International Dental Journal (2007) 57, 399-410

Oral hygiene and periodontal

considerations in preventing and
managing dentine hypersensitivity
Connie Drisko
Georgia, USA

The onset of dentine hypersensitivity is almost exclusively associated with exposed den-
tine due to tooth wear or to gingival recession, or at times both tooth wear and gingival
recession. Recession secondary to periodontal disease is thought to be related to poor
oral hygiene, while overzealous, incorrect tooth brushing may be responsible for the
recession associated with good oral hygiene. However, the aetiology of gingival reces-
sion is multifactorial and is therefore unlikely to be caused by any single factor. Dentine
hypersensitivity is preceded by gingival recession and exposure of the root surface. Acidic
and erosive foods and drinks combined with vigorous tooth brushing and highly abrasive
dentifrices are likely to elicit dentine hypersensitivity. Successful treatment of patients
with mild sensitivity and minimal recession can be accomplished in most cases simply by
correcting destructive oral hygiene habits in conjunction with use of a desensitising den-
tifrice. Moderate to severe dentine hypersensitivity in the presence of gingival recession
≥1 mm usually requires a surgical root coverage procedure with or without daily use of
desensitising toothpastes and/or professional application of desensitising agents, dentine
bonding materials, or cervical restorations.

Key words: Oral hygiene, periodontal disease, dentine hypersensitivity

The onset of dentine hypersensitivity is almost exclusively
associated with exposed dentine due to tooth wear or
to gingival recession, or at times both tooth wear and
gingival recession. Dentine hypersensitivity is a painful
condition characterised by short sharp pain frequently
in response to thermal, tactile, or chemical stimuli1-3.
Typically, dentine hypersensitivity is the only or most
significant symptom of gingival recession and when ad-
dressing that symptom the dental professional should
also investigate the factors contributing to the recession,
if present. If the recession process is allowed to progress
it is unlikely that the management of the hypersensitivity
will be successful.
Factors associated with dentine hypersensitivity
Although the process of recession is not well-under-
stood4-5, early histological studies in the rat and monkey
showed that periodontal inflammation is essential to the
formation of cleft defects principally by the growth and
anastomosis of the rete pegs of the oral epithelium and
© 2007 FDI/World Dental Press
0020-6539/07/06399-12
the epithelium lining the periodontal pocket. Since the
studies have not been duplicated in the human, it is not
known definitively if the pathogenesis of recession is
the same for humans. However, it is highly plausible that
vigorous tooth brushing in the presence of subclinical
or frank inflammation would most likely result in the de-
velopment of clefts and subsequently gingival recession
much like that observed in animals.
Longitudinal studies have provided significant evi-
dence to support the premise that gingival recession is
associated with excessive oral hygiene and plaque control
habits producing lesions that are exacerbated in the pres-
ence of certain anatomic factors4-8. The most common
anatomic factors that predispose sites to recession6-15
include:
• Root prominence in the presence of thin mucosa
• Dehiscences and fenestrations in the underlying
alveolar bone
• Frenum pulls
• Orthodontic movement of teeth/roots outside the
alveolar housing16-27 (Figure 1).
400

Figure 1. 20-year-old female with thin scalloped gingivae, root prominence and lack of keratinised gingivae on the
canines puts this patient at risk for future additional gingival recession. Recession lesions are in the early stages
of development on the first premolars. Photographs courtesy of Dr. Terry Rees.

