Clinical considerations of dentin Related to 1.color 2. Hardness 3.Permeabilty 4.Related to Caries 5.Age related changes 6.Dentin hypersensitivity 7.

Related to bonding

Dentin

Pashley defined dentin as a porous biological composite composed of apatite crystal filler particles in a collagen matrix.

Dentin properties-considerations

Dentin is softer than enamel and provides greater yield to the pressure of a sharp explorer tine, which tends to catch and hold in dentin. When moving an explorer tine over the tooth, enamel surfaces provide a sharper, higher-pitched sound than dentin surfaces. The hardness of dentin averages one fifth that of enamel . hardness near the DEJ is about three times greater than near the pulp Dentin becomes harder with age, primarily due to increases in mineral content.

COLOR

Dentin is normally yellow white and slightly darker than enamel. In older patients dentin is darker. It can become brown or black in cases where it has been exposed to oral fluids, old restorative materials, or slowly advancing caries. Dentin surfaces are more opaque and dull, being less reflective to light than similar enamel surfaces, which appear shiny.

A key function of enamel and dentin is thermal insulation of the pulp. Most restorative materials are not as insulating as dentin and therefore thermal insults may occur during intraoral temperature changes The need for insulation is greatest for metallic restorations. Thermal insulation is proportional to the thickness of the insulating material.
Approximately 2 mm of dentin, or an equivalent thickness of material, should exist to protect the pulp . This thickness is not always possible, but 1 to 1.5 mm of insulation is accepted as a practical thickness.

While dentin is a hard, mineralized tissue, it is somewhat flexible, with a modulus of elasticity of 1.67 X 106 PSI. This flexibility helps support the more brittle, nonresilient enamel.

The surface area of dentin is much larger at the dentinoenamel or dentinocemental junction than it is on the pulp cavity side. The number of tubules increases from 15,000 to 20,000/mmz at the DEJ to 45,000 to 65,000/mmz at the pulp

The lumen of the tubules also varies from the DEJ to the pulp surface. In coronal dentin, the average diameter of tubules at the dentinoenamel junction is 0.5 to 0.9 /-tm, but this increases to 2 to 3 /.Lm at the pulp

Tubules in superficial dentin close to the dentinoenamel junction (A), are smaller and more sparsely distributed compared to deep dentin (B). The tubules in superficial root dentin (C), and deep root dentin (D) are smaller and less numerous than those in comparable depths of coronal dentin.

Dentin permeability is not uniform throughout the tooth. Coronal dentin is much more permeable than root dentin. There are also differences within coronal dentin . Dentin permeability is primarily dependent on the remaining dentin thickness (i.e., length of the tubules) and the diameter of the tubules. Since the tubules are shorter, become more numerous, and increase in diameter closer to the pulp, deep dentin is a less-effective pulpal barrier than is superficial dentin near the dentinoenamel or dentinocemental junctions

Dentin must be treated with great care during restorative procedures to minimize damage to the odontoblasts and pulp. Air-water spray should be used whenever cutting with high-speed handpieces to avoid heat buildup. The dentin should not be dehydrated by compressed air blasts; it should always maintain its normal fluid content .Protection is also provided by judicious use of liners, bases, dentin-bonding agents,and nontoxic restorative materials. Restorations must adequately seal the preparation to avoid microleakage and bacterial penetration.

A, Excessive drying of tooth preparations can cause odontoblasts to be aspirated into dentinal

tubules.

What is Dental Caries?

It is a microbial disease of the calcified tissues of the teeth,

characterized by demineralization of the inorganic portion

and destruction of the organic substance of the tooth.

Progression of caries in dentin is different from progression in the overlying enamel because of the structural differences of dentin.

Begins with the natural spread of the process along the DEJ and rapid involvement of the dentinal tubules. The dentinal tubules act as tracts leading to the pulp (path for microorganisms).

