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Surface Alteration

The cervical area of the tooth interfaces with the gingiva just above the cementoenamel junction and creates a unique biologic junction. This region can be altered by gingival disease as well as tooth destructive processes. Periodontal inflammation and toothbrush trauma may combine to cause recession. Intensive toothbrushing and concentrated dentifrices can then result in abrasion of the tooth. This process is intensified by the presence of acidic PHs from environmental factors like soft drinks, gastric disease or reduced salivary flow. This abrasion, aided by erosive factors, is but one of several pathological processes affecting the dentogingival junction. In this issue we examine the four pathological conditions that affect the tooth-gingival interface. Understanding the origins of these problems increases the likelihood of successful treatment. The following table lists the four conditions that most often create cervical tooth structure loss along with the definition and clinical appearance of the lesions.

Erosion    Progressive loss of hard dental tissue by chemical processes not involving bacterial action. Broad cupping of smooth surface enamel, wear on non-occluding surfaces, "raised amalgams," enamel "cuff" persists in gingival crevice.    Broad cupping of smooth surface enamel, wear on non-occluding surfaces, "raised amalgams," enamel "cuff" persists in gingival crevice.
         
Abrasion   Loss by wear of dental tissue caused by abrasion by foreign substances (for example, toothbrushing and/or dentifrices) Usually located at cervical areas, wider than deep lesion, premolars and cuspids commonly affected.   Usually located at cervical areas, wider than deep lesion, premolars and cuspids commonly affected.
         
Abfraction   Loss of tooth surface at the cervical areas of teeth caused by compressive and tensile forces during tooth flexure. Affects buccal/labial surfaces, deep narrow v-shaped notch, commonly affects single teeth with occlusal alloys and eccentric loads.   Affects buccal/labial surfaces, deep narrow v-shaped notch, commonly affects single teeth with occlusal alloys and eccentric loads.
         
Resorption   Loss of root surface tissue by uncontrolled inflammation of the soft tissues, usually of unknown origin. Associated with trauma, orthodontic care, stress and internal bleaching of endo treated teeth, sometimes erodes CEJ area causing "pink spot"   Associated with trauma, orthodontic care, stress and internal bleaching of endo treated teeth, sometimes erodes CEJ area causing "pink spot"

Erosion is the condition most easily diagnosed in its pure state. Prevalence studies, conducted largely in Europe suggest the incidence of this entity to range from 5% to 25%, with a significant presence in children aged 5-14. The presence of an enamel "cuff" apical to the free gingival margin is pathognomonic and represents the fact that the gingiva somehow protects against the tooth dissolution process. Erosion is caused by extrinsic or intrinsic sources of acid that do not penetrate the gingival sulcus. Extrinsic sources are carbonated drinks, sports drinks, fruits, fruit juices and acid inducing medications. Intrinsic acids are most commonly associated with gastric regurgitation. Diseases that are associated with this condition include GERD (gastro esophageal reflux disease), bulimia, anorexia nervosa, diabetes and alcoholism. Not only do these conditions increase the acid content of the mouth, but the medications used to treat them often result in reduced salivary flow. Patients with erosion have been found to have lower acid buffering capacity in saliva than control groups. Salivary flow is an important factor in the etiology of erosion. Erosion is best managed through the control of acid pH inducing factors, improving the buffering capacity of saliva through increased flow and remineralization of remaining enamel. Large degrees of dentin exposure invite secondary caries. Many situations necessitate full coverage restorations when dentin exposure is extensive or sensitivity develops.

In contrast to lesions that are primarily erosion, abrasion lesions are broad and involve the cementoenamel junction. Enamel surfaces may be worn to a smooth transition to dentin, losing the definitive cervical bulge of enamel. Cervical areas can be hard, with what appears to be sclerotic dentin. If the buffering capacity of saliva is low, or acid concentration in the mouth is high, secondary caries can develop in the area of prior recession. The root surface portion of these lesions can be treated with root coverage procedures such as connective tissue grafts. However, the portion of the abrasion which involves enamel coronal to the interproximal bone is unlikely to be resolved by surgical care. If esthetics is a significant consideration, the coronal portion of such a lesion would need to be restored with a resin bonded restoration. Gingival coverage of the dentin prior to restoration reduces the problems associated with retention of dentin bonded restorations and tooth sensitivity.

In 1991, Grippo coined the term "abfraction" to describe v-shaped notches in the cervical region of the tooth, which he attributed to the presence of occlusal loads on the teeth. Since that time, various researchers have demonstrated the presence of v-shaped notches on one tooth in a segment, but not in other teeth in the segment or at different angles than adjoining teeth. This reduces the probability that these lesions are toothbrush initiated. In 1998, Rees published a two dimensional finite analysis of tooth stress. He found that the presence of an occlusal restoration greatly increased the stress on the cervical enamel, raising the stress above the level needed for enamel rod fracture. Whitehead showed in laboratory conditions, that natural bicuspids placed under axial loads in low pH environments developed non-carious cervical lesions. Mayhew, in a clinical study of abfractive lesions, found that 95% of cervical lesions correlated with facet wear on the occlusal surfaces. A high percentage of the teeth noted to have abfractive lesions had occlusal restorations. It has been suggested that bonding failures in Class V restorations may be related in many cases to increased loads on the cervical area from loads spread secondary to bruxism or increased function. Clinicians have experienced the effect of cuspal flexure in a different way that may support this idea. When bonded restorations are placed in large bulk rather than incrementally built along lateral preparation walls, the cusps may be pulled towards the center of the shrinkage that occurs with light polymerization. The patient develops discomfort from the occlusal stresses deforming the dentin after restoration. Occlusal adjustment or replacing the restoration are necessary to eliminate the sensitivity. When cusps are loaded occlusally and the load is transmitted to the cervical region the enamel may undergo microfracture or the existing restoration may be lost. It is interesting to note that the loss of periodontal support moves the stress concentration apically on the tooth, off the cervical enamel. Periodontally involved teeth seem to have less abfractive lesions and progression of these lesions is lessened. These non-carious lesions are best managed through restoration as many are confined to enamel. However, deep lesions involving the dentin may be candidates for soft tissue augmentation.

In distinction to abfraction, cervical root resorption is an inflammatory process. It occurs just below the epithelial attachment, whether the epithelial attachment is at the CEJ of on root surface. Cervical root resorption occurs as a delayed reaction to trauma and can be seen following tooth movement, orthognathic surgery, periodontal care, trauma and non-vital bleaching. The cause is unknown, but most authorities suggest an alteration in the root surface which does not resist cementoclasts when inflammation develops near the affected surface. Spread of the root resorption undermines the cervical enamel producing a "pink spot," similar to the process of internal resorption. These lesions are asymptomatic, and often they are misdiagnosed as periodontal vertical deformities in their early stages. External resorption shows on radiographs and is different than internal resorption as the pulp chamber's outline remains clearly distinguishable in external resorptioin. When these lesions are exposed surgically, a band of intense inflammatory tissue surrounds the lesion. The recommended method of treatment is surgical exposure and debridement of the lesion with endodontic therapy when the lesion approaches the pulpal tissues. The exposed lesion is restored beyond the margins of the resorption as far as tooth structure allows. Left untreated the process destroys so much tooth structure that the tooth is not restorable. Some lesions continue to destroy tooth structure after restorative care so patients need to be appraised of a future risk for breakdown.
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