Definitive Desensitization of Dentin: The Prevention and Treatment of Postoperative Hypersensitivity

 Physiology of Tooth Sensitivity

Dentin is a vital tissue, harder than bone, weaker than enamel with a physiological elasticity preventing tooth fracture.  Dentin is approx. 74% mineral;—the organic phase approx. 26% type-1 collagen with small amounts of proteins and water.  Its collagen is secreted as a biologically “plastic” material, which hardens by a variety of mechanisms.  Normal dentin is composed of millions of tubules, running from the pulpal wall to the DEJ;—through a collagen and calcium-rich zone of intertubular dentin.  Tubule diameter at the DEJ is 0.06 µm, and 3.0 µm at the pulpal wall (approx. 60,000 tubules / mm²).  Most tubules are filled with fluid, an odontoblast process, collagen, and occasional non-myelinated pulpal nerves coursing approx. 150 µm towards the DEJ   (Ten Cate 1998).

In normal (non-anesthetized) patients, Gysi (1900) reported that fluid distortion on the cavity floor caused sharp pain.  Brännström et al. (1966, 1969, 1976, 1979, 1980, 1996) demonstrated that hypersensitivity (sharp pain) is the result of rapid fluid movement in the tubule complex, aggravated by aggressive air-drying.  Physiological testing in various animal studies (Heyeraas 1985, Narhi 1983, 1985) confirmed the “hydrodynamic mechanism” (Brännström 1966) as the prime cause of sudden dentin pain.

Enamel defects: Fluid-flow through human enamel is dependent upon morphology and age.  Enamel is a mineralized crystalline calcium phosphate of approx. 96% with 4% organic component and water.  Its hardness is comparable to brittle steel especially when allowed to dry.  Its basic structural unit is an enamel rod;—tightly packed and mechanically adherent to other rods, providing resistance to stress fractures (Ten Cate 1998).  Lamellae are thin sheets of organic debris which extend from the DEJ to the enamel surface as strain faults in young teeth, becoming cracks in older individuals.  Lamellae are the most widespread defect in enamel.  Following eruption and exposure to foods, acidic drinks and oral hygiene (mouthwashes), lamellae become filled with exogenous matter originating from saliva and food debris.  These cracks represent initiation pathways for caries and fluid diffusion through the enamel to the pulp;—resulting in hypersensitivity.  Other organic enamel defects are enamel tufts, which are proteins that fail to mature during development and maturation.  Tufts extend from the DEJ to approx. one third of the enamel thickness.  Enamel spindles are organic remnants of odontoblast processes that persist in the enamel.   Lamellae, tufts and spindles all contribute to crack propagation resulting in hypersensitivity.

Clinical scenario: Physiologically, any rapid bi-directional fluid flow is the result of a sudden shift in tubule fluid from stimuli i.e. cold or rapid airflow (Brännström 1996). Hypersensitivity is also the consequence of scaling and root planing of cementum and dentin, related to calculus removal (Hartzell 1911, Riffle 1952, 1953, Garrett 1977, Rabbani et al. 1981, Fleischer et al. 1989).  In patients without anesthesia, rapid flow of fluid at the restoration interface or at (cracks) lamellae and exposed root dentin rapidly evaporates fluid.  Upon release of the air syringe, patients generally report severe pain for several minutes (Brännström 1996) however, immediate application of warm water on a cotton pellet provides immediate temporary relief.

 Blockage of open tubules

 Physiological closure of enamel cracks (lamellae) and open tubules of root dentin occur by formation of salivary plaque and its eventual mineralization.  This closure is often referred to as the placebo effect, which is any non-active substance that measures psychological or CNS changes in the patients perception of hypersensitivity (Mumford 1962, 1982, McGrath 1986, Chapman et al. 1987).  Dentinal sclerosis is the natural occlusion of minerals in the tubules which then blocks the outward fluid-flow (Adrięns et al. 1974).  Sclerosis occurs as an aging phenomenon in root dentin and underneath the tubules of various restorative agents (Stanley et al. 1980).

Mechanical instrumentation of enamel and dentin creates a smear layer that covers the instrumented surface and pushes grinding debris into the dentinal tubules for several micrometers as smear plugs.  The smear layer only provides transient relief to dentin hypersensitivity as it degrades within a few weeks;—to be replaced by bacteria (Brännström 1996).  Removal of the smear layer and smear plugs with any acidic agent permits a dramatic outward fluid-flow and without blockage, the patients report increased postoperative dentin hypersensitivity.

Physical blockage: The goal of any clinical procedure is to prevent and treat the patients hypersensitive dentin by sealing the dentinal tubules.  Most commercial toothpaste’s contain fine grit which provide a transient blockage of the dentinal tubules which stops the fluid-flow.  Clinicians have also burnished various agents (Lasho et al. 1983) i.e. Ca(OH)₂ into cervical lesions, into exposed root dentin as well as onto the entire instrumented surface of crown preparations in an attempt to physically block fluid flow.  In addition, application of adhesive systems to these areas also reduces hypersensitivity (Brännström 1966, Dayton et al. 1974, Nordenvall et al. 1980, Greenhill & Pashley 1981, Hirvonen et al 1984, Hosoda et al. 1990).  These and other treatments have enjoyed a short period of popularity, but due to their transient effect, they have proved unacceptable to the greater numbers of the clinical profession.  In addition, cost and placement factors for adhesive systems often places them out of reach for the average patient;—and they tend to limit the type of temporary and final cement by compromising luting mechanism.  Hypersensitivity has also been treated by iontophoresis (Gangarosa & Park 1978, Lutins et al. 1984) with solutions such as, fluoride formaldehyde or glutaraldehyde with limited efficacy.

 Chemistry of tooth desensitization:

 Recent development of biologically compatible oxalate chemistry such as Super Seal™ removes the smear layer, demineralizes the peritubular dentin and expose the hydroxyapatite due to its low pH (Hafez et al. 2000).  Super Seal™ desensitizer is applied with a cotton pellet using gentle rubbing pressure to abfraction lesions, exposed root dentin and to crown preparation surfaces for one minute.  A chemical crystalline calcium complex is then precipitated to the surface of dentin and enamel.  This crystalline complex layer forms insoluble precipitates on enamel and dentin surfaces on and within the dentinal tubule complex.  When applied in vivo Super Seal™ precipitates a calcium-oxalate barrier in the tooth substrate and stops the rapid fluid flow (Greenhill & Pashley 1981, Niazy et al., 1999, 2000).

Conclusion

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