Gingival recession is characterized by the displacement of the gingival margin apically from the cementoenamel junction, or CEJ, or from the former location of the CEJ in which restorations have distorted the location or appearance of the CEJ. Gingival recession can be localized or generalized and be associated with one or more surfaces.1 The resulting root exposure is not esthetically pleasing and may lead to sensitivity and root caries. As a result, we reviewed studies that described the prevalence, etiology and factors associated with gingival recession.
Many people may exhibit generalized gingival recession without having any awareness of the condition.
Many authors have attempted to explain the phenomenon of gingival recession. There is a theory that the gingival margin, rather than retracting apically, may remain largely static while the tooth moves occlusally by eruption or extrusion and lifts the CEJ clear of the gingival margin.2 This appears to be an unlikely or a rare explanation for recession. During studies in which teeth were extruded purposely, the epithelial attachment remained at the same position on the tooth.3 In addition, some grossly supererupted teeth have no gingival recession and, in many cases in which teeth are in occlusion, the extent of gingival recession far exceeds any possible overeruption. Consequently, the theory of supereruption with gingival recession does not provide proof of supereruption leading to recession, as the primary etiology may be due to other factors.
Many people may exhibit generalized gingival recession without having any awareness of the condition. Many others, however, often are anxious about gingival recession for reasons such as fear of tooth loss, dentinal hypersensitivity and poor esthetics.1 Dentists also may be challenged by questions regarding prevention of future attachment loss. Due to interaction among many possible contributing factors, it is difficult to predict whether further changes in gingival recession may occur at a given site.
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AGING
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Albandar and Kingman4 studied the prevalence of gingival recession among subjects 30 to 90 years of age. Using a sample of 9,689 subjects, they projected that 23.8 million people have one or more tooth surfaces with gingival recession of 3 millimeters or more. They also found that the prevalence of 1 mm or more recession in people aged 30 years and older was 58 percent and increased with age. Men and African-Americans had significantly more gingival recession than did women and other racial/ethnic groups, respectively. Recession also was more prevalent and severe at buccal than at inter-proximal surfaces of teeth.
Where gingival recession has developed, the underlying presence of dehiscences may be considered and possibly discovered during flap procedures.
Similarly, Gorman5 found that the frequency of gingival recession increased with age and was greater in men than in women of the same age. Malpositioned teeth and toothbrush trauma were found to be the most frequent etiologic factors associated with gingival recession. Recession associated with labially positioned teeth occurred in 40 percent of patients 16 to 25 years of age and increased to 80 percent of patients in the 36 to 86 years of age group. Those findings were corroborated by Murray,6 who examined 4,000 subjects and found that the incidence of gingival recession increased with age.
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ANATOMICAL FACTORS
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One etiologic factor that may be associated with gingival recession is a prior lack of alveolar bone at the site.10 The deficiencies in alveolar bone may be developmental (anatomical) or acquired (physiological or pathological).11
Anatomical factors that have been related to recession include fenestration and dehiscence of the alveolar bone, abnormal tooth position in the arch, aberrant path of eruption of the tooth and individual tooth shape.12 All those anatomical factors are interrelated and may result in an alveolar osseous plate that is thinner than normal and that may be more susceptible to resorption.
Anatomically, a dehiscence may be present due to the direction of tooth eruption or other developmental factors, such as buccal placement of the root relative to adjacent teeth so that the cervical portion protrudes through the crestal bone.13 One surgical study found a correlation between gingival recession and bone dehiscence.14 A correlation between the pattern of eruption and gingival recession also has been suggested.15 Dehiscences may be present where the buccolingual thickness of a root is similar to or exceeds the crestal bone thickness.16 Those authors postulated that people with morphological biotypes characterized by narrow, long teeth are more prone to dehiscences than are people with broad short teeth. Where gingival recession has developed, the underlying presence of dehiscences may be considered and possibly discovered during flap procedures.
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PHYSIOLOGICAL FACTORS
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Physiological factors may include the orthodontic movement of teeth to positions outside the labial or lingual alveolar plate, leading to dehiscence formation.17 Such studies suggested that the acquired loss of alveolar bone might be associated with a number of identifiable physiological or pathological conditions for which bone loss is part of a physiological or pathological process.