Figure 2. Presence of dehiscence significantly correlated to gingival recession

The thickness of marginal tissue rather than the
apico-coronal width of keratinised and attached gingivae
appear to be a more important determining factor for
the development of gingival recession during orthodon-
tic therapy27. It has also been reported that recession will
increase over time with the use of abrasive toothpastes
and tobacco, and frequency of brushing with or without
hard bristle brushes1,14,23,28-31.
Smokers with higher frequency of gingival recession
in excess of 2mm (23%) compared to non-smokers
(7%) were not at increased risk for development of
gingival recession in 19-30-year-olds after adjusting for
other confounding variables in a short longitudinal 6
month study15. However, this finding is not in agreement
with another report that found more gingival recession
in smokers than in non-smokers after adjusting for
mean plaque index, race, gender and age30. In a large
cross sectional study, cigarette smoking and presence
of supragingival calculus were associated to a high level
with localised and generalised recession in an urban
Brazilian population14.
Frequency of gingival recession has been shown to
increase with age and women have less recession than
International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)
men of the same age11,23. Socioeconomic status and
number of dental visits may not be significant risk indi-
cators in all populations14. In one study investigating the
relationship between age and tooth position in the arch,
recession was also associated with labially positioned
teeth in 40% of 16-25-year-old patients increasing to
80% in the 36-86-year-old group23. Teeth that erupt with
the cervical portion protruding through the crestal bone
may result in bony dehiscence. Presence of dehiscence
in the bone is significantly correlated with recession26
(Figure 2).
Recession secondary to inflammatory periodontal
disease is thought to be related to poor oral hygiene,
while overzealous, incorrect tooth brushing may be
responsible for the recession associated with good
oral hygiene9,12. Low plaque scores are frequently as-
sociated with increased frequency of brushing and
gingival recession. The relationship of traumatic tooth
brushing, lower plaque levels and brushing frequency
was confirmed in a recent 5 year study of Italian dental
students that revealed an increase in the percentage of
sites with recession despite a reduction in the frequency
of destructive tooth brushing habits. The prevalence

of gingival buccal recession nearly doubled between
baseline (47.8%) and the five year exam (82.6%) in this
young healthy population. Maxillary and mandibular
premolars had the highest number of receded surfaces
at baseline compared to maxillary and mandibular mo-
lars and premolars at the second exam. Plaque scores
were significantly lower at the second exam as was the
percentage of subjects using an approved Bass or roll
technique of brushing. Thus, as has been reported in
other studies, patients with a high standard of oral hy-
giene are at greater risk of developing buccal gingival
recessions.
Others have compared the effect of right and left
hand preference and found that recession is more
prominent on maxillary and mandibular canines and
premolars on the right side of right handed individuals
and conversely, on the left maxillary and mandibular
canines and premolars of left handed individuals11.
The greatest amount of gingival recession was found
in those who used the horizontal scrub technique, with
gingival recession increasing as tooth brushing frequen-
cy and duration increased11. In general, the frequency of
gingival recession is significantly higher in the maxilla.
Soft and hard tissue abrasion is less well understood,
but has frequently been associated with gingival reces-
sion11,12,,28-31 (Figures 3a-d). Toothbrush trauma may not
3a. Gingival abrasion second
3c. Healing two weeks
Figure 3 (a-d). Self inflicted gingival abrasion lesions evident on maxillary premolar facial gingivae
Photographs courtesy of Dr. Terry Rees.
401
cause recession directly, but may abrade the tooth at
the cemento-enamel junction, with subsequent loss of
cementum, periodontal attachment and alveolar bone1,12
(Figure 4a-g). Poor plaque control in addition to abrasion
of the soft and hard tissue may exacerbate inflammation
in the connective tissue leading to acceleration of the
process. Clinical identification of soft tissue brushing
lesions has been shown to be comparable to that seen
by electron microscopic examination, however, strong
evidence to establish the direct relationship between
soft tissue abrasion and recession has not been reported
to date28.
It is generally accepted that repetitive iatrogenic
lesions due to overzealous brushing produce multiple
soft tissue erosive lesions leading to loss of marginal
tissue. However, strong histological evidence is lacking
in the literature despite the fairly wide acceptance of
this theory1,8.
In contrast to the soft tissue abrasion theory to
which many ascribe, a recent investigation proposed a
completely different theory based on the premise that
cell damage caused by brushing may help keep gums
healthy36. Bristles engaged with even gentle force tear
holes in the epithelial cells that line the gingivae and
tongue, causing a momentary rupture. According to
this study, tearing of the epithelial cells enables calcium,
3b. Gingival abrasion second
3d. Healing two weeks
Drisko: Preventing and managing dentine hypersensitivity
402
4a. Facial view pre-treatment with acellular dermal
allograft. Note extensive recession and tooth surface
loss extending onto exposed root surfaces
4b. Surgical exposure of dehiscence on all teeth
4 c-d. Close up view of excessive wear on all roots
Figure 4 (a-g). Advanced gingival recession and tooth wear in 30-year-old physician
Photographs courtesy Dr. Henry Greenwell, University of Louisville, School of Dentistry, Graduate Periodontics Program.
which is abundant in saliva, to move in to the cells,
stimulating internal membranes to move up and patch
the hole (Figure 5). However, in the seconds that repair
takes, growth factors that promote growth of collagen,
new cells and blood vessels leak out of the injured cells.
According to the authors, the resultant cell injury also
turns on expression of the c-fos-gene, an early-response
gene often activated under stress that may be the first
step in a response such as cell division or growth. They
concluded that in addition to removal of harmful bac-
International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)
4e. Coronally positioned flap sutured over acellular
dermal allograft right premolars to left premolars (10 teeth)
4 f. Pretreatment
4g. Three years post treatment acellular dermal allograft
terial plaque and debris from the teeth, that “brushing
could lead to local cell-adaptive responses ultimately
of benefit to gingival health” 36. Other areas of inter-
est identified by the authors include determining if the
method and/or type of brush might strongly influence
the extent of epithelial cell-wounding and subsequent
liberation of factors that promote gum health. Accord-
ing to the corresponding author on this paper, more
work will be needed to confirm their theory. However,
earlier indications from investigators working with Asian
 403

