dentin reaction to caries

بسم الله الرحمن الرحيم

Dentin and pulp reaction to caries and operative procedure
Assist prof. Dr. Emad Alkhalidi PhD conservative dentistry


Clinical and Histologic Characteristics of Dentinal Caries, Acid Levels, and Reparative Responses.
Progression of caries in dentin is different from progression in the overlying enamel Dentin contains much less mineral and possesses microscopic tubules that provide a pathway for the ingress of acids and egress of mineral. dentinal caries is V-shaped in cross-section with a wide base at the DEJ and the apex directed pulpally. Caries advances more rapidly in dentin than in enamel. Caries produces a variety of responses in dentin, including pain, demineralization, and remineralization

Episodes of short duration pain may be felt occasionally during earlier stages of dentin caries. Once bacterial invasion of the dentin is close to the pulp, toxins and possibly even a few bacteria enter the pulp, resulting in inflammation of the pulpal tissues. Initial pulpal inflammation is thought to be evident clinically by production of sharp pains, with each pain lingering only a few seconds (10 or less) in response to a thermal stimulus. A short, painful response to cold suggests reversible pulpitis or pulpal hyperemia. Reversible pulpitis: is a limited inflammation of the pulp from which the tooth-can recover if the caries producing the irritation is eliminated by timely operative treatment.

When the pulp becomes more severely inflamed, a thermal stimulus will produce pain that continues after termination of the stimulus, typically longer than 10 seconds. This clinical pattern suggests irreversible pulpitis, when the pulp is unlikely to recover after removing the caries.( Pulp extirpation and R.C.T is the treatment of choice) Throbbing, continuous pain suggests partial or total pulp necrosis (R.C.T. OR Exo.)


The pulp-dentin complex reacts to caries attacks by attempting to initiate remineralization and blocking off the open tubules. These reactions result from odontoblastic activity and the physical process of demineralization and remineralization. Three levels of dentinal reaction to caries can be recognized: (1) reaction to a long-term, low-level acid demineralization associated with a slowly advancing lesion (2) reaction to a moderate-intensity attack. (3) reaction to severe, rapidly advancing caries characterized by very high acid levels.

slowly advancing caries

sclerotic dentin
Infected dentin
Normal dentin
Sclerotic dentin : dark colored, hard to the explorer tip. lacks a shiny, reflective surface function is to wall off a lesion by blocking (sealing) the tubules. The permeability greatly reduced because of the decrease in the tubule lumen diameter.


The second level of dentinal response is to moderate intensity (or intermediate) irritants: More intense caries activity results in bacterial invasion of the dentin. Infected dentin contain debris,bateria,hydrolytic enzyme These materials can cause the degeneration and death of the odontoblasts and their tubular extensions. Groups of these dead, empty tubules are termed dead tracts.

The pulp may be irritated sufficiently from high acid levels or bacterial enzyme production to cause the formation (from undifferentiated mesenchymal cells) of replacement odontoblasts (secondary odontoblasts). These cells produce reparative dentin (reactionary dentin) on the affected portion of the pulp chamber wall The structure of reparative dentin can vary from well-organized tubular dentin (less often) to very irregular tubular dentin (more often), depending on the severity of the stimulus Reparative dentin is a very effective barrier to diffuser of material through the tubules. Severe stimuli also can result in the formation within the pulp chamber of unattached dentin, termed pulp stones, in addition to reparative dentin.


The success of dentinal reparative responses, either by remineralization of intertubular dentin and apposition of peritubular dentin or by reparative dentin, depends on the severity of the caries attack and the ability of the pulp to respond. The pulpal blood supply may be the most important limiting factor to the pulpal responses.

The third level of dentinal response is to severe irritation. Acute, rapidly advancing caries with very high levels of acid production overpowers dentinal defenses and results in infection, abscess, and death of the pulp. the pulp is poorly tolerant of inflammation. Small, localized infections in the pulp produce an inflammatory response involving capillary dilation, local edema, and stagnation of blood flow. Because the pulp is contained in a sealed chamber and its blood is supplied through very narrow root canals, any stagnation of blood flow can result in local anoxia and necrosis.