 The dentinoenamel junction has the least resistance to caries attack and allows rapid lateral spreading once caries has penetrated the enamel. Because of these characteristics, dentinal caries is V-shaped in crosssection with a wide base at the DEJ and the apex directed pulpally. Caries advances more rapidly in dentin than in enamel because dentin provides much less resistance to acid attack because of less mineralized content.

DENTINAL FLUID

Dentinal fluid is found in the dentinal tubules along with od ontoblastic processes . An ultra filtrate of plasma in the pulp capillaries Composition resembles plasma Play a role in the pain sensing mechanism Interfere with the bonding Generally there is an outward flow of the dentinal fluid from pulp.

TERTIARY DENTIN
Also known as Reactionary or Reparative dentin. Formed as a reaction to noxious stimuli only by those cells affected by it. 2 types:Reactionary-formed by preexisting odontoblasts. Reparative-formed by newly differentiated odontoblast like cells.

DEAD TRACTS

When the odontoblasts are injured beyond repair they retract their processes leaving behind empty dentinal tubules filled with air,these are known as dead tracts. They appear black in transmitted and white in reflected light. It is the initial step in formation of sclerotic dentin. Mostly seen in coronal dentin.

Dead tract

Reparative dentin

INTERGLOBULAR DENTIN

These are regions of hypomineralisation in dentin where the calcospherites fail to fuse. Most common in circumpulpal dentin immediately below mantle dentin. Occurs due to Vit.D defn. or due high exposure to fluoride.

Sclerotic dentin results from aging or mild irritation

(such as slowly advancing caries) and causes a change in the composition of the primary dentin. The peritubular dentin becomes wider, gradually filling the tubules with calcified material, progressing pulpally from the DEJ .These areas are harder, denser, less sensitive,and more protective of the pulp against subsequent Irritations.

Sclerosis resulting from aging is physiologic dentin sclerosis; sclerosis resulting from a mild irritation is reactive dentin sclerosis. Reactive dentin sclerosis often can be seen radiographically in the form of a more radiopaque (lighter) area in the S-shape of the tubules.

Eburnated dentin refers to the outward (exposed) portion of reactive sclerotic dentin, where slow caries has destroyed formerly overlying tooth structure, leaving a hard, darkened, cleanable surface.

Dentin SENSITIVITY
Sensitivity of dentin is encountered whenever odontoblasts and their processes are stimulated during operative procedures, even though the pain receptor mechanism appears to be within the dentinal tubules near the pulp.

The most accepted theory of pain transmission is the hydrodynamic theory, which accounts for pain transmission through small, rapid movements of fluid that occur within the dentinal tubules. Because many tubules contain mechanoreceptor nerve endings near the pulp, small fluid movements in the tubules arising from cutting, drying, pressure changes, osmotic shifts, or changes in temperature account for the majority of pain transmission.

Stimuli that induce fluid movements in dentinal tubules distort odontoblasts and afferent nerves (arrow), leading to a sensation of pain. Many operative procedures such as cutting or airdrying induce such fluid movement.

Restoration requiring extensive and deep removal of dentin would open more and larger dentinal tubules and increases the pulpal irritation- thus the importance of REMAINING DENTINAL THICKNESS
Clinical judgments about the need for specific liners and bases are linked to the amount of remaining dentin thickness (RDT), considerations of adhesive materials, and the type of restorative material being used.

INTRINSIC CHANGES

MOST COMMONLY THE RESULT OF TRAUMA. BREAKDOWN OF BLOOD SUPPLY WHICH LEADS TO PULPAL NECROSIS (PULP DEATH). PULPAL BREAKDOWN PRODUCTS PENETRATE THE DENTINAL TUBULES LEADING TO DISCOLORATION.

LYSIS OF BLOOD CELLS, THE RESULT OF INTRAPULPAL HEMORHAGE, WITH SUBSEQUENT PENETRATION INTO THE TUBULES LEADS TO STAINING.

