ORIGINAL ARTICLE

Gingival clefts revisited: Evaluation of the

characteristics that make one more
susceptible to gingival clefts
Dina Stappert,a Robert Geiman,b Zahra Heidari Zadi,a and Mark A. Reynoldsc
Baltimore, Md, Madison, CT

Introduction: Orthodontic space closure after premolar extraction commonly results in the formation of a
gingival cleft, which may contribute to orthodontic relapse and poor periodontal health. The purpose of this study
was to examine clinical parameters that may predispose patients to gingival clefts. Methods: Twenty-nine
patients planned for treatment with premolar extractions (n 5 87) and orthodontic space closure were evaluated
in this prospective study. The clinical measures included width of keratinized buccal gingiva, thickness of buccal
gingiva, thickness of buccal bone, time of space closure, and the occurrence (presence or absence) and severity
(volume) of cleft formation. The association of the clinical measures with gingival cleft formation and severity was
assessed separately for patients according to age group: young adolescent (#13 years of age), adolescent
(14-18 years of age), and adult ($19 years of age). Results: The overall incidence of gingival cleft formation
was 73.2%, with a trend toward greater cleft formation in the young adolescents (79.4%) than in the adolescent
and adult groups (69.2% and 68.2%, respectively). The mean severity of clefts exhibited a significant positive
association with age group—young adolescent (26.6 mm2), adolescent (27.9 mm2), and adult (41.5 mm2).
Buccal bone thickness was significantly correlated with gingival phenotype in the adolescent and adult groups
(r 5 0.42 and r 5 0.52, respectively; both, P \0.05). Rate of space closure was significantly correlated with cleft
formation (r 5 0.71; P \0.001) in the adult group. Conclusions: The formation of gingival clefts is common after
premolar extraction and space closure. Adults with a thinner gingival phenotype were more likely to develop
gingival clefts of greater severity. The rate of space closure was significantly and inversely correlated with cleft
formation in adults, reflecting a greater likelihood of cleft formation with slower space closure. Although various
clinical parameters show a correlation to both severity and incidence of clefts, all patients undergoing
postextraction space closure appear to be at risk and should be monitored. (Am J Orthod Dentofacial Orthop
2018;154:677-82)

P
remolar extractions are commonly indicated
during orthodontic therapy to treat tooth
size-arch length discrepancies.1 Practice surveys
have shown that tooth extractions are performed
in about 10% to 15% of orthodontic patients.2
Orthodontic space closure, most notably at premolar
extraction sites, is commonly associated with the
formation of gingival clefts, or invaginations, that may
a
Department of Orthodontics and Pediatric Dentistry, University of Maryland,
Baltimore, MD.
b
Private practice, Madison, CT.
c
School of Dentistry, University of Maryland, Baltimore, MD.
All authors have completed and submitted the ICMJE Form for Disclosure of
Potential Conflicts of Interest, and none were reported.
Address correspondence to: Dina Stappert, University of Maryland, School of
Dentistry, 650 W Baltimore St (3209), Baltimore, MD 21201; e-mail,
dstappert@umaryland.edu.
Submitted, September 2017; revised and accepted, January 2018.
0889-5406/$36.00
Ó 2018 by the American Association of Orthodontists. All rights reserved.
https://doi.org/10.1016/j.ajodo.2018.01.018
contribute to orthodontic relapse and poor periodontal
health.3 The incidence of gingival cleft formation
appears to be relatively high, with reported rates ranging
from 35% to 100% of patients undergoing extractions
and orthodontic space closure.4,5 Nevertheless, clinical
factors that predispose patients to gingival cleft
formation remain unclear.
