Gingival recession. Part 1: prevalence and aetiology

Gingival recession affects more than 50% of the population, across all age groups, with almost all middle to older aged people exhibiting the condition.^1–4 It has a multifactorial aetiology and is defined, in broad terms, as the migration of the gingival margin apical to the cemento-enamel junction (CEJ), with the distance between the two giving a measure of the recession. This definition was modified in 2017 by the World Workshop to ‘an apical shift of the gingival margin caused by different conditions/pathologies’ and can apply to any surface of the tooth.⁵ Gingival recession is often an incidental finding, rarely causes symptoms and can affect one or more teeth. Although considered a silent condition, it has been reported that gingival recession can negatively influence quality of life by causing physical pain and psychological discomfort.⁶ This is the first of two articles that address the prevalence and aetiology of gingival recession, along with the different classification systems used to define it.

Prevalence of gingival recession

The prevalence of gingival recession varies in different populations and is influenced by age, with the overall prevalence ranging from 58% to 99.7%.^1–4,7,8 The reported differences in the variation across different populations are influenced by the geographic distribution of the population, variable socio-economic and educational status, as well as the way in which the recession is measured (Table 1).

Gender has been identified as a significant factor when considering gingival recession, with males more affected than females.^1,9,10 Recession can develop at a very young age and can progressively worsen over time. The degree by which the recession progresses is population dependent, for example 100% of 40-year-old Sri Lankans were reported to have recession when compared to 90% of 50-year-old Norwegians.¹¹

Almost any teeth present can be affected by gingival recession with it seen more frequently in the mandible when compared to the maxilla.^10–12 The teeth most commonly affected are considered to be the mandibular incisors.^8,10,11

The severity of gingival recession can be grouped into mild (up to 1 mm), moderate (1–3 mm) and severe (4 mm and over).¹² The majority of the population has been shown to experience at least one mild site, with studies suggesting up to 30% experiencing moderate recession. Others have shown that 5.9–40.7% of the population experiences severe recession, with the variance being related to different countries.^13,14 Buccal surfaces of the teeth are the most commonly affected, especially in young people, followed by the lingual and interproximal surfaces.¹¹ Multiple factors can affect the initiation and development of the recession which are discussed below.

Aetiology

Gingival recession has a multifactorial aetiology with a predominance of factors that play a role in its development. A healthy mucogingival complex, as shown in Figure 1, is made up of free and attached gingivae, mucogingival junction and alveolar mucosa. It is essential to maintain the health of the attachment to the teeth. When this complex is disrupted, it can present as a closed disruption, through pocket formation, or through an open disruption, leading to cleft formation or recession.¹¹ The factors that cause this can be categorized into either predisposing or precipitating risk factors (Table 2). Predisposing factors will usually place the gums at risk of developing recession and usually include anatomical factors, such as bone dehiscence, tooth malposition, thin gingival tissue biotype, high frenal attachments and a lack of keratinized tissue. Precipitating factors, on the other hand, increase the risk of the recession developing, and include traumatic tooth brushing, dental treatment (orthodontic and restorative), poor plaque control, piercings and self-inflicted trauma. While the precipitating factors will increase the chance of the recession developing, there would have to be underlying predisposing factors present for the recession to develop.

Predisposing risk factors

Anatomical

Bone dehiscence. A bone dehiscence is characterized by a missing buccal plate where the alveolar crestal margin is located apically. In contrast, a fenestration is where there is a window of missing bone on the buccal surface with the alveolar bone margins intact (Figures 2 and 3). Studies have shown up to 40% of adults will have a dehiscence, with the most commonly affected teeth being the canines, and up to 62% will have fenestrations.¹⁵ Dehiscences are also reported to affect the buccal aspects of the teeth, most frequently the coronal third of the tooth, which could explain why the buccal surfaces of the teeth are more commonly affected by recession (Figures 2 and 3).¹⁶

Tooth position. Malocclusions and malalignment of teeth lead to an unfavourable position of the root in the alveolar bony housing. Usually in these patients, the alveolar bone at the crest is either void or thin, especially buccally, thus increasing the risk of gingival recession developing.^9,17,18 The tooth position is also important because it influences the quality of the gingival tissue biotype (Figure 4).

Gingival tissue biotype. The different biotypes of gingival tissues have been described using the anatomical characteristics of the mucogingival complex. This includes a description of the gingival tissue thickness and has been described in three categories – thin scalloped, thick flat and thick scalloped.¹⁹ The thin scalloped has a narrow zone of keratinized tissue with thin gingival tissue and thin alveolar bone. The thick flat biotype usually has a broad zone of keratinized tissue and thick alveolar bone, and the thick scalloped has a narrow zone of keratinized tissue with thick bone. The main variance in these two groups is the thickness of the underlying bone and the amount of keratinized tissue. Thin tissue has a bone thickness of approximately 0.3 mm and thick tissue that of 0.8 mm.²⁰ Examples of the clinical appearance of thin and thick biotypes are shown in Figure 5. The thickness of the tissue is usually difficult to assess and is often measured by inserting a probe into the sulcus (Figure 6). If the probe is visible through the sulcus it is considered thin.