Figure 5. Cell wounding in the gingival tissues and tongue induced by brushing. (A) Confocal fluorescence image of epithelium and
underlying connective tissue from the undisturbed (not brushed) maxillary gingivae. (B) Confocal fluorescence image of epithelium
and underlying connective tissue from the brushed, mandibular gingival (taken 15 minutes after brushing.) Epithelial cells labeled
with fluorescein-labeled dextran are observed in all strata. (C) Confocal fluorescence image of epithelium and underlying connective
tissue from the brushed mandibular gingival (taken 3 hours after brushing. Epithelial cells labeled with fluorescein-labeled dextran are
observed in all strata. (D) Skelatal muscle of a tongue with the fluorescein-labeled individual myocytes. The myocytes themselves are
not labeled intracellularly with the fluorescein-labeled dextran. (E) Skeletal muscle of a tongue 15 minutes after brushing. Many of
the mycytes display strong cytoplasm labeling with fluorescein-labeled dextran. (F) Skeletal muscle of a tongue 3 hrs. after brushing.
Again, many of the myocytes are strongly labeled with dextran.

Reprinted with permission Figure 1, J Dent Res 2007 86: 770, Breaking biological barriers with a toothbrush. Aman, Miyake, Borke and McNeil.

subjects, showed similar positive effects of brushing.
Their studies37-42 confirm that brushing may indeed have
significant beneficial effects at the cellular level on the
fibroblast proliferation and procollagen Type I collagen
synthesis in dogs42.
There is some evidence to support the importance
of end-rounding of toothbrush bristles to avoid soft
tissue abrasion and injury29-35. A recent meta-analysis
showed that compared to manual brushes, powered
brushes with rotation oscillation action reduced gin-
givitis and plaque more effectively but were no more
likely to cause injuries to the gums32. Other investigators
inspected filament end-rounding quality in 15 electric
toothbrushes and reported nine of 15 brands examined
showing a high acceptability of end rounding, with
four products showing a medium acceptability and two
with poor end-rounding qualities (Table 1). Given the
increased number of strokes complicit with powered
brushes, it would appear that more attention should be
paid by both the consumer and professional to the bris-
tle end-rounding in the selection and recommendation
of toothbrushes. Unwanted side effects of tissue abra-
sion and gingival recession might be better prevented
if greater emphasis was placed on the manufacture and
promotion of brushes with a higher standard of bristle
end rounding.
Besides traumatic brushing as the primary risk fac-
tor for receding gums in a healthy dentition, gingival
recession is a common manifestation of periodontal dis-
ease. In a study of 1,460 subjects in an urban Brazilian
population, more than half (51.6%) of individuals and
17% of their teeth had ≥3mm of recession associated
with chronic periodontitis14. In addition 22% of indi-
viduals had ≥5mm of recession in 5.8% of their teeth.
The authors reported that gingival recession was also
shown to be associated with other risk factors such as
age. Males ≥30 years of age showed the highest extent,
prevalence and severity of recession in this study. Using
a multivariable model approach to the analysis, smok-
ing and presence of supragingival calculus were also
factors most often associated with both localised and
generalised recession but gender, dental visits and so-
cioeconomic status were not significant risk indicators.