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PATHOLOGICAL FACTORS
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Pathological factors include bone resorption as a sequel to microbially induced periodontal diseases. In this case, however, the process of recession may be more complex since the teeth involved may extrude, tilt and become mobile. A rat study demonstrated a possible mechanism of gingival recession, showing that loss of attachment was the result of localized inflammatory processes in connective tissue with the accumulation of mononuclear cells.18 It also was suggested that inflammation may persist subclinically and therefore cannot be eliminated as a factor in recession.18 Similarly, recession has been related to inflammation in periodontal connective tissue in monkeys.19–22
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TRAUMA
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In addition to psychological factors, various forms of trauma—such as vigorous toothbrushing, aberrant frenal attachment, occlusal injury, operative procedures and tobacco chewing—have been thought to play a role in the etiology of recession. Clinical and case report studies also have associated gingival recession with chronic trauma, including habits such as chronic impaction of foreign bodies within the gingiva or gingival injury.23 In a case report, an unusual cause of gingival recession secondary to trauma induced by a lower-lip piercing also has been observed.24
Traumatic mechanical toothbrushing is a factor in the etiology of gingival recession.25–27 The effects of toothbrushing have been studied by many investigators with general agreement that vigorous or incorrect use of the toothbrush can produce recession. One study found that recession due to toothbrushing was characteristically localized on facial surfaces and frequently "V" shaped, often occurring in association with tooth abrasion.28
Epidemiologic studies have supported the idea that traumatic toothbrushing may be associated with gingival recession, with buccal gingival recession noted more frequently on the left side of the jaw.29 These findings likely are related to the fact that most people are right-handed and brush more thoroughly on the left sides of their mouths.30 In patients with dentin hypersensitivity, more gingival recession and sensitivity are found on the left side of the mouth and the lowest amount of plaque is seen on teeth with recession and sensitivity.29–31 Repeated root planing in shallow pockets resulted in gingival recession and crestal bone resorption.32 It was suggested that when a developmental or acquired crestal bone inadequacy pre-exists, brushing may be more likely to induce gingival recession due to repeated mild trauma on possibly thin and inflamed gingival tissue.17,18
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HYGIENE
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The frequency of gingival recession in subjects with excellent oral hygiene has been reported to be more frequent at buccal than proximal or lingual surfaces.7,8 In an epidemiologic study, gingival recession was positively correlated with the frequency of toothbrushing.9
Recession occurs more frequently in patients with good rather than poor oral hygiene.5,33 O’Leary and colleagues33 found that recession increased two years after oral hygiene instruction. Those findings could be due to the vigorous toothbrushing in the subjects in both of these studies. The concept of multiple etiologies of gingival recession also has been supported by parallel longitudinal studies in Norwegian and Sri Lankan populations during 1969 to 1990 among 15- to 50-year-olds.34
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ABERRANT FRENAL ATTACHMENT
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Aberrant frenal attachment also has been mentioned as a cause of localized recession, but the evidence is not overwhelming. Some studies did not find any correlation between frenal pull and recession,35,20 whereas others did find an association.36,22
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CLASSIFICATION SYSTEMS
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Since the presentation of gingival recession varies widely in the population, classification systems have been established to better describe it. An early study of recession associated with mandibular incisor teeth used the descriptive terms "narrow," "wide," "shallow" and "deep" to classify recession into four groups.37 Another study classified gingival recession into "shallow-narrow" defects as less than 3 mm in both dimensions, and "deep-wide" defects as more than 3 mm in both dimensions.38
The Index of Recession, or IR, was introduced by Smith.1 Recession was described by two digits separated by a dash (for example, F2-4), and the prefixed letter F or L denotes whether the recession is on the facial or lingual aspects of the tooth. If an asterisk were present, it would denote involvement of the mucogingival junction.
The digits describe the horizontal and vertical components of a recession site in that order. The horizontal component is expressed as a whole number value (from the range 0–5) depending on what proportion of the CEJ is exposed on either the facial or lingual aspects of the tooth, between the mesial and distal midpoints (Table 1
). Table 2 shows the second digit of the IR that gives the vertical extent of recession measured in millimeters (on a range from 0–9). Nordland and Tarnow39 presented a classification system for loss of papillary height, as described in Table 3.
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