Lack of keratinized gingivae. Keratinized gingiva is the part of the oral mucosa that surrounds the teeth and extends from the free gingival margin to the mucogingival fold and is made up of the free and attached gingivae.²¹ The width of the keratinized tissue varies in the different biotypes and ranges from 2.8 mm to 5.4 mm in thin biotypes, and from 5.1 mm to 6.7 mm in the thick biotypes.²⁰ While keratinized tissue is not essential, it has been reported that a minimum thickness of 2 mm is necessary to maintain periodontal health and without this, recession may occur (Figure 7).⁵

High frenal attachment. Frenal attachments are fibrous collagenous tissue folds that connect the lip to the alveolar process, and when positioned too close to the gingival margin, often affect a person's ability to maintain an optimal level of plaque control. This, along with the possible mechanical retraction of the gingival tissue, is thought to contribute to the development of recession (Figure 8). While the latter has been hypothesized, it is more likely that frenal presence impairs the ability to maintain oral hygiene leading to inflammation and subsequent recession.^22,23

Precipitating factors

Iatrogenic

Orthodontic tooth movement. This does not inherently cause gingival recession as usually the induced tooth movement is undertaken within the boundaries of the alveolar complex. However, in cases with underlying predisposing anatomical factors, the recession occurs because the tooth movement induces changes in the bone morphology (Figure 9). Therefore, if there is a thin buccal plate, or dehiscence, along with thin gingival tissue biotype, high muscle attachment and a malpositioned tooth, the risk of gingival recession developing becomes greater.^24–27 Others have reported that fixed orthodontic retainers may induce gingival recession post-treatment; however, it is more likely that this is related to the type of retainer (fixed or removable) and the plaque retention around this resulting in inflammation characteristic of periodontal disease.^28,29 The effects of occlusal trauma caused by a deep overbite whereby the lower incisor teeth cause stripping of the gingival tissues palatal to the maxillary incisors can also induce recession with soreness often expressed by patients owing to the secondary inflammation of the gingival tissues.³⁰

Orthodontic tooth movement can, in some cases, assist in improving the severity of the gingival recession by moving the tooth into a more favourable position within the alveolar housing.³¹ Gebistorf et al demonstrated that patients with orthodontically treated malocclusion exhibited less gingival recession 10–15 years post-treatment when compared to those with an untreated malocclusion.³¹

Restorative treatment. Restorative treatment, particularly in the presence of predisposing factors, such as overhangs and subgingival restoration margins, can lead to gingival recession by damaging the gingival complex both during and after treatment. This is seen particularly in patients with thin gingival tissue biotype when subgingival restorations encroach on the biological width.^5,32 The gingival tissue biotype should therefore be assessed prior to any fixed prosthetic treatment, especially when subgingival margins are being considered. If the tissues are thin, then either supragingival or equigingival margins should be considered to minimize the risk of gingival recession.^33,34 Poorly designed dentures, the so called ‘gum strippers’, also cause recession by trauma to the gingival tissues that is exacerbated in the presence of poor plaque control (Figure 10).³⁵ Poorly designed denture clasps, especially gingivally approaching clasps, can also lead to recession over time on the abutment teeth. Thus, the need for well-designed dentures with attention to the gingival tissue biotype should not be underestimated.³⁵

Traumatic

Traumatic tooth brushing. This is often seen in patients who are overzealous with their brushing, with trauma associated with the incorrect use of oral hygiene aids. It is theorized that the repeated trauma physically injures the gingival tissues progressively, causing gingival recession over time. The direct relationship between traumatic homecare regimens and gingival recession is inconclusive. Although most short-term studies suggest an association between gingival trauma and abrasion, there are no long-term studies that support the notion of gingival recession developing following toothbrush trauma.^5,36 If, however, there are underlying predisposing factors, then it seems logical that traumatic tooth brushing could contribute to the occurrence of gingival recession (Figure 11).

Piercings. Tongue and lip piercings are the most common site for oral piercing, with 43% being placed in the tongue, and 33% in the lip.³⁷ The incidence of gingival recession is reported to be 44% in people with tongue piercing and 50% in those with lip piercing, with the latter being at a four-times higher risk of recession than those without a piercing.³⁸ Overall, 68–80% of lip piercings have been associated with gingival recession owing to the intra-oral position of the ‘stud’ of the piercing.³⁹ This constantly traumatizes the labial mucosal tissues, with the severity of recession being dependent on the degree of keratinized tissue present, and the quality of the gingival tissue biotype.⁴⁰ In comparison, tongue piercings have been associated with a higher prevalence of lingual recession, which ranged from 3% to 33%.³⁹ This is thought to be related to the trauma caused by the ‘dumbbell’ during protrusion of the tongue.