Two current theories attempt to explain the etiology
of gingival clefts. The first relates cleft formation to the
underlying bony architecture of the extraction site. Loss
of alveolar bone due to trauma, resorption, or both is
thought to predispose to gingival invagination.3,6
Araujo and Lindhe,7 for example, documented a
reduction in the volume of the dental alveolar ridge,
particularly the buccal aspect, after extraction of
mandibular premolars. The second explanation
attributes gingival cleft formation to the transseptal
fiber system, which may be displaced rather than
remodeled during tooth movement, resulting in
677
678
bunching, pressure on the subjacent bone, and
concomitant invagination of the gingival tissues. This
hypothesis is based, in part, on the clinical occurrence
of reopening of previously closed extraction spaces.8,9
As space closure occurs, tissues on the tension side are
stretched, whereas tissues on the pressure side are
compressed. The pressure side is presumably
responsible for gingival invagination, but the tension
side contributes to the relapse.10,11
Gingival clefts may delay or prevent complete space
closure, and it has been shown that there is decreased
interdental bone in sites with gingival invaginations.12
Incomplete space closure, with open contacts, is
associated with an increased likelihood of food
impaction and gingival trauma.8 Many studies have
shown reduced interproximal bone height relative to
original alveolar dimensions.10
An important clinical question is whether it is
possible to predict extraction sites at risk for gingival
cleft formation after orthodontic space closure. Gingival
phenotype can be characterized using several soft and
hard tissue anatomic parameters, including gingival
thickness, width of keratinized gingiva, alveolar bone
thickness, and osseous architecture.13 Although there
are different classifications of gingival phenotype,
most classifications are based on several common
clinical and anatomic features.14 A thick gingival
phenotype is characterized by a flat gingival margin, a
broad zone of keratinized gingiva, and a thick
underlying bony architecture.13 A thin gingival
phenotype is characterized by a scalloped gingival
contour, a thin band of keratinized gingival, and a thin
underlying bony architecture. Importantly, different
gingival phenotypes have been shown to respond
differently to inflammation and injury. When there is
chronic inflammation, the gingival phenotype appears
to be predisposed to distinctly different clinical
outcomes—a thick gingival phenotype tends to develop
periodontal pockets, whereas a thin gingival phenotype
tends to undergo recession.15-18
The purpose of this prospective cohort study was to
examine the association between clinical measures of
cleft formation and severity after orthodontic space
closure of premolar extraction sites related to gingival
phenotype.
MATERIAL AND METHODS
Thirty-six participants were recruited from patients
requiring premolar extractions as part of comprehensive
orthodontic care at the University of Maryland, School of
Dentistry, in Baltimore. All participants had complete
orthodontic records (models, lateral cephalometric and
panoramic radiographs, intraoral and extraoral photos,
November 2018  Vol 154  Issue 5 American Journal of Orthodontics and Dentofacial Orthopedics
Stappert et al
Fig 1. Transgingival probing.
and examinations) and screening before enrollment in
the study. Inclusion criteria included a full permanent
dentition and a comprehensive orthodontic treatment
plan that included 2 or 4 premolar extractions and space
closure with fixed orthodontic appliances. Exclusion
criteria included periodontitis and systemic conditions.
Consent or assent and HIPAA authorization forms were
reviewed with each participant or guardian. All
participants provided verbal and written consent.
Subjects contributed either 2 or 4 premolar extraction
sites, and all measurements were performed on the study
sites in triplicate. Measurements were averaged to create
a mean score for analysis. This study was approved by
the Institutional Review Board at the University of
Maryland.
Initial gingival measurements were taken immedi-
ately before and after each tooth extraction. The width
of the keratinized gingiva was measured with
a Maryland/Moffitt color-coded periodontal probe
(Hu-Friedy, Chicago, Ill) (millimeters) from the gingival
margin to the mucogingival junction at the midfacial
surface. After topical anesthesia with 20% benzocaine,
local infiltration (2% xylocaine and epinephrine,
1:100,000) was administered on the buccal and lingual
or palatal surfaces. After anesthesia, measurements of
gingival thickness were obtained by transgingival
probing using an endodontic probe with a stopper.
Measurements were taken with bone sounding on the
direct facial surface before extraction (Fig 1).