In contrast, other authors have reported significant as-
sociations between gender, age and frequency of tooth
brushing and gingival recession in a US population29. It
is apparent that aetiologic factors and other risk factors
vary across countries and cultures and must be taken
into consideration when looking at epidemiologic data
relative to gingival recession.
Although many clinicians assume that highly abrasive
dentifrices also contribute to the overall problem of soft
tissue abrasion and consequently recession, there is lit-
tle evidence to support this assumption1, 31. Much more
research is needed to guide the practitioner in selection
of appropriate dentifrices for their patients, but until
Drisko: Preventing and managing dentine hypersensitivity
404

Table 1 Number of tufts and percentage of acceptably end-rounded filaments of the toothbrush brands examined (n=5)
Product Manufacturer No. of Tufts Acceptable (%)

Rowenta Dentaclip ZH-07 SEB group 22 98

Waterpik BH-4U Waterpik 21 98
Rowenta rotoclip ZH-11 SEB Group 14 96
Dr. Best e-FLEX3 GlaxoSmithKline, Buhl, Germany 40 93
Rowenta Dentaclip ZH 010 SEB group 14 91
Krups 548 Krups, Solingen, Germany 26 91
Oral-B EB3 Braun Oral-B 28 90
Oral B Plak Control Kids Braun Oral-B 24 90
Broxo hard Broxo 28 89
Blend-a-dent Wellenprofil 2000 Hart Procter & Gamble 28 84
Blend-a-dent Wellenprofil 2000 mittel-welch Procter & Gamble 28 78
Blend-a-Dent Medic for kids Procter & Gamble 23 78
Braun Oral-B Flexisoft EB 17-8 Braun Oral-B 26 76
Butler Gum for E1 Butler 23 38

UltraSonex Dent-O-Care 35 34

Reprinted with permission Meyer-Lueckel et al. J Clin Periodontol 2005; 32:29-32 Table 1

Table 2 Abrasivity of common toothpastes

Relative Dentin Abrasivity Score - Dentifrice brand and variety

04 ADA reference toothbrush and plain water 94 Rembrandt Plus

07 Plain baking soda 94 Plus White
08 Arm & Hammer Tooth Powder 95 Crest Regular (possibly 99)
30 Elmex Sensitive Plus 101 Natural White103 Mentadent
35 Arm & Hammer Dental Care 103 Arm & Hammer Sensation
42 Arm & Hammer Advance White Baking Soda Peroxide 104 Sensodyne Extra Whitening
44 Squigle Enamel Saver 106 Colgate Platinum
48 Arm & Hammer Dental Care Sensitive 106 Arm & Hammer Advance White Paste
49 Arm & Hammer Peroxicare Tartar Control 107 Crest Sensitivity Protection
49 Tom’s of Maine Sensitive (given as 40’s) 110 Colgate Herbal
52 Arm & Hammer Peroxicare Regular 110 Amway Glister (given as upper bound)
53 Rembrandt Original (“RDA”) 113 Aquafresh Whitening
54 Arm & Hammer Dental Care PM Bold Mint 117 Arm & Hammer Advance White Gel
57 Tom’s of Maine Children’s, Wintermint (given as mid-50’s) 117 Arm & Hammer Sensation Tartar Control
62 Supersmile 120 Close-Up with Baking Soda (canadian)
63 Rembrandt Mint (“Hefferren RDA”) 124 Colgate Whitening
68 Colgate Regular 130 Crest Extra Whitening
70 Colgate Total 133 Ultra brite
70 Arm & Hammer Advance White Sensitive 144 Crest MultiCare Whitening
70 Colgate 2-in-1 Fresh Mint (given as 50-70) 145 Ultra brite Advanced Whitening Formula
79 Sensodyne 150 Pepsodent (given as upper bound)
80 AIM 165 Colgate Tartar Control (given as 155-165)
80 Close-Up 168 Arm & Hammer Dental Care PM Fresh Mint
83 Colgate Sensitive Maximum Strength 175 Colgate Luminous (given as 150-200)
91 Aquafresh Sensitive 200 Colgate 2-in-1 Tartar Control/Whitening or Icy Blast/Whitening
93 Tom’s of Maine Regular (given as high 80’s low 90’s) (given as 190-200)
200 FDA recommended limit
250 ADA recommended limit
(Sourced from http://www.epinions.com/content_3128664196)