Self-inflicted injury. These injuries are repetitive acts that cause physical damage to the gingivae usually in the form of scratching, rubbing or picking the gingivae using a fingernail or abrasive objects and are more common in children, especially females.^41,42 The local application of cocaine to the gingival tissues has also been associated with localized gingival recession.^43,45 These cases are difficult to manage owing to the complex underlying social and medical issues, and early intervention often helps minimize the risk of progression.

Pathogenic

Periodontal disease. If left untreated, periodontal disease ultimately results in bone loss and gingival recession. The disease, once initiated and if not managed, results in the apical migration of the gingival tissues with pocket formation, the so called, closed destruction of the mucogingival complex.¹¹ The pathogenesis of the disease results in bone resorption related to the inflammatory process affecting the alveolus, with the recession often being masked by the tissue inflammation and oedema (Figure 12). Untreated, the disease progresses, which results in gingival tissue recession. However, even if treatment is initiated, once the inflammation is eliminated, there is a retraction of the gingival tissues with root surface exposure as the gingival tissues adopt a healthier position. Surgical forms of treatment also lead to recession, the extent of which is dependent on the type of procedure being undertaken. While bacterial plaque is the causative factor of periodontal disease, risk factors for periodontal disease, such as smoking and diabetes, have also been associated with a higher risk of recession developing.^23,45,46

Oral mucosal disorders. These disorders are autoimmune and per se, will not cause the gingival recession; however, the condition affects the patient's ability to perform optimal plaque control, thereby generating an inflammatory reaction. Additionally, these patients may have thin quality gingival biotype, lack of keratinized tissue and underlying bone dehiscences, which, as discussed earlier, contribute to the condition. Specifically, gingival recession has been reported as a consequence of graft versus host disease and morphea.^47,48

Occlusal trauma. Historical studies suggested that gingival recession may be induced by excessive occlusal force, although more recent evidence does not support this.⁴⁹ If this were to contribute, the extent of the contribution would be dependent on the thickness of the buccal/cortical bone plate. In the presence of buccal dehiscences, the classical V-shaped defect may be seen in these cases, which anecdotally may often be associated with abfraction and recession.⁵⁰

Classification of gingival recession

Classifications have been used to aide communication, but also as decision-making tools for the clinician when considering the best course of action when taking into account the multiple factors that may influence the outcome. The multifactorial aetiology of gingival recession can make the management of the condition challenging; however, with careful consideration of the aetiological factors, the outcome to treatment can be successful.

Table 3 shows the different classification systems used to describe gingival recession. Most are complicated to use, relying on defining the recession using objective criteria, including an assessment of gingival tissue thickness. Miller's classification system (1985, 2011, 2018) uses the extent of the recession, in relation to the mucogingival fold, in conjunction with presence of hard and soft tissue interdentally (see Table 4).^51,52

Until 2018 when the World Workshop introduced the new classification, this was the most commonly used classification for gingival recession. The new classification combines Miller's Class I and II into a single category, and uses the interdental clinical attachment loss as the descriptor, measuring the attachment loss to the apical limit (Table 5). While aimed at making the classification simpler, it does not take into consideration the extent of keratinized tissue present, which could influence the choice of treatment.

More recently, Cortellini and Bissada²⁰ undertook a systematic review that outlined the multifactorial issues that influence the diagnosis and management of gingival recession and outline a novel treatment-oriented classification that takes into consideration the gingival tissue biotype, the gingival recession severity and associated cervical lesions to assist the clinicians' decision-making process using a 4 x 5 matrix (Table 6). The classification is based on two groups:

• Group 1: no recession Based on the assessment of the gingival tissue biotype, the gingival tissue thickness and width of the keratinized tissue either in single site or the whole mouth. This is then further divided into Case A, with thick gingival tissue biotype, and Case B, with thin gingival tissue biotype, and the modality of monitoring described.
• Group 2: recession present Based on a treatment-oriented approach using the interdental clinical attachment level score described by Cairo et al (RT1-3).⁵³ These are further quantified by measurements of the recession depth (distance from the cemento-enamel junction to the free gingival margin), gingival tissue thickness, keratinized tissue width (distance from the free gingival margin to the mucogingival fold) and root surface condition (i.e. abrasion present or not). Other factors such as tooth position, cervical wear, and adjacent recessions are also recorded. Depending on the assessment analysis, the management is divided into case C, where a conservative attitude is adopted, or case D where a treatment-orientated approach is adopted influenced by the patient's complaint.

This classification is the first of its kind where an assessment of all the factors, predisposing and precipitating, are considered when making the decision of how best to manage the recession. However, its use in daily practice can be challenging and Miller's classification, along with the 2018 classification, remain the more popular ways of classifying gingival recession.

Conclusion

This article highlights the difficulties that clinicians often face when assessing gingival recession and provides an overview of its prevalence and multifactorial aetiology. The need to take these factors into consideration is highlighted, and the challenges with the different classification systems that have been used highlights the importance of using objective criteria, along with the different prognostic factors that may influence treatment outcome. The second article will focus on the management of gingival recession and the decision-making process to optimise treatment outcomes.