SYSTEMIC STAINING

EXAMPLE HERE WOULD BE TETRACYCLINE GIVEN DURING TOOTH DEVELOPMENT.

IT EFFECTS THE HYDROXY-APPETITE CRYSTALS OF BOTH THE ENAMEL AND THE DENTIN.

BONDING TO THE DENTIN

Bonding of resins to dentin is far more difficult & less predictable than bonding to enamel asMore complex histologic structure than enamel, which also varies more with location Alterations in the mineral content and structure of dentin as in caries-affected or sclerotic areas Not a separate entity, but a part of a complex with the pulp

Most dentin bonding systems remove or solubilize smear layer, allowing resins to penetrate and form

"hybrid layer" with dentin structures. Ideally, smear

plugs would not be removed.

PRECAUTIONS TO BETAKEN

Dentin should not be etched for more than 15 secs, as this will cause post operative sensitivity & increased microleakage, leading to early failure. After etching, dentin should not be dried. Blotting should be done to remove excess water & the dentin should be left moist.

The bond strength is primarily related to micromechanical bonding to the intertubular dentin which occurs between tubules along the cut dentin surface. Dentin adhesion relies primarily on the penetration of adhesive monomers into the filigree of collagen fibers left exposed by acid etching. In deep dentin the greater number of tubules and the diameter of tubules reduce the amount of the intertubular dentin available for bonding.

DEVELOPMENTAL DEFECTS

Dentinogenesis Imperfecta

Definition: A genetic disorder affecting dentine collagen during embryogenesis. Gray to yellowish Broad crowns with constriction of the cevical area resulting in a tulip shape. Radiographically, the teeth appea4r solid,lacking pulp chambers and root canals

Dentinogenesis Imperfecta
Classification of DI Type I: DI without osteogenesis imperfecta TypeII: Brandywine type a shell-like appearance and multiple pulp exposures

dentinogenesis imperfecta

The premature loss of enamel exposes the dentin to occlusal forces that can lead to severe attrition. As in this patient, full crown coverage is often used to preserve occlusal height.

Dentinogenesis imperfecta (note obliterated pulp chambers & canals, short roots, relatively normal crowns with thin enamel)

Radiological features: --characteristic short roots --obliteration of pulp chambers

TREATMENT:

The treatment is directed primarily towards preventing the loss of enamel and subsequent loss of dentin through attrition. Cast metal crowns on the posterior teeth and jacket crowns on the anterior teeth. Fillings are not usually permanent because of the softness of the dentin.

DENTIN DYSPLASIA (ROOTLESS TEETH)

A hereditary defect in dentin formation in which the coronal dentin and tooth colour is normal; the root dentin is abnormal with a gnarled pattern and associated shortened and tapered roots. type I radicular dysplasia normal crowns of regular or slightly amber translucency type II coronal dysplasia semi-transparent opalescent primary teeth

 Dentin dysplasia type II note thistle-shaped pulp chambers, bell shaped crowns This is a rare phenomenon in which there is abnormal dentin development and aberrant root formation. The dentin is poorly formed with large amounts of interglobular dentin present, and pulp chambers and pulp canals are virtually nonexistent. These teeth quickly become mobile, and are commonly extracted because they cannot withstand the forces of occlusion.

DENTIN HYPOCALCIFICATION

There is a failure of union of many of the globules, leaving interglobular areas of uncalcified matrix. But there is no alteration in clinical appearance. Hypocalcified dentin is softer than well calcified dentin.

REGIONAL ODONTODYSPLASIA (GHOST TEETH)

This is an unusual dental anomaly in which one or several teeth in a localized area are affected in an unusual manner. The etiology is unknown. It has been suggested that the condition may represent a somatic mutation, although the possibility has also been raised that it could be due to a latent virus reciding into the odontogenic epithelium, which subsequently becomes active during the development of the tooth.