Detecting and Quantifying Cervical Dentin Hypersensitivity Using Air Indexing Combined with the T-Scan System

Detecting and Quantifying Cervical Dentin Hypersensitivity Using Air Indexing Combined with the T-Scan System

Thomas A. Coleman, DDS (Private Practice, USA)
DOI: 10.4018/978-1-4666-6587-3.ch009
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Abstract

This chapter introduces the Air Indexing method for detecting and quantifying cervical dentin hypersensitivity as a companion to the T-Scan Occlusal Analysis System, which evaluates occlusal force and timing values of contacting teeth. The chapter discusses detection, diagnosis, and treatment of clinical signs and/or symptoms of Cervical Dentin Hypersensitivity (CDH). A 17-year-long retrospective study conducted between 1979 and 1996 is presented that illustrates the correlation between Cervical Dentin Hypersensitivity and its resolution following occlusal adjustment. Resulting stress from occlusal contact force is etiologic for non-carious cervical lesion formation and root degradation. This chapter details how biocorrosion and lost protective glycoproteins hasten the effects of applied force, creating CDH symptoms and cervical abfractions. Lastly, the Air Indexing method of CDH diagnosis is melded with T-Scan occlusal analysis to diagnose and treat CDH symptoms. Together, these two methods yield more CDH/occlusal insight than either method can alone.
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Background

Occlusal stress may result from chronic microtrauma or macrotrauma (Speck et al., 1979). Chronic microtrauma is defined as the repetitive low force inter-arch contact of teeth over time. This type of trauma occurs during swallowing, habitual function, parafunction, or mastication (Dejak et al., 2003; Grippo, 1991; Grippo et al., 2004; Kydd, 1957; Shore, 1976; Straub, 1960). Microtrauma may exist with or without food bolus.

Microtrauma may be considered pathologic when it results in premature signs and/or symptoms of OD, by disrupting masticatory system health. The term Occlusal Disease, first appeared in the literature during 1990 (Lytle, 1990), was further modified 17 years later (Ruiz, 2007), and then redefined again, 1 year later (Ruiz & Coleman, 2008). Occlusal Disease includes clinical findings of occlusal wear, fractures of teeth or restorations, hypersensitivity of teeth during mastication, cervical dentin hypersensitivity (CDH) (Coleman et al., 2003; Coleman & Kinderknecht, 2000), tooth hypermobility (Harrel et al., 2006), fremitus (Harrel et al., 2006; Ruiz, 2007), abfractive stress (Coleman et al., 2003; Grippo, 1991; Ruiz, 2003, 2005, 2007), vertical bone loss or localized bone destruction (secondary to inflammatory and bacterial periodontal disease) (Harrel et al., 2006), and masticatory muscle or TMJ pain (Gremillion, 2006; Ruiz, 2005; Sipila et al., 2006). Originally published in Compendium. © 2008 to AEGIS Publications, LLC. All rights reserved. Reprinted with permission from the publishers.

In 1971, Ramfjord and Ash suggested that the Central Nervous System (CNS) reflex that stimulates bruxism, seems to emanate from the periodontal proprioceptors, specifically from within the Sharpey’s fiber complex of the periodontal ligament (Ramfjord & Ash, 1971). This “nociceptive reflex” results from polysynaptic noxious stimuli (Okeson, 1998). It has been observed during the years when the dentition is transitional, but applies to all ages as a periodontal reflex response to the muscles of mastication resultant from dental mobility (Okeson, 1998).

Key Terms in this Chapter

Cervical Dentin Hypersensitivity (CDH): Sensitivity of the CEJ to external stimuli, such as air, cold, tactile stimulation, electrical stimulation, and/or acid exposure.

Microtrauma: The repetitive low-force interdigitation and compressions of teeth during inter-arch contact. It may be generalized or localized with or without active Occlusal Disease.

Friction: Friction results from mechanical surface interaction during motion, when the substrate surfaces are under solid, liquid, and/or gaseous applied force.

Occlusal Disease (OD): The premature presence of wear facets, fractures of teeth or restorative materials, tooth hypermobility seen without gingival inflammation or periodontal bone loss, isolated CDH episodes, tooth fremitus, hypersensitivity of teeth during mastication without the presence of a cracked tooth, localized vertical bone loss secondary to periodontal bone loss, masticatory muscle or TMD pain, without respective anatomic pathology.

Biocorrosion: Electrical, biochemical, and/or electrochemical degradation of dental tissue. Its effect may degrade both hard and soft tissue.

Nociception: A neural polysynaptic muscular response to stimuli from distant receptors. A threshold of receptor stimulation must be reached, to effect the clinical detection of contractions of the muscle.

Cervical Stress: The resultant vectored deformation in the cervical regions of teeth upon the hydroxyapetite crystal arrangement, in response to tensile and/or compressive force applied on the tooth’s occlusal surface. Adequate periodontal bone levels assist in the tooth’s deformation by resisting the applied occlusal load, inducing the tooth to accommodate the load by flexing.

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