N

220

ingival 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
Many authors have attempted to
may exhibit explain the phenomenon of gingival
generalized recession. There is a theory that the
gingival gingival margin, rather than
retracting apically, may remain largely
recession
static while the tooth moves occlusally
without having by eruption or extrusion and lifts the
any awareness CEJ clear of the gingival margin.2 This
of the appears to be an unlikely or a rare
condition. 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

MOAWIA M. KASSAB, D.D.S., M.S.; ROBERT E.

COHEN, D.D.S., Ph.D.

Background. Gingival recession in its

localized or generalized form is an undesirable condition resulting in root exposure.
A D A
J
The result often is not esthetic and
may

lead to sensitivity and root caries. Exposed

root surfaces also are prone to abrasion.
The purpose of this article is to describe the
N
C
U
U
IN
prevalence, etiology and factorsAassociated
D
1
RT G E
with gingival recession.
ICLE
Types of Studies Reviewed. The
authors reviewed cross-sectional epidemiologic studies of gingival recession and found
that they correlated the prevalence of recession to trauma, sex, malpositioned teeth,
inflammation and tobacco consumption.
The recent surveys they reviewed revealed
that 88 percent of people 65 years of age
and older and 50 percent of people 18 to 64
years of age have one or more sites with
recession. The presence and extent of gingival recession also increased with age.
Results. More than 50 percent of the population has one or more sites with gingival
recession of 1 mm or more. The prevalence
of gingival recession was found in patients
with both good and poor oral hygiene. It has
been proposed that recession is multifactorial, with one type being associated with
anatomical factors and another type with
physiological or pathological factors. Recession has been found more frequently on
buccal surfaces than on other aspects of the
teeth.
Clinical Implications. Dentists should
be knowledgeable about the etiology, prevalence and associating factors of gingival
recession, as well as treatment options, so
that appropriate treatment modalities can
be offered to patients. Treatments for gingival recession include gingival grafting,
guided tissue regeneration and orthodontic
therapy. Such treatments typically result in
esthetic improvement, elimination of sensitivity and a decreased risk of developing
root caries.
CON

The etiology and

prevalence of gingival
recession

ABSTRACT

IO
N

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

JADA, Vol. 134, February 2003

Copyright 2003 American Dental Association. All rights reserved.

T R E N D S

changes in gingival recession may occur at a

given site.
AGING

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.

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.
PHYSIOLOGICAL FACTORS
Recession also was more prevalent
and severe at buccal than at interPhysiological factors may include
Where gingival
proximal surfaces of teeth.
the orthodontic movement of teeth
recession has
Similarly, Gorman5 found that
to positions outside the labial or
developed, the
the frequency of gingival recession
lingual alveolar plate, leading to
increased with age and was greater
dehiscence formation.17 Such
underlying presence
in men than in women of the same
studies suggested that the acquired
of dehiscences may
age. Malpositioned teeth and toothloss of alveolar bone might be assobe considered and
brush trauma were found to be the
ciated with a number of identifiable
possibly discovered
most frequent etiologic factors assophysiological or pathological condiduring flap
ciated with gingival recession.
tions for which bone loss is part of a
procedures.
Recession associated with labially
physiological or pathological
positioned teeth occurred in 40 perprocess.
cent of patients 16 to 25 years of age
PATHOLOGICAL FACTORS
and increased to 80 percent of patients in the 36
to 86 years of age group. Those findings were corPathological factors include bone resorption as a
roborated by Murray,6 who examined 4,000 subsequel to microbially induced periodontal disjects and found that the incidence of gingival
eases. In this case, however, the process of recesrecession increased with age.
sion may be more complex since the teeth
involved may extrude, tilt and become mobile. A
ANATOMICAL FACTORS
rat study demonstrated a possible mechanism of
One etiologic factor that may be associated with
gingival recession, showing that loss of attachgingival recession is a prior lack of alveolar bone
ment was the result of localized inflammatory
at the site.10 The deficiencies in alveolar bone may
processes in connective tissue with the accumulabe developmental (anatomical) or acquired (physition of mononuclear cells.18 It also was suggested
11
ological or pathological).
that inflammation may persist subclinically and
Anatomical factors that have been related to
therefore cannot be eliminated as a factor in
recession include fenestration and dehiscence of
recession.18 Similarly, recession has been related
the alveolar bone, abnormal tooth position in the
to inflammation in periodontal connective tissue
arch, aberrant path of eruption of the tooth and
in monkeys.19-22
12
individual tooth shape. All those anatomical facTRAUMA
tors are interrelated and may result in an alveolar osseous plate that is thinner than normal
In addition to psychological factors, various forms
and that may be more susceptible to resorption.
of traumasuch as vigorous toothbrushing, aberAnatomically, a dehiscence may be present due
rant frenal attachment, occlusal injury, operative
to the direction of tooth eruption or other developprocedures and tobacco chewinghave been
mental factors, such as buccal placement of the
thought to play a role in the etiology of recession.
root relative to adjacent teeth so that the cervical
Clinical and case report studies also have assoJADA, Vol. 134, February 2003
Copyright 2003 American Dental Association. All rights reserved.

