E G O P E R I O D O N T O LP O R I Y D O N T O L O G Y

The Aetiology of Gingival Recession

PAUL BAKER AND CHARLOTTE SPEDDING
distribution within different populations suggests that a variety of aetiological factors may be involved in gingival recession (Table 1). Populations with poor levels of oral hygiene show greater amounts of interproximal recession, as well as buccal recession, as a result of periodontal disease causing loss of the attachment apparatus (Figure 1). In populations that are highly motivated, the pattern of recession may be more easily explained by toothbrush trauma (Figure 2).

Abstract: Gingival recession affects a large proportion of the adult population. This
paper discusses the aetiology and mechanisms behind the formation of gingival recession, and considers the relevance of gingival recession to both orthodontics and restorative dentistry. It is followed by a second paper on the management of gingival recession. Dent Update 2002; 29: 5962

Clinical Relevance: This paper aims to highlight the causes and sequelae of
gingival recession.

ingival recession has been defined by the American Academy of Periodontology as the location of the marginal tissue apical to the cementoenamel junction. Gingival recession may occur not only on the labial/buccal and lingual/palatal surfaces, but also interproximally and may present circumferentially.

INCIDENCE/PREVALENCE
The prevalence of recession was examined in the Third National Health and Nutrition Examination Survey in America.1 Not surprisingly, it was found that the prevalence of gingival recession increases with age, with 0.5% of 1824 year olds having one or more sites with severe recession (>3 mm), increasing to 45% in those aged 65+. On an individual
Paul Baker, BDS, MSc, FDS RCS(Eng.), MRD, MClinDent,and Charlotte Spedding,BDS, MSc, MRD RCS(Eng.), MClinDent, Specialists in Periodontics, Clinical Demonstrators, Department of Periodontology and Preventive Dentistry, Guys, Kings and St Thomas Dental Institute, Guys Hospital, London.

site basis, the prevalence of severe recession remained small until the age of 45 (1%), though this increases with age, reaching 11% in people over 65. Gingival recession has been studied as part of Les classic studies on the natural history of periodontal disease in man, a comparison of Sri Lankan tea workers not exposed to dental care with a group of Norwegian dental students.2 This study found that gingival recession affecting the buccal surfaces presented in early adult life in the dentally motivated Norwegian population, occurring in 60% of 20 yearolds. By the age of 50, more than 90% had gingival recession, affecting 25% of buccal surfaces but only 4% of interproximal sites. In the Sri Lankan population, recession also started in early adult life, but there was a greater tendency for the recession to occur on all tooth surfaces, with 70% of buccal surfaces and 40% of interproximal surfaces affected by the age of 50.

MECHANISMS OF GINGIVAL RECESSION

The exact pathological changes that occur during recession are not fully understood. It is generally accepted that thin tissues overlying the root surface are more prone to recession than thick tissues, possibly because the inflammatory infiltrate that occurs adjacent to subgingival plaque will occupy the tissues to a distance of about 2 mm. Where the tissues are thin this may be the entire width of the attachment apparatus; where the tissues are thick, a more superficial layer of

AETIOLOGY
The change in prevalence and

Periodontal disease Toothbrush trauma Tooth malposition Traumatic overbite Alveolar bone dehiscences Muscle attachments and fraenal pull Iatrogenic: restorative treatment periodontal treatment orthodontics Self inflicted Drug related (cocaine abuse)4

Table 1. Causes of gingival recession.3 59

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Figure 1. Circumferential recession as a result of periodontal disease.

Figure 2. Recession due to toothbrush trauma.

uninvolved tissue will surround this 2 mm of inflammatory infiltrate. One theory is that gingival recession is caused by opposing rete ridges of the gingival and sulcular epithelia coalescing. The rete ridges are known to form in the junctional epithelium as a result of the inflammation occurring in chronic gingivitis. In thin tissues, this proliferation may allow the rete ridges to come in contact with the rete ridges of the opposing oral gingival epithelium, causing epithelial bridges across the width of the gingival tissues. Baker and Seymour looked at the histological changes that occurred during an induced recession.5 They found that, as an inflammatory infiltrate developed in the subepithelial connective tissue, the basal layers of the epithelium proliferated into this area. In what appeared to be an effort to maintain the epithelial thickness, superficial desquamation occurred in this area, leading to the formation of epithelial clefts within the gingival tissues.5

cause attachment loss or gingival recession. However, there are some factors which should be considered when planning orthodontic treatment in patients with gingival recession or those at risk of developing recession. Not least of these is the fact that the two primary causes of recession (gingival inflammation and toothbrush trauma) may be associated with the periodontal tissues when orthodontic appliances are being worn. Also, alveolar bone dehiscences appear to be associated with gingival recession. These may be present as a result of malaligned teeth or be created by orthodontic tooth movement (Figures 3 and 4). In children, continued growth of the alveolar process, along with changes in the position of the teeth, will alter the position of the gingival margin. Recession associated with a buccally placed tooth may resolve if the tooth moves lingually back into the arch, either as a result of increasing space due to alveolar growth, or as a result of orthodontic movement. For these reasons, mucogingival surgery is generally deferred until after facial growth is complete.

