Den Ti No Genesis

DENTINOGENESIS AND DENTIN REPAIR

SUBMITTED BY DR.GANESH 1 YEAR ENDODONTICS

DENTIN REPAIR dentin repair is a process response to external influences-including such as dental caries, tooth wear, trauma, and other tissue injuries etc Dentin repair is nothing but tertiary Dentinogenesis Primary secondary dentine

Tertiary dentine

tubular matrix, regular dentinal tubules

dysplastic matrix, atubular,irregular

Tertiary Dentinogenesis is sub classified in to 2 types

Tertiary dentin

reactionary

reparative

reactionary : dentin matrix secreted by surviving post mitoticodontoblast Reparative : dentin matrix secreted by new generation of odontoblastic like cells in response to stimulus to an appropriate stimulus after the death of the original post mitotic Odontoblasts

Reparative Dentinogenesis The intensity of the response will reflect both the degree and duration of the stimulus Such a response will normally be made to stronger stimuli and represents a much more complex sequence of biologic processes . Reparative dentin actually encompasses a broad range of responses, some of which appear to be relatively specific while others are classified as tertiary dentinogenesis only because they occur in the pulpodentin complex. It is appropriate to consider these two variants of tertiary dentinogenesis individually in view of the diversity of the biologic processes taking place

Reparative dentin actually encompasses a broad range of response Reparative dentin will often be a sequel of reactionary Dentinogenesis Both may be observed with in the same lesion

Reactionary Dentinogenesis Reactionary dentin is, by definition, secreted by surviving primary Odontoblasts The biologic processes responsible for reactionary Dentinogenesis represent focal up-regulation of the secretory activity of the surviving Odontoblasts The intensity of the response will reflect both the degree and the duration of the stimulus, although the extent of the response is limited to those cells in direct tubular communication with the initiating stimulus.

beneath a cavity preparation, the reactionary Dentinogenesis response is generally limited to those areas where the dentinal tubules communicate with the cavity. In unetched preparations, variable plugging of the tubules may lead to differential stimulation of individual Odontoblasts beneath the preparation and an irregular Reactionary Dentinogenesis response interface between the beneath an unetched and unexposed cavity (top) reactionary dentin and prepared in a ferret canine tooth in which a Odontoblasts, possibly with lyophilized preparation of isolated dentin matrix proteins have been implanted. finger-like projections of Reactionary dentin secretion is restricted to matrix that area in which the dentinal tubules are in direct communication with the cavity. Note th finger-like

Growth factor TGF B - implicated these molecules in the cellular signaling responsible for reactionary Dentinogenesis • TGF-B1,TGF-B2,TGF-33,isoforms are expressed by Odontoblasts • considerable endogenous tissue pools of this growth factor are found within the dentin matrix, and these are available for release if the matrix is solubilized or degraded.

During caries Plaque Bacterial acid

diffusing through demineralization to growth factor release

During caries, plaque bacterial acids diffusing through and demineralizing the dentin matrix might be expected to solubilized some of this tissue pool of growth factor. In cavity preparation, the use of etchants or cavity conditioning agents may also release these molecules Cavity preparation Etching

Release molecules

cavity conditioning

EDTA --- most commonly induce reactionary dentin CAOH--- also has the same mechanism

Growth factor Insulin like growth factor IGFs 1 and IGFs 2 Bone morphogenetic protein BMPs Angiogenetic growth factor

All growth factor provides a powerful Cocktail of bioactive molecules that May be released and involved In cellular signaling during injury and Repair to the pulpo dentin complex

The presence of angiogenic growth factors in dentin may explain the stimulation of angiogenesis at sites of tertiary dentin formation

Factors Influencing Reactionary Dentinogenesis  The activity of a caries lesion  Restoration  The method of cavity preparation,  The dimensions of the cavity,  The residual dentin thickness (RDT) of the cavity  Etching of the cavity  Nature of the dental materials used  Method of their application for the restoration  The pulpal changes in response

correlation between reactionary dentin secretion    

RDT, patient age, cavity floor surface area restoration width .