221

T R E N D S

TABLE 1

THE HORIZONTAL EXTENT OF RECESSION.*

SCORE

CRITERIA

No clinical evidence of root exposure

No clinical exposure of root exposure plus a subjective awareness of

dentinal hypersensitivity in response to a one-second air blast is
reported, and/or there is clinically detectable exposure of the CEJ for
up to 10 percent of the estimated midmesial to middistal distance

Horizontal exposure of the CEJ more than 10 percent but not

exceeding 25 percent of the estimated midmesial to middistal distance

Exposure of the CEJ more than 25 percent of the midmesial to

middistal distance but not exceeding 50 percent

Exposure of the CEJ more than 50 percent of the midmesial to

middistal distance but not exceeding 75 percent

Exposure of the CEJ more than 75 percent of the midmesial to

middistal distance up to 100 percent

* Source: Smith.1
CEJ: Cementoenamel junction.

TABLE 2

THE VERTICAL EXTENT OF RECESSION.*

SCORE

CRITERIA

No clinical evidence of root exposure

No clinical exposure of root exposure plus a subjective awareness of

dentinal hypersensitivity is reported and/or there is clinically
detectable exposure of the CEJ not extending more than
1 millimeter vertically to the gingival margin

2 to 8

Root exposure 2 to 8 mm extending vertically from the CEJ to the base

of the soft-tissue defect

Root exposure more than 8 mm from the CEJ to the base of the
soft-tissue defect

An asterisk is present next to the second digit whenever the vertical

component of the soft-tissue defect encroaches into the mucogingival
junction or extends beyond it into alveolar mucosa; the absence of an
asterisk implies either absence of mucogingival junction involvement
at the indexed site or its noninvolvement in the soft-tissue defect

* Source: Smith.1
CEJ: Cementoenamel junction.

ciated 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
222

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 righthanded 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

HYGIENE

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
OLeary and colleagues33 found that recession
increased two years after oral hygiene instruc-

JADA, Vol. 134, February 2003

Copyright 2003 American Dental Association. All rights reserved.

T R E N D S

tion. 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
ABERRANT FRENAL
ATTACHMENT

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
CLASSIFICATION
SYSTEMS

TABLE 3

CLASSIFICATION OF PAPILLARY HEIGHT.*

CLASSIFICATION

CRITERIA

Normal

Interdental papilla fills embrasure space to the apical extent of

the interdental contact point/area

Class I

The tip of the interdental papilla lies between the interdental

contact point and the most coronal extent of the interproximal
CEJ (space present but interproximal CEJ is not visible)

Class II

The tip of the interdental papilla lies at or apical to the

interproximal CEJ but coronal to the apical extent of the facial
CEJ (interproximal CEJ visible)

Class III

The tip of the interdental papilla lies level with or apical to the
facial CEJ

* Source: Nordland and Tarnow.39

CEJ: Cementoenamel junction.

