natural teeth rather than relying on a porcelain replacement.Major Surgical Intervention In some cases, major surgical intervention may be the only treatment option available. In this case the dentist will combine several procedures, including sinus lifting, bone augmentation and grafting, and dental replacementRegional OdontodysplasiaUnusual dental anomaly in which one or several teeth in a localized area affected in an unusual manner. Maxillary teeth are involved more frequently than mandibular teeth. Most frequently affected is Maxillary permanent Central Incisor, Lateral Incisor, and Cuspid. Both the deciduous and permanent dentition may be involved.Synonyms:Odontodysplasia, Ghost teeth, Odontogenic dysplasia, odontogenesis imperfecta.Etiology:Is unknown. It has been suggested that the condition may represent a somatic mutation, may be due to a latent virus residing in odontogenic epithelium which becomes active during development of tooth.Clinical features:There is delay or total failure in eruption of teeth. Tooth shape becomes irregular with evidence of defective mineralization.Radiographic features:Tooth shows thin enamel and dentin with large pulp chambers thereby giving it a floating appearance. There is a marked reduction in radiodensity so that the teeth give a Ghost appearance. The enamel layer is often not evident.Histological features:There is marked reduction in amount of dentin with widening of pre dentin layer. There is presence of large areas of interglobular dentin and irregular tubular pattern of dentin.Treatment:Because of poor cosmetic appearance of these teeth, extraction with restoration by a prosthetic appliance is usually indicated.Dentin HypocalcificationEtiology:Similar to those of environmental enamel hypoplasia and enamel hypoplasia. Other factors like rickets, parathyroid deficiency could also produce hyocalcification.Normal dentin is calcified by deposition of calcium salts in the organic matrix in the form of globules. These increase in size by further peripheral deposition of salts until all the globules are finally united into a homogeneous structure. In dentinal hypocalcification there is failure of union of a number of globules, leaving Interglobular areas of uncalcified matrix.Clinical features:Hypocalcified dentin would be much softer than well calcified dentin.

ConclusionAlthough only a limited understanding of the biologic mechanisms responsible for control of odontoblast secretion currently exist, the very close understanding of primary dentinogenesis is known to result in a remarkable degree of reproducibility in tooth form and shape. Thus, developing an understanding of the blueprint for physiologic dentinogenesis and its age changes holds the key for a new biologic era in restorative dentistry.References Orbans oral histology and Embryology-12th edition Oral histology By A. R Tencate -7th edition Oral anatomy, histology & embryology Berkovitz- 3rd edition Dental Pulp- Seltzer and Benders Shafer textbook of Oral pathology- 5th edition