International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)


such time that a stronger evidence base to support selec-
tion of dentifrice decisions is available, common sense
would dictate recommending use of the least potentially
abrasive dentifrice. It is difficult to evaluate the abrasivity
of products that are constantly entering and leaving the
market place, however the chart in Table 2 shows the
relative dentine abrasivity (RDA) of some dentifrices
currently available for use that are within manufactur-
ing guidelines for safety. Whereas there are currently
no clinical data indicating the clinical significance of
different abrasive levels, empirically it makes sense to
recommend a low abrasive toothpaste for patients at risk
of soft tissue abrasion (and of wear to the dental hard
tissues too). It is noteworthy that the more “whitening
and lightening” claims that are associated with a denti-
frice, the more likely it is to have increasing abrasivity,
required for increased surface stain removal capability.
It is therefore important for the dental professional to
explore not only tooth brushing habits but selection of
toothpaste as well.
Factors associated with the prevalence and
severity of gingival recession and dentine
hypersensitivity
The prevalence of clinically defined dentine hypersensi-
tivity in a general dental practice has been shown to be
as little as 3.8% in the UK16 and up to 57% in the gen-
eral US population. It is difficult to compare different
studies as the methodologies employed and criteria used
differ widely. Albandar and Kingman6 reported epide-
miological data on 9,689 subjects 30-90 years of age in
the United States and projected that over 23.8 million
people have one or more tooth surfaces with gingival
recession of ≥3mm. They found that the prevalence of
recession of ≥1mm in this population was 58% and that
it increased with age. In addition, males have been found
to have increased recession compared to females7,8,11.
Similarly, others7 reported earlier that the frequency of
Figure 6a. Pre treatment
405
gingival recession increased with age and was greater
in men than in women of the same age. They also as-
sociated recession with labially positioned teeth in 40%
of their patients 16-25 years of age and noted that the
prevalence increased to an impressive 80% of patients
between 36 and 86 years of age. Additionally, crowd-
ing in the lower anterior segment increases the risk of
gingival recessions of >3.5mm and shallow periodontal
pockets in older patients ≥35 years of age according
to a study conducted in an orthodontic clinic18. Similar
findings have been reported for the association be-
tween crowded dentition and recession in children and
adolescents19-23. The degree of crowding was found to
correlate with tooth fracture in younger patients and
with gingival recession and shallow periodontal pockets
in older patients18.
In addition to the adverse affects of over-brushing,
there is compelling evidence to show that the rep-
etitious instrumentation of healthy shallow pockets in
periodontitis patients leads to increased gingival reces-
sion concomitant with bone and attachment loss 43-44.
Scaling with either curettes or ultrasonic scalers causes
a mean attachment loss of 0.75mm immediately after
instrumentation which should recover, but may have
some long-lasting effects as demonstrated in the stud-
ies looking at attachment loss after instrumentation of
shallow sites43. The authors caution practitioners to
resist scaling and root planing in shallow pockets lest
they cause an additional 0.3mm of gingival recession in
health sites over time. Tooth cleaning has been associ-
ated with increased hypersensitivity24 and may be one of
the major factors that influence the distribution and the
occurrence of dentine hypersensitivity.
Besides the concern over gingival recession as a
result of non-surgical and surgical therapy, periodontal
patients in general have an increased incidence of 72.5-
98.0% of dentine hypersensitivity associated with reces-
sion induced by periodontal therapy25,44-49 (Figures 6a-b).
The patient was extremely hypersensitive following
Figure 6b. Post treatment. Right maxillary and
mandibular quadrants received scaling and root planing
only. Left quadrants received osseous surgery.
Drisko: Preventing and managing dentine hypersensitivity
406
surgical pocket reduction on the left half of his mouth
and refused further treatment beyond scaling and root
planing on the right side. Both areas were successfully
treated with use of a desensitising dentifrice (Sensodyne)
and chlorhexadine mouthrinses. Interestingly, over time,
significant recession was noted on the right side that
received scaling and root planning (SRP) only, however
the use of the desensitising dentifrice and mouthrinse
immediately following SRP successfully prevented sig-
nificant hypersensitivity on the non-surgical side com-
pared to the excruciating pain the patient experienced
for over three months on the surgical side.
Treatment for gingival recession and dentine
hypersensitivity
Hypersensitivity due to minimal exposure of dentine
is usually the most easily treated symptom of gingival