TABLE 4

CLASSIFICATION OF MARGINAL TISSUE RECESSION.*

CLASSIFICATION

CRITERIA

Class I

Marginal tissue recession that does not extend to the

mucogingival junction

Class II

Marginal tissue recession that extends to or beyond the

mucogingival junction, with no periodontal attachment loss
(bone or soft tissue) in the interdental area

Class III

Marginal tissue recession that extends to or beyond the

mucogingival junction, with periodontal attachment loss in the
interdental area or malpositioning of teeth

Since the presentation of

Marginal tissue recession that extends to or beyond the
Class IV
mucogingival junction, with severe bone or soft-tissue loss in
gingival recession varies
the interdental area and/or severe malpositioning of teeth
widely in the population,
40
* Source: Miller.
classification systems have
been established to better
describe it. An early study of recession associated
what proportion of the CEJ is exposed on either
with mandibular incisor teeth used the descripthe facial or lingual aspects of the tooth, between
tive terms narrow, wide, shallow and deep
the mesial and distal midpoints (Table 1). Table 2
to classify recession into four groups.37 Another
shows the second digit of the IR that gives the
study classified gingival recession into shallowvertical extent of recession measured in millimenarrow defects as less than 3 mm in both dimenters (on a range from 0-9). Nordland and Tarnow39
sions, and deep-wide defects as more than 3 mm
presented a classification system for loss of papilin both dimensions.38
lary height, as described in Table 3.
The Index of Recession, or IR, was introduced
These two indexes are used primarily in crossby Smith.1 Recession was described by two digits
sectional and longitudinal epidemiologic studies
separated by a dash (for example, F2-4), and the
to describe the prevalence, incidence, severity and
prefixed letter F or L denotes whether the recesetiology of gingival recession. Clinically, Millers40
sion is on the facial or lingual aspects of the tooth.
classification probably is the most widely used for
If an asterisk were present, it would denote
describing gingival recession (Table 4). Millers
involvement of the mucogingival junction.
classification also is illustrated in the figure.
The digits describe the horizontal and vertical
TREATMENT OPTIONS
components of a recession site in that order. The
horizontal component is expressed as a whole
Different gingival grafting techniques have been
number value (from the range 0-5) depending on
proposed to treat gingival recession, including the
JADA, Vol. 134, February 2003
Copyright 2003 American Dental Association. All rights reserved.

223

T R E N D S

D
Figure. The Miller classification system. A. Class I recession. B. Class II recession. C. Class III recession. D. Class IV
recession.

lateral sliding flaps, coronally positioned flaps

and connective tissue grafts, resulting in mean
root coverage of 65 to 98 percent.41,42 Guided
tissue regeneration was introduced later to treat
recession, using bioabsorbable or nonabsorbable
membranes, and studies showed similar results
with a mean root coverage of 48 to 92 percent.43,44
Orthodontic treatment can be considered with or
without periodontal surgery, especially in
situations were teeth are malpositioned.
CONCLUSIONS

The induction of gingival recession by a single

factor is unlikely.1,34 In reality, several factors
may play a part, but not necessarily simultane224

ously or equally. To identify and quantify the

influence of each factor may not be possible, and
recession at a given site may be the endpoint or
outcome of several different factors. Further
investigation needs to be done to fully understand
those relationships.
The authors would like to thank Peter Bush and the Instrumentation
Center at the State University of New York at Buffalo for their contribution. They also would like to thank Dr. Hala Badawi for her support
and assistance.
1. Smith RG. Gingival recession: reappraisal of an enigmatic condition and a new index for monitoring. J Clin Periodontol 1997;24:201-5.
2. Ainamo J, Talari A. The increase with age of the width of attached
gingiva. J Periodontal Res 1976;11(4):182-8.
3. Kajiyama K, Murakamai T, Yokota S. Gingival reactions after
experimentally induced extrusion of the upper incisors in monkeys. Am
J Orthod Dentofacial Orthop 1993;104(1):36-47.