RDT was apparently the most significant factor determining the secretion of reactionary dentin,

CORRELATION BETWEEN MATERIALS AND REACTIONARY DENTINOGENESIS A weaker correlation was observed between choice of restoration material and reactionary Dentinogenesis;

ZOE

CaOH Amalgam

No effect on reactionary Dentinogenesis

More effect on reactionary Dentinogenesis

Relation between reactionary Dentinogenesis and residual dentin thickness { RDT }

LESS Reactionary Dentinogenesis was seen

RDT

Maximum reactionary Dentinogenesis was seen above 0.5 m Below 0.25 mm RDT is 0.5 mm to 0.25 mm

Maximum reactionary Dentinogenesis was seen Rank based on Odontoblasts survival Stimulation of RDT

Rank CaOH > resin composite > resin modified GIC > ZOE

Relation between reactionary Dentinogenesis and cavity cutting process RDT after cavity cutting has the potential to influence odontoblastic cell survival. in deep (RDT less than 0.25 mm) cavities, little more than 50% Odontoblasts survival may be seen whereas in shallower cavities, Odontoblasts survival is about 85% or greater, and despite the likely cutting of the Odontoblasts process, the cells respond by secretion of reactionary dentin Cutting process receptor present near pulp this receptor send signaling to

Etching process treatment with EDTA

EDTA Chemical released Reached dentin matrix Released TGF 31 Diffuse to dentin tubules Bind to receptor Signaling

reactionary Dentinogenesis

Etching process treatment with EDTA for 0 sec, 60 sec, 120 sec

Rank 60 sec > 120 sec > 0 sec 0, 120 sec ---- decreed Odontoblasts survival 60 sec ---------- more Odontoblasts survival Phosphoric acid ------ less stimulatory action

Reparative Dentinogenesis In nonexposed pulps, reparative Dentinogenesis may be a sequel to reactionary Dentinogenesis or it may occur independently Reparative Dentinogenesis always take place at sites of pulp exposure because of the loss of Odontoblasts and the need for dentin bridge formation Reparative Dentinogenesis involves a much more complex sequence of biologic events than reactionary Dentinogenesis in that progenitor cells from the pulp must be induced to differentiate into Odontoblasts-like cells before their secretion may be up-regulated to form the reparative dentin matrix

Ground section of dentin stained to demonstrate dentin phosphophoryn (mauve).

Reparative Dentinogenesis will often be preceded by secretion of a fibrodentin matrix, which is atubular and is associated with rather cuboidal cells with poorly developed organelles on its formative surface. Deposition of tubular matrix by polarized cells is then seen later on the surface of this fibrodentin.

Pulpal exposure

Reparative Dentinogenesis

Death of Odontoblasts

Stimulus of pluri-potent steam cells

Undifferentiated mesenchymal cells

Stimulate Odontoblasts like cells

Secretion of dentinal matrix

Atubular,irregular,dentinal tubules

Undemineralized section of the mature dentin-pulp complex. The vascularity of the pulp is evident. The cell-free zone of Weil can be clearly seen beneath the odontoblast layer

Primary dentin. Odontoblasts border the pulp chamber and line the predentin surface. Below the odontoblasts is a cell-free zone followed by a cell-rich zone.

Reparative Dentinogenesis Stem cells are pluri-potent, and their presence in tissues can offer opportunities for regeneration in response to growth and differentiation signals. There are many genes that control the behavior and expression potential of stem cells, including the highly conserved Notch signalling pathway, which can enable equivalent precursor cells to adopt different cell potentials. Reappearance of Notch in subodontoblast cells during reparative responses to injury and in association with vascular structures in apical areas of the root of the tooth may indicate the role of cells in these areas to contribute to reparative Dentinogenesis If this is the case, then both undifferentiated mesenchymal cells and pericytes may be progenitors of Odontoblasts-like cells.

Reparative Dentinogenesis Although the specific components in the matrix that are responsible for these effects remain to be identified, TGF-B1 is known to be chemotactic for fibroblasts, macrophages, neutrophils, and monocytes during dermal wound healing. Attraction of inflammatory cells to the site of injury may further enhance the chemotaxis of other cells, including pulpal progenitor cells, since many will also produce TGF. TGF-(31 has also been reported to be mitogenic for cells in the subodontoblast layer, and thus may provide both a migratory stimulus for progenitor cells and stimulate their proliferation to expand the available population of progenitor cells.