recession that is ≤1mm. Dentifrices that contain potas-
sium salts have been shown to be effective in reducing
dentine hypersensitivity within the first few weeks of
daily use in a large segment of the population with
hypersensitivity by depolarising the pain mechano-re-
ceptors around the odontoblast processes. Therefore,
when minimal recession of 1mm or less is present, after
recognition and correction of destructive oral hygiene
habits, use of a desensitising dentifrice is frequently suf-
ficient to eliminate dentine hypersensitivity.
If sensitivity persists in the presence of minimal
recession, other options are available. A recent in vitro
study47 compared Sensodyne™ dentifrice (formulated
with a strontium salt as a tubule occluding agent) to a
Nd:YAG laser to occlude dentinal tubules on slabs of
dentine. Using a double-blind technique to measure ink
penetration (in mm) for each group, researchers found
there were no significant differences in the occluding
effect of Nd:YAG laser and Sensodyne toothpaste.
Both treatments have the ability to reduce permeation
through exposed dentinal tubules. The laser therapy may
produce immediate results however it must be delivered
by a dental professional, increasing the overall cost of
therapy. Conversely, the desensitising dentifrice can
be used at home by the patient for relatively little cost
and only takes about 2-3 weeks to achieve equivalent
results.
In addition to sensitive exposed dentine, recession
may present significant aesthetic problems prompting
the patient to seek solutions that address both concerns.
Long term relief of moderate to severe dentine hyper-
sensitivity associated with gingival recession >1mm is
more difficult to achieve and may require surgical inter-
vention using a periodontal plastic surgical procedure to
cover the exposed root. A variety of root coverage tech-
niques are available that have been shown to be highly
successful over time48. Recent meta-analyses of certain
root coverage techniques show the connective tissue
graft has some advantages over guided tissue regenera-
International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)
tion for root coverage. The most common procedure
used by most dentists worldwide for root coverage is
the connective tissue graft (Figures7a-d).
Selection of a particular surgical technique is rou-
tinely based on the depth and width of the recession
according to the Miller Classification system (Table 3),
that also takes into consideration the height of the
interproximal bone which is a strong predictor of the
root coverage that is possible in each classification of
recession defects50. Other considerations in selecting a
particular surgical technique are based on the number
of teeth with recession, the width and thickness of the
keratinised gingiva at the recession site, and availability
of host tissue that may be transplanted from one area
of the mouth to another.
When several adjacent teeth are in need of root cov-
erage procedures, multiple surgical procedures may be
needed to treat large recession areas. Fortunately, within
the last few years, an acellular dermal allograft material
has become available commercially that may be used in
lieu of autogenous grafts harvested from distant donor
sites within the mouth (Figures8a-e). Although use of
the acellular dermal allograft material is highly operator
technique sensitive, success rates are similar to autog-
enous grafts48. Patient acceptance is usually good except
that some reject the idea of receiving donor material
from a cadaver. Many patients prefer the use of their
own tissue despite the need for a second surgical site
for harvesting the graft(s) that may take several surgical
procedures to correct large areas of recession (Figures
4a-g). The patient represented in these figures represents
a case of overzealous tooth brushing with resultant wear
of the dentine and significant gingival recession in rather
thick gingival tissue. Figure 4g is the patient three years
post acellular dermal allograft surgery.
Regardless of the surgical technique or donor mate-
rial, grafting to cover roots has become commonplace
and although the procedures can be rather technique
sensitive, they are predictable means of helping to
alleviate dentine hypersensitivity due to recession. It
should be noted that one in every five teeth affected by
gingival recession is susceptible to deepening recession
if alveolar bone dehiscence was identified as the major
predisposing aetiologic factor in the recession defect
originally17. Therefore careful monitoring of recession
sites, particularly after surgical grafting, is highly rec-
ommended since regeneration and repair of the bony
dehiscence is seldom accomplished, leaving some areas
at higher risk for further recession. It is notable that
the left canine in Figure 5g is beginning to show some
relapse of the recession at three years. Self-inflicted
(iatrogenic) gingival injuries caused by over-zealous oral
hygiene practices can easily reverse the positive results
achieved by even the most successful tissue augmenta-
tion procedures51-58.
The recent popularity of lip and tongue jewellery
is responsible for a new type of recession defect that
 407