JADA, Vol. 134, February 2003

Copyright 2003 American Dental Association. All rights reserved.

T R E N D S

4. Albandar JM,
Kingman A. Gingival
recession, gingival
bleeding, and dental
calculus in adults 30
years of age and older
in the United States,
1988-1994. J Periodontol 1999;70(1):
When this article was
Dr. Cohen is a pro30-43.
written, Dr. Kassab was
fessor, Department of
5. Gorman WJ.
a clinical assistant proPeriodontics and
Prevalence and etifessor, Department of
Endodontics, and the
ology of gingival
Periodontics and
director, Postgraduate
recession. J PeriEndodontics, School of
Periodontics, School of
odontol 1967;38:
Dental Medicine, State
Dental Medicine, State
316-22.
University of New York
University of New York
6. Murray JJ. Ginat Buffalo. He now is a
at Buffalo.
gival recession in
periodontist, The
tooth types in high
Forsyth Institute, 140
fluoride and low fluoride areas. J Periodontal
The Fenway, Boston,
Res 1973;8:243-51.
Mass. 02115, e-mail
7. Le H, Anerud A, Boysem H, Smith M.
mkassab@forsyth.
The natural history of periodontal disease in
org. Address reprint
man: the rate of periodontal destruction before
requests to Dr. Kassab.
40 years of age. J Periodontol 1978;49:607-20.
8. Kallestal C, Matsson L, Holm AK. Periodontal conditions in a group of Swedish adolescents (I): a descriptive
epidemiologic study. J Clin Periodontol 1990;(17):601-8.
9. Vehkalahti M. Occurrence of gingival recession in adults. J Periodontol 1989;60:599-603.
10. Watson PJ. Gingival recession. J Dent 1984;12(1):29-35.
11. Geiger AM. Mucogingival problems and the movement of
mandibular incisors: a clinical review. Am J Orthod 1980;78:511-27.
12. Alldritt WA. Abnormal gingival form. Proc R Soc Med 1968;61(2):
137-42.
13. Lost C. Depth of alveolar bone dehiscences in relation to gingival
recessions. J Clin Periodontol 1984;11:583-9.
14. Bernimoulin J, Curilovie Z. Gingival recession and tooth mobility.
J Clin Periodontol 1977;4(2):107-14.
15. Modheer T, Odenrick L. Post-treatment periodontal status of labially erupted maxillary canines. Acta Odontol Scand 1980;38:253-6.
16. Olsson M, Lindhe J. Periodontal characteristics in individuals
with varying form of the upper central incisors. J Clin Periodontol
1991;18(1):78-82.
17. Wennstrm JL, Lindhe J, Sinclair F, Thilander B. Some periodontal tissue reactions to orthodontic tooth movement in monkeys. J
Clin Periodontol 1987;14(3):121-9.
18. Baker DL, Seymour GJ. The possible pathogenesis of gingival
recession: a histological study of induced recession in the rat. J Clin
Periodontol 1976;3:208-19.
19. Hopps RM, Johnson NW. Relationship between histological
degree of inflammation and epithelial proliferation in macaque gingiva.
J Periodontal Res 1974;9:273-83.
20. Powell RN, McEniery TM. Disparities in gingival height in the
mandibular central incisor region of children aged 6-12 years. Community Dent Oral Epidemiol 1981;9(1):32-6.
21. Akpata ES, Jackson D. The prevalence and distribution of gingivitis and gingival recession in children and young adults in Lagos,
Nigeria. J Periodontol 1979;50:79-83.
22. Stoner JE, Mazdyasna S. Gingival recession in the lower incisor

region of 15-year-old subjects. J Periodontol 1980;51(2):74-6.