should be examined for their thickness and as to whether a dehiscence is present or whether movement will cause one. This may require augmentation at some stage of treatment, or meticulous plaque control as a preventive measure. The presence of a bony dehiscence is assumed to be associated with a greater risk of developing recession. This may occur where teeth are malpositioned, or where the gingival morphology is of a thin phenotype. Providing that teeth are moved within the envelope of the alveolar process, there is little risk of recession-type defects developing. The width (height) of keratinized tissue, or indeed its presence at all, does not seem to be a factor in predicting the development of recession during orthodontic movement.

RECESSION AND RESTORATIVE TREATMENT Margin Location

The concept of a biological width

Lingual Tooth Movement

It has been shown in animal experiments that movement of a tooth lingually will allow alveolar bone growth where previously there was a dehiscence. Lingual tooth movement will also be associated with a coronal shift in the position of the gingival margin as the overlying soft tissues increase in thickness. Any thin tissues or recession defect present before lingual movement should be left and reassessed after completion of orthodontic tooth movement.

Figure 3. At the start of orthodontic treatment, minimal recession is present around the lower incisors.

Labial tooth movement

Labial tooth movement will reduce the thickness of the tissues (bone and gingivae) overlying the tooth root, and may affect the level of the gingival margin. When considering labial movement, the overlying soft tissues

ORTHODONTICS AND RECESSION 68

Orthodontic treatment itself does not
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Figure 4. Same patient as in Figure 3 following orthodontics: note the increased recession around the central incisors. Dental Update March 2002

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Figure 5. Gingival inflammation associated with the crown margin on the upper right central incisor.

Restorations should be designed to allow adequate access for circumferential cleaning, and patients should always be instructed in how to maintain their restorations at home. If periodontal health is achieved before restorative treatment and is maintainable on its completion, recession need not occur and optimal aesthetics can be maintained in the long term.

requirement to have a minimal width of attached tissue. The concept that a minimum thickness of attached gingiva is required to maintain gingival health is now disregarded. The absence of keratinized tissue may be associated with a redder gingival margin, which may give the appearance of inflammation (Figure 6) but this is a result of the more visible vasculature associated with unkeratinized tissue.

determining the distance between the alveolar bone and gingival tissues is now widely accepted. When the biological width is encroached upon, the attachment apparatus will recede to ensure the biological width is maintained. Subgingivally placed restoration margins become supragingival with time.9,10 If aesthetics demand that a margin cannot be placed supragingivally, then it should be placed just below the gingival margin to minimize the occurrence of marginal tissue recession.

ANATOMY OF THE GINGIVAL TISSUES Significance of Attached Tissue Width

Originally it was thought that a minimum width of 2 mm of keratinized gingivae, and hence 1 mm of attached gingiva, was required to maintain gingival health: Lang and Le, in a study of dental students with supervised oral hygiene procedures,11 observed greater clinical inflammation at sites of narrow keratinized gingivae than in sites with more than 2 mm of keratinized tissue. However, Miyasato et al.12 examined similar sites in a group of hygienists and dental nurses and found minute amounts of gingival exudate associated with both widths of keratinized tissue in health, and no appreciable difference in the amounts of gingival exudate, plaque or clinical inflammation with experimentally induced gingivitis in the same subjects. Wennstrm and Lindhe13 found a possible explanation for Lang and Les observation when examining different widths of keratinized gingivae with experimentally induced gingivitis. Clinically, sites with minimal width appeared to show greater amounts of inflammation, but histologically the amounts of inflammatory infiltrate were the same. They concluded that the vasculature is more visible in this unkeratinized tissue. Thus, although it may be easier and more comfortable for the patient to keep clean, it is not an essential

Significance of Tissue Thickness

Thin gingival tissues may be more prone to gingival recession by the processes already described. Where tissues are thin, they may be associated with alveolar bone dehiscences. It is easy to see the difficulty in fitting a periodontal ligament, alveolar bone and associated connective tissues, overlying gingival lamina propria and epithelium into the limited space available.

Eruption and Position of Teeth

Teeth erupt into the mouth into a position dictated by the forces applied to the tooth during that eruption. Where eruption movement or orthodontic movement takes the tooth outside the envelope of the alveolar bone, a bony dehiscence will result. It is unclear whether the presence of a dehiscence is a risk factor for recession, or whether it is the thin tissues which are often present in such areas.

Plaque Retention
The presence of poor marginal fit, poor crown emergence angles and rough restoration surfaces will all lead to plaque retention in the critical dentogingival area (Figure 5). This will contribute to the development of recession in the susceptible patient. The placement of margins subgingivally is associated with increased difficulties in assessing the presence of marginal deficiencies and overhangs.