Extractions were completed as atraumatically as
possible to preserve the bony architecture, followed by
gentle debridement and irrigation of the extraction
socket with sterile saline solution. After extraction, the
thickness of the buccal bone was determined using a
bone caliper. Buccal bone thickness was measured at
the midfacial surface at the crest of the bone.
Patients needing orthodontic treatment with
premolar extraction were consecutively recruited until
enrollment ended. Each subject was treated by 1
assigned orthodontist, ensuring consistency of care. All
orthodontic care was delivered by 4 practitioners.
When space closure was at or near (\2 mm) completion,
the incidence and severity of clefting was measured
Stappert et al
Fig 2. A, Occlusal and B, buccal views of gingival cleft.
using the coding system of Reichert et al.19 Soft tissue
measurements were taken in 3 planes: mesiodistal
(x-axis dimension), buccolingual (y-axis dimension),
and incisal-gingival (z-axis dimension); the degree of
clefting was determined by volumetric measurement
(Fig 2).
The following variables were categorized for analysis:
age—young adolescent (#13 years), adolescent
(14-18 years), and adult ($19 years); and gingival
phenotype (thickness)—thin (#2.5 mm) and thick
(.2.5 mm).14
Statistical analysis
The association of clinical parameters with the
formation and severity (volume) of clefts was assessed
separately in the age groups using the nonparametric
Spearman rank correlation. Statistical significance was
set at P #0.05.
RESULTS
Twenty-nine of the 36 subjects completed the study.
Two patientts underwent extractions under sedation,
which precluded clinical evaluation; 5 subjects failed
to complete treatment or did not come for the
follow-up evaluation. Four subjects were planned for
treatment with extraction of 3 premolars; consequently,
data on the third premolar were not included in the
American Journal of Orthodontics and Dentofacial Orthopedics
679
Table. Intergroup comparison for formation of
gingival clefts and gingival cleft severity based on age
Young adolescent Adolescent Adult
(#13 y) (14-18 y) ($19 y)
Cleft formation (%) 79.4 69.2 68.2
Cleft severity (mm2) 26.6 27.9 41.5
Frequency of cleft formation did not differ significantly between age
groups (chi-square 5 0.62; not significant). Cleft severity differed
significantly between age groups (Kruskal-Wallis analysis of variance
by ranks (2, n 5 65) 5 7.9; P #0.05).
analysis. A total of 82 premolar extraction sites were
evaluated for cleft formation and cleft severity.
The overall incidence of gingival cleft formation was
73.2% (n 5 60), with a similar frequency of cleft
formation in the maxillary and mandibular extraction
sites (72.9% vs 73.5%, respectively). Soft tissue
measurements ranged from 0 to 1 mm in the mesiodistal
dimension, 0 to 9 mm in the buccolingual dimension,
and 0 to 7 mm in the incisal-gingival dimension. Clefts
developing at maxillary and mandibular extraction sites
were similar in average severity (31.4 and 29.8 mm2,
respectively). The number of extraction sites (2 vs 4)
contributed by subjects had no association with the
occurrence and severity of clefts (r 5 0.06 and
r 5 0.08, respectively).
Clefts formed in 79.4%, 69.2%, and 68.2% of
subjects in the young adolescent, adolescent, and adult
groups, respectively. Although the percentage of
subjects with clefts had a modest inverse relationship
with age group, this association was not significant.
The mean severity of clefts, however, exhibited a
significant positive association with age group. The
mean severity values of clefts were 26.6, 27.9, and
41.5 mm2 in the young adolescent, adolescent, and
adult groups, respectively (Table).
Buccal bone thickness was significantly and
positively correlated with gingival phenotype in the
adolescent and adult groups (r 5 0.42 and r 5 0.52,
respectively; both, P \0.05); however, no association
was observed in the young adolescent group.
The width of buccal keratinized gingiva, gingival
phenotype, and bone thickness showed no associations
with cleft formation or cleft severity in the age groups.