23. Jenkins WM, Allan CJ. Guide to periodontics. 3rd ed. Oxford,
England: Wright; 1994:155-85.
24. ER N, zkavaf A, Berberoglu A, Yamalik N. An unusual case of
gingival recession: oral piercing. J Periodontol 2000;71:1767-9.
25. Sandholm L, Niemi ML, Ainamo J. Identification of soft tissue
brushing lesions: a clinical and scanning electronmicroscopic study. J
Clin Periodontol 1982;9:397-401.
26. Bergstrom J, Eliasson S. Cervical abrasion in relation to toothbrushing and periodontal health. Scand J Dent Res 1988;96:405-11.
27. Khocht A, Simon G, Person P, Denepitiya JL. Gingival recession
in relation to history of hard toothbrush use. J Periodontol
1993;(64):900-5.
28. Gillette WB, Van house RL. Ill effects on improper oral hygiene
procedures. JADA 1980;10(1):476-80.
29. Addy M, Mostafa P, Newcombe RG. Dentine hypersensitivity: the
distribution of recession, sensitivity and plaque. J Dent 1987;15:242-8.
30. Addy M, Griffiths G, Dummer P, Kingdom A, Shaw WC. The distribution of plaque and gingivitis and the influence of toothbrushing
hand in a group of South Wales 11-12 year-old children. J Clin Periodontol 1987;14:564-72.
31. Niemi ML, Sandholm L, Ainamo J. Frequency of gingival lesions
after standardized brushing as related to stiffness of toothbrush and
abrasiveness of dentifrice. J Clin Periodontol 1984;11:254-61.
32. Lindhe J, Nyman S, Karring T. Scaling and root planing in
shallow pockets. J Clin Periodontol 1982;9:415-8.
33. OLeary TJ, Drake RB, Crump PP, Allen MF. The incidence of
recession in young males: a further study. J Periodontol 1971;42:264-7.
34. Le H, Anerud A, Boysen H. The natural history of periodontal
disease in man: prevalence, severity, and extent of gingival recession. J
Periodontol 1992;63:489-95.
35. Trott JR, Love B. An analysis of localized gingival recession in
766 Winnipeg High School students. Dent Pract Dent Rec 1966;16:
209-13.
36. Parfitt GJ, Mjr JA. A clinical evaluation of local gingival recession in children. J Dent Child 1964;31:257.
37. Sullivan HC, Atkins JH. Free autogenous gingival grafts, 3: utilization of grafts in the treatment of gingival recession. Periodontics
1968;6(4):152-60.
38. Mlinek A, Smukler H, Buchner A. The use of free gingival grafts
for the coverage of denuded roots. J Periodontol 1973;(44):248-54.
39. Nordland WP, Tarnow DP. A classification system for loss of papillary height. J Periodontol 1998;69:1124-6.
40. Miller PD Jr. A classification of marginal tissue recession. Int J
Periodontics Restorative Dent 1985;5(2):9-13.
41. Bouchard P, Etienne D, Ouhayoun JP, Nilveus R. Subepithelial
connective tissue grafts in the treatment of gingival recessions: a comparative study of 2 procedures. J Periodontol 1994;65:929-36.
42. Wennstrm JL, Zucchelli G. Increased gingival dimensions: a significant factor for successful outcome of root coverage procedures?a 2year prospective clinical study. J Clin Periodontol 1996;23:770-7.
43. Trombelli L, Scabbia A, Tatakis DN, Calura G. Subpedicle connective tissue graft versus guided tissue regeneration with bioabsorbable
membrane in the treatment of human gingival recession defects. J Periodontol 1998;69:1271-7.
44. Harris RJ. A comparison of 2 root coverage techniques: guided
tissue regeneration with a bioabsorbable matrix style membrane versus
a connective tissue graft combined with a coronally positioned pedicle
graft without vertical incisionsresults of series of consecutive cases. J
Periodontol 1998;69:1426-34.

JADA, Vol. 134, February 2003

Copyright 2003 American Dental Association. All rights reserved.

225