ADVANCED CARIOUS LESIONS:

Necrotic dentin is recognized clinically as a wet, mushy, easily removable mass. This material is structureless or granular in histologic appearance and contains masses of bacteria. Infected dentin (zones 4 and 5) is both softened and contaminated with bacteria. It includes the superficial, granular necrotic tissue and the softened, dry, leathery dentin. Affected dentin is softened, demineralized dentin that is not yet invaded by bacteria (zones 2 and 3).

Indirect pulp capping : Indicated In a tooth with a deep carious lesion, no history of spontaneous pain, normal responses to thermal stimuli, and a vital pulp (demonstrated by electric testing), a deliberate, incomplete caries excavation. and is characterized by placement of a thin layer of calcium based materials on the questionable dentin remaining over the pulp. Direct pulp capping: is the placement of calcium based materials directly on exposed pulpal tissue (pulpal exposure) and the surrounding deeply excavated dentinal area. The techniques of indirect and direct pulp capping may stimulate the formation of reparative dentin.

The use of cutting instruments can harm the pulp by exposure to mechanical vibration, heat generation, desiccation and loss of dentinal tubule fluid, and/or transection of odontoblastic processes. As the thickness of remaining dentin decreases, the pulpal insult (and response) from heat or desiccation increases.
Pulpal precautions during cavity preparation


Slight to moderate injury produces a localized, protective pulpal response in the region of the cut tubules. In severe injury, destruction extends beyond the cut tubules, often resulting in pulpal abscess and death of the pulp. These pulpal sequel (recovery or necrosis) take from 2 weeks to 6 months or longer, depending on the extent and degree of the trauma. Although a young pulp is more prone to injury, it also recovers more effectively when compared with an older pulp, in which the recuperative powers are slower and less effective.



Enamel and dentin are good thermal insulators and will protect the pulp if the quantity of heat is not too great and the remaining thickness of tissue is adequate. The longer the time of cutting and the higher the local temperature produced, the greater is the threat of thermal trauma. Steel burs produce more heat than carbide burs because of inefficient cutting. Burs and diamond instruments that are dull or plugged with debris do not cut efficiently, resulting in heat production. When used without coolants, diamond instruments generate more damaging heat than carbide burs.


The most common instrument coolants are air or air-water spray. Air alone as a coolant is not effective in preventing pulpal damage because it desiccates the dentin and damages the odontoblasts Air has a much lower heat capacity than water and is much less efficient in absorbing unwanted heat.
instrument coolants


Air-water spray is universally used to cool , moisten, and clear the operating site during normal cutting procedures. In addition, the spray lubricates, cleans, and cools the cutting instrument, thereby increasing it is efficiency and service life .


During normal cutting procedures a layer of debrise described as a smear layer, is created that covers the cutting surfaces of the enamel and dentin The smear layer on dentin is moderately protective because it occludes dentinal tubules and inhibits the outward flow of tubular fluid and the inward penetration of microleakage contaminants. However, the smear layer is still porous. When air alone is applied to dentin local desiccation may produce fluid flow and affect the physiologic status of the odontoblastic processes in the underlying dentin.

Mechanism of pulp protection

In response to mild, long-term chemical or mechanical insults, the odontoblast processes slowly recede toward the pulp while occluding the tubules with peritubular dentin by depositing hydroxyapatite crystals If the insult is strong and/or near to the pulp, the odontoblastic processes are retracted more rapidly from that region and a thin local bridge of hydroxyapatite is created across the affected tubules. Both of these responses are natural defense mechanisms to insulate the pulp from chemical, thermal, mechanical, or biologic challenges.


If the insult produces fluid flow, in or out of the dentinal tubules, the pressure change is sensed by mechanoreceptors within the pulp, and the patient experiences sensitivity. If leakage of chemical irritants from dental materials or bacteria occurs, then the pulp complex can become inflamed. To protect against these events, it is important to seal the outer ends of the tubules along the dentinal tooth preparation wall.

Tooth preparation with rotary instruments generates cutting debris, material called smear layer Enamel and dentin smear layers are left in place for unbonded amalgam restorations. The dentin smear layer produces some degree of dentinal tubule sealing, although it is 25% to 30% porous. Halving the diameter of the opening produces a sixteenfold reduction in flow. Therefore the smear layer is a very effective barrier. However, because it is partially porous, it cannot prevent slow long-term diffusion.

Smear plugs 2-5 deep

Dentinal tubule
Smear layer
Fluid flow