The rate of space closure was significantly and
positively correlated with cleft formation (r 5 0.71;
P \0.001) in the adult group, reflecting a greater
likelihood of cleft formation with slower space closure.
No association was observed between rate of space
closure and cleft formation in the young adolescent
and adolescent groups. Rate of space closure had no
association with cleft severity in the age groups.
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680
DISCUSSION
The overall incidence of gingival cleft formation in
this study was 73.2%, ranging from 79.4% in the young
adolescent group to 68.2% in the adult group. This rate
of cleft formation was intermediate to rates previously
reported: from 35%5 to 100%.4 In this study, maxillary
sites had a nonsignificantly higher percentage of clefts
than did mandibular sites, consistent with several earlier
studies. An apparent greater propensity for maxillary
sites to develop clefts has been attributed to denser
mandibular than maxillary bone, with a resulting slower
tooth movement.20,21 In this study, rate of space closure
was significantly and positively correlated with cleft
formation in the adult group, reflecting a lesser
likelihood of cleft formation with faster space closure.
However, rate of space closure was not associated with
cleft formation in the younger age groups; this may
explain observations that are consistent with those
across studies with respect to cleft formation.4,5,22
One postulated explanation for the development of
gingival clefts is loss of underlying hard tissue support
after extractions. In addition to the potential for alveolar
bone dehiscence or bone loss secondary to surgical
trauma, extractions are characteristically associated
with progressive alveolar ridge resorption resulting in a
reduction of ridge volume.23 The decrease in alveolar
ridge volume is most commonly attributable to
resorption of the buccal bone plate.24 The rate of
resorption of the alveolar ridge is most rapid in the initial
healing after the extraction.25 Available evidence
suggests that the risk of gingival cleft formation is
greatest when orthodontic space closure beins late after
tooth extractions and remodeling of the alveolar
ridge.6,22
A thin buccal bone phenotype (#1 mm thick) is
considered a risk factor for bone resorption, since
bundle bone appears to be the first bone to be
resorbed.26 The thinner the buccal wall, the greater
the proportion of bundle bone.27,28 The buccal bone
plate experiences more resorption because it is
generally thinner than the lingual plate. Several recent
studies examining the effect of ridge preservation after
extractions, using guided bone regeneration or bone
replacement grafts before orthodontic space closure,
have reported reductions in the incidence of gingival
invagination.29-33 In our study, no association was
found between crestal buccal bone thickness and
development of gingival clefts. Space closure begun
immediately after extraction may have contributed to
a reduction in the occurrence in gingival invagination.
Another hypothesis for the development of gingival
clefts is that the transseptal fiber system may be dis-
placed rather than remodeled during tooth movement,
November 2018  Vol 154  Issue 5 American Journal of Orthodontics and Dentofacial Orthopedics
Stappert et al
resulting in bunching, pressure on the subjacent
bone, and concomitant invagination of the gingival
tissues.
The collagenous nature of connective tissue and its
adherence to the underlying mucoperiosteum are the
primary determinants of the firmness of the attached
gingiva. The thick network of closely packed collagen
fibers helps to resist loading and withstand compressive
and shear forces.34 If gingival compression and
bunching during tooth movement contribute to gingival
invagination, then the width of attached keratinized
gingiva should be correlated with cleft formation.35 In
this study, however, the width of keratinized gingiva,
which contains the attached keratinized gingiva,
exhibited no association with cleft formation or cleft
severity in any age group. In contrast, however, gingival
thickness had a negative association with gingival
invagination and severity of cleft formation in the adult
group; patients with a thin gingival phenotype had a
greater predisposition for clefting than did those with
a thick phenotype. A similar but nonsignificant
correlation emerged between gingival thickness and
cleft formation in the adult group. Collectively, these
findings suggest that gingival phenotype is a
predisposing factor in cleft formation and severity,
because of the positive relationship between gingival
thickness and alveolar bone volume, an association
also seen in our adult group.