Fig 3-23 Schematic diagram of possible derivations of signaling molecules contributing to pulpal injury and repair responses

Dentin bridge formation At sites of pulp exposure, dentin continuity may be restored through dentin bridge formation across the exposure. There have been reports bridging after pulp-capping with a variety of agents, the most common being calcium hydroxide although resin composites are gaining in usage. Dentin bridge formation is not distinct from reparative dentinogenesis but rather represents a particular situation under which reparative dentin is formed. However, the extent of the injury and the reparative processes required may influence the quality or structure of the new matrix secreted within the bridge

Journal of Oral Pathology & Medicine Volume 20 Issue 10, Pages 502 - 508 Published Online: 28 Apr 2006

Electron microscope characteristics of dentin repair after hydroxylapatite direct pulp capping in rats In order to study the osteogenic action of hydroxylapatite (HA) on the dental pulp, a pulp capping experiment was designed using the rat upper molar. Under general anaesthesia, molar teeth in 14 male rats were pulp capped with Osteogen (HA) or with Dycal as a control material. After pulp capping, the maxillary molars cavities were restored with amalgam and a pedodontic steel crown was adjusted and sealed over the molar teeth on either side of the maxilla. After 7 days, the areas of necrosis and acute inflammation were more evident in the pulps treated with Dycal than with Osteogen. Hard tissue formation began to appear around dentinal chips in the pulp and extended from the cavity walls into the pulp regardless of the material that was used.

Furthermore, this calcified material was scattered throughout the pulp when Osteogen was used, but was not observed in the Dycal treated pulps. The hard tissue formation was thought to be due to the fibroblasts and odonloblasts found in the pulp. After 28 days dense dentinal tissue was observed bridging the exposure site when Dycal was used, The dentinal tissues formed with Osteogen was always of a globular type, and showed an irregular distribution. Since Osteogen tends to cause areas of dystrophic calcification in the pulp, its use is not be recommended for pulp capping purposes in humans, because these areas of calcification would make future endodontic treatment difficult.

Restorative pulpal and repair responses Vol 132, No 4, 482-491. 2001 American Dental Association The presence of bacteria within the cut dentinal tubules of cavities appeared to influence tertiary dentin repair activity .The mean area of tertiary dentin beneath a cavity preparation with an RDT between 2.993 and 0.501 mm was 235.9 percent. A similar comparison of cavities with an RDT between 0.500 and 0.251 mm showed that the area of tertiary dentin increased by 60.4 percent. However, once the RDT was reduced to between 0.250 and 0.040 mm, the effect of bacterial microleakage did not appear to have much influence on tertiary dentin activity (– 6.2 percent) in comparison with uncontaminated cavity preparations.

Vol 132, No 4, 482-491. 2001 American Dental Association

We found that the number of odontoblasts per square millimeter decreased in density beneath cavity preparations, with the RDT being the most important influence . The general trend after restoration with all materials was for the mean odontoblast density to decrease by 24.3 percent for those preparations with an RDT between 0.500 and 0.251 mm, in comparison with cavity preparations with an RDT between 2.993 and 0.501 mm . Deeper cavity preparations—that is, those with an RDT between 0.250 and 0.040 mm— were found to have 30.5 percent fewer odontoblasts per square millimeter than cavity preparations with an RDT between 0.500 and 0.251 mm.

In important influence on the number of odontoblasts per square millimeter beneath cavity preparations was the type of material used to restore the teeth . The hierarchy of materials in order of reduced odontoblast density between areas independent of the cavity and beneath cavities with an RDT between 0.250 and 0.040 mm is as follows (with reductions in parentheses): Ca(OH)2 : 11.3 percent ZnOE : 29.1 percent resin-based composite bonded to dentin : 32.percent ZnPC : 36.5 percent resin-based composite bonded to enamel : 55percent RMGI : 62.5 percent.

REFERENCE Dental Pulp ---- Seltzer and Bender's Ten Caste's Oral Histology, Sixth Edition Vol 132, No 4, 482-491. 2001 American Dental Association

Journal of Oral Pathology & Medici Volume 20 Issue 10, Pages 502 - 508 Published Online: 28 Apr 2006

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