Figure 6. Lack of attached tissue width giving an unaesthetic appearance. (Courtesy of Mr N. Meekin.) Dental Update March 2002

Figure 7. Fraenal attachment associated with gingival recession. 61

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Class II, it should be possible to get complete coverage but partial coverage is all that can be expected for Class III and Class IV.

Class I Marginal tissue recession not extending to the mucogingival junction. No loss of interdental bone or soft tissue. Class II Marginal tissue recession extending to or beyond the mucogingival junction. No loss of interdental bone or soft tissue. Class III Marginal tissue recession extending to or beyond the mucogingival junction. Loss of interdental bone or soft tissue apical to the cementoenamel junction but coronal to the apical extent of the marginal tissue recession. Class IV Marginal tissue recession extending to or beyond the mucogingival junction. Loss of interdental bone extends to a level apical to the extent of marginal tissue recession.

SUMMARY
This paper has introduced the aetiology of gingival recession, and attempted to discuss the relevance of gingival recession to the general dental practitioner. The second paper in this series covers the treatment of gingival recession, with an emphasis on the various surgical techniques that can be used.

Figure 8. Recession extending to the depth of the vestibule.

Fraenal Attachment and Vestibular Depth

In some clinical situations the local anatomy makes oral hygiene difficult. For instance, where a fraenal attachment is associated with the gingival margin (Figure 7), or where previous recession has moved the gingival margin to the depth of the vestibule (Figure 8), it may be extremely difficult for the patient to render the area plaque free.

R EFERENCES
1. Brown LJ, Brunelle JA, Kingman A. Periodontal status in the United States, 198891: Prevalence, extent and demographic variation. J Dent Res 1996; 75: 672683. Le H, nerud , Boysen H. The natural history of periodontal disease in man: Prevalence, severity and extent of gingival recession. J Periodontol 1992; 63: 489495. Wennstrm JL. Mucogingival therapy. Ann Periodontol 1996; 1: 671701. Kapila YL, Kashani H. Cocaine-associated rapid gingival recession and dental erosion. A case report. J Periodontol 1997; 68: 485488. Baker DL, Seymour GJ. The possible pathogenesis of gingival recession. J Clin Periodontol 1976; 3: 208 219. Wennstrm JL. Mucogingival considerations in orthodontic treatment. Semin Orthod 1996; 2: 46 54. Moriarty JD. Mucogingival considerations for the orthodontic patient. Curr Opin Periodontol 1996; 3: 97102. Matthews DP, Kokich VG. Managing treatment for

Table 2. Millers classification of gingival recession.14

the orthodontic patient with periodontal problems. Semin Orthod 1997; 3: 2138. Valderhaug J, Birkland JM. Periodontal conditions in patients 5 years following insertion of fixed prostheses. Pocket depth and loss of attachment. J Oral Rehabil 1976; 3: 237243. Valderhaug J. Periodontal conditions and carious lesions following the insertion of fixed prostheses. Int Dent J 1980; 30: 296304. Lang NP, Le H. The relationship between the width of keratinized gingiva and gingival health. J Periodontol 1972; 43: 623627. Miyasato M, Crigger M, Egelberg J. Gingival condition in areas of minimal and appreciable width of keratinized gingiva. J Clin Periodontol 1977; 4: 200 209. Wennstrm JL, Lindhe J. Plaque-induced gingival inflammation in the absence of attached gingiva in dogs. J Clin Periodontol 1983; 10: 266276. Miller PD. A classification of marginal tissue recession. Int J Periodont Restor Dent 1985; 5: 913.

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CLASSIFICATION OF RECESSION
Gingival recession has been classified by Miller, as shown in Table 2.14 The Miller classification is useful when considering root surface coverage procedures. It is not possible to cover the root surface above the level of the proximal tissue. When treating recession defects that are Class I or

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ABSTRACT
SHOULD WE STOP MAKING APICAL STOPS? An In Vitro Experiment on the Effect of an Attempt to Create Apical Matrix during Root Canal Preparation on Coronal Leakage and Material Extrusion. A. Kastakova, M.-K. Wu and P.R. Wesselink. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2001; 91: 462467. The commonly taught method for preparing the apical part of the root
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canal system is the apical stop (apical matrix), by enlarging the root canal to three sizes greater than the first file that binds at working length. However, a more recent suggestion has been to create an apical taper through a serial shaping technique. It is thought that the apical stop may only prevent further passage of the master file, and not reduce microleakage or the extrusion of obturating materials. These workers prepared 60 roots by each technique, and obturated the canals using a variety of techniques. They then examined the roots for both

of the criteria above, (microleakage using a fluid transport technique, and extrusion of the restorative material). In both the leakage and the extrusion tests, no significant difference was found between the canals prepared with either technique. It is therefore suggested that the hypothesis that preparing an apical stop as traditionally taught will reduce the amount of filling extruded and the leakage is not substantiated, thus confirming current teaching of canal preparation techniques. Peter Carrotte Glasgow Dental School
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