When we considered the rate of space closure,
2 considerations appeared to be important in relation
to the potential for cleft formation. First, by closing
the extraction space faster, there is less time for bone
remodeling and loss of alveolar ridge volume and,
therefore, a potentially smaller risk for gingival cleft
formation. However, with faster space closure, the
gingival fiber complex might not have time to
reorganize. Teeth typically move faster in younger
patients than inolder patients, and it was thought that
the younger the patient, the less likely the risk for
gingival cleft formation. In this study, however, the
frequency of cleft formation had a nonsignificant
difference between age groups, with cleft frequencies
highest in the young adolescent group and lowest in
the adult group. In contrast, the severity of cleft
formation showed a consistent significant positive
relationship with age group, with the most severe clefts
in the adult group and the least severe in the young
adolescent group. The young adolescent group had the
smallest mean cleft severity, especially in contrast to
the adult group (26.6 vs 41.5 mm2, respectively). It is
unclear whether orthodontic techniques designed to
accelerate tooth movement, such as corticotomies,
micro-osteoperforation, vibration methods, lasers, or
Stappert et al
piezosurgery, may influence the risk of gingival cleft
formation.
There is limited research regarding the prevention of
gingival clefts. The inverse correlation observed in this
study between rate of closure and cleft formation in
adults suggests that decreasing the time it takes to close
the extraction site may reduce the risk of gingival cleft
formation. This interpretation, however, must be made
cautiously, given the observational nature of the data
and the modest strength of the association. Several
recent studies examining the effect of ridge preservation
after extractions, using guided bone regeneration or
bone replacement grafts, before orthodontic space
closure have reported reductions in the incidence of
gingival invagination.29-33 Tiefengraber et al30
performed socket preservation procedures in a study
with a split-mouth design. Gingival cleft formation
was compared between premolar extraction sites
(control) and premolar extraction sites covered with a
nonresorbable barrier membrane (experimental).
Gingival clefts of varying size were seen at all
nonmembrane sites, whereas no gingival clefts were
observed at extraction sites treated with a barrier
membrane.31 The benefit of ridge preservation
techniques, therefore, including barriers and bone
grafts, on reducing cleft formation may be attributable
to both ridge stabilization and reducing the rate of space
closure.
There were several limitations in the study,
including the clinical applications of various
orthodontic biomechanics—power chains, T-loops,
nickel-titanium coils, and elastics—to accomplish
orthodontic space closure. Assessment of periodontal
phenotype, particularly bone architecture, was limited
to point measurements of buccal bone thickness using
a bone caliper, rather than radiologic measurements
(eg, cone-beam computed tomography). In addition,
no adjustment in Type I error rate was made for
multiple correlations in this exploratory study.
Moreover, the potential for confounding due to a
patient effect is possible, since the analysis did not
control for multiple observations related to subjects.
We strongly expect that the clinical prediction of risk
for cleft formation will require information on several
predictor variables.
CONCLUSIONS
We found that gingival cleft formation is a relatively
common occurrence after extractions and orthodontic
tooth movements to achieve postextraction space
closure. In addition, this study suggests that age is
an important factor in assessing the risk for gingival
American Journal of Orthodontics and Dentofacial Orthopedics
681
cleft formation and severity. We found that the rate
of space closure was significantly and inversely
correlated with cleft formation in adults, reflecting a
greater likelihood of cleft formation with slower space
closure. These results suggest that clinicians need to be
cautious when predicting the long-term stability of
orthodontic treatment involving premolar extractions.
In particular, they should inform patients about the
possibility of relapse and unfavorable treatment
outcomes. All patients, especially adults, undergoing
postextraction space closure should be monitored for
the development of gingival clefts. Multivariate models
are likely to be necessary for the clinical prediction of
cleft formation.
ACKNOWLEDGMENTS
The first author thanks the American Association of
Orthodontists Foundation for the grant (Orthodontic
Faculty Development Fellowship Award: T. M. Graber
Teaching Fellowship Award). We thank Robert Williams
for proofreading the manuscript.
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