Gingival Recession and Classification

The gingival margin is clinically represented by a scalloped line that follows the outline of the cemento-enamel junction (CEJ) or 1-2 mm coronal to it. Gingival recession is an apical shift of the gingival margin from the physiologic position with exposure of the root surface to the oral cavity.

In the literature, there are many classification systems for gingival recessions. Among the others, Miller’s classification system is one of the most widely used classification system. This classification aims the diagnosis of the severity of gingival recessions and the prognostic evaluation of the treatments. Gingival recessions have been classified into four groups based on the level of gingival margin with respect to the mucogingival junction and the underlying alveolar mucosa by Miller.

  • Miller I Gingival Recession; recession does not extend to the mucogingival line and there is no interdental attachment loss.
  • Miller II Gingival Recession; gingival margin reaches to mucogingival line and there is no interdental attachment loss.
  • Miller III Gingival Recession; defect is located at or beyond to the mucogingival line with interproximal attachment and bone loss.
  • Miller IV Gingival Recession; interproximal attachment loss is severe and/or there is malpositioning of the teeth.

However, after many years, on the basis of an exact classification on the use of more complicated mucogingival surgical approaches, new classification systems have been revealed.

Pini-Prato et. al (2010) have classified dental surface and exposed root surfaces with a new system. This system is based on the presence/visibility of CEJ (A) or absence of CEJ (B), and presence (+) or absence (-) of abrasions on the dental surface. Then, four possible classes have been identified (A+, A-, B+, B-).

More recently, Cairo et al.  (2011) proposed a new classification system which detailed the severity of interproximal bone loss. According to this classification system;

  • Recession type I (RT1); defects include gingival recession with no interproximal bone loss.
  • Recession type II (RT2); defects consist of interproximal attachment loss less than or equal to the buccal site.
  • Recession type III (RT3); defects with more interproximal bone loss than buccal site.

Gingival Recession 2021

Etiology of Gingival Recessions

Although microbial dental plaque and inflammation are the key factors for all periodontal defects, the etiology of the gingival recessions is more complex2. Etiological factors can be grouped under the headings of anatomical, physiological, pathological factors leading to gingival recessions.

Anatomical factors

Dehiscence and fenestration of the alveolar bone is one of the most widely seen etiological factor that may lead to gingival recession. Additionally, the abnormal tooth position in the arch and the shape of the tooth can also be considered as predisposing factors for gingival recessions.

Physiological factors

Orthodontic treatment, fingernail biting, sucking objects like pen, pencil or toothpicks are the physiological etiologic factors that may lead to gingival recessions.

Pathological factors

Faulty toothbrushing is commonly associated with gingival recession and partly explains low plaque levels found at sites of gingival recession. Soft-tissue ulcers and hard-tissue cervical abrasions are clinical signs of gingival recessions caused by traumatic toothbrushing .

Incorrect flossing techniques, peri-oral and intra-oral piercings, direct trauma associated with malocclusion, partial denture/restorative therapy, periodontal disease, bacterial plaque and herpes simplex can be listed as the other pathological etiologic factors.

Pathogenesis of Gingival Recessions

There is limited source of knowledge in the literature investigating the pathogenesis of gingival recession. The most rationally related study to pathogenesis has been proposed by Baker and Seymour in 1976, which reports histological findings associated with inflammatory gingival recession in Wistar rats. Baker and Seymour has introduced that gingival recession occurs with the presence of inflammation affecting epithelial and connective tissues. Proliferation of the epithelial cells into the connective tissue brings about a subsidence of the epithelial surface, which is manifested clinically as a gingival recession.

Three recognizable zones have been described during the experimental gingival recessions formation that can be simulated to human gingival recessions. (Figure1)

Diagram of the zones in the gingival recession

Figure 1. Diagram of the zones in the gingival recession process from which sections are taken vertically, parallel to the zone line. (NT: Natural tooth, GNT: Gingiva of Natural Tooth, RG: Receding Gingival Margin)

Appearance of Unaffected Tissues (Zone I)

This zone is described as the control zone. Tissue between epithelial layer of the periodontal pocket and palate is thick but does not contain alveolar bone. The rete pegs of the oral epithelium and pocket-lining epithelium are in normal configuration and not elongated into the intervening connective tissue.

Hyperplasia of Rete Pegs (Zone II)

Reduced thickness of the epithelial layer of the pocket and palate is observed. Lengthening of the rete pegs is noticeable. In the connective tissue, rete pegs are surrounded by the mononuclear cell infiltration. Section from a more advanced stage; the mesial and distal basal layers have produced a common granular layer, which has begun to split where a common keratinized layer has differentiated.

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