is especially hard to repair on the mandibular arch. Conclusions

Tongue piercing is associated with lingual recession of
Recession secondary to periodontal disease is thought
mandibular anterior teeth and chipping of posterior
to be related to poor oral hygiene, while overzealous,
teeth (Figure 9). The length of time worn, and increased
incorrect tooth brushing may be responsible for the re-
barbell length results in increased prevalence of these
cession associated with good oral hygiene. The aetiology
effects. Current use of acellular dermal matrix graft
of gingival recession is multifactorial and unlikely to be
and autogenous connective tissue grafts has increased
caused by any single factor1,8. Dentine hypersensitivity is
the opportunities for clinicians to address these unusual
preceded by gingival recession and exposure of the root
gingival defects successfully, however, recurrence of
surface. Acidic and erosive foods and drinks combined
recession defects are highly likely unless the patient is
with vigorous tooth brushing and highly abrasive den-
counselled to remove the barbell or lip piercing.

7a. Pre-operative 7b. Graft placement

7c. Two weeks post-operative 7d. Three months post-operative

Figure 7 (a-d). Connective tissue graft

Photographs courtesy of Dr Glenn Maze, Periodontal Program
Director, Medical College of Georgia.

Table 3 Miller 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 malpositioned teeth.

Class IV Marginal tissue recession that extends to or beyond the mucogingival junction with severe bone or
soft-tissue loss in the interdental area or malpositioned teeth.

Source Miller50

Drisko: Preventing and managing dentine hypersensitivity

408

8a Pre-treatment 8b Exposure of the defect

8c Placement of acellular dermal allograft 8d Flap closure

8e 6 months post-operative

Figure 8 (a-e) .
Photographs courtesy Dr. Henry Greenwell, University of Louisville, School of Dentistry, Graduate Periodontics Program.

Figure 9. Lip piercing. Design of jewellery and placement technique

are critical if gingival clefts are to be avoided. Arrows indicate
early clefting associated with the highlighted jewellery piece
Photograph courtesy of Betsy Reynolds, RDH, MS, in association
with Association of Professional Piercers.

International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)


tifrices are likely to elicit dentine hypersensitivity1,9. Suc-
cessful treatment of patients with mild sensitivity and
minimal recession can be accomplished in most cases
simply by correcting destructive oral hygiene habits in
conjunction with use of a desensitising dentifrice. Mod-
erate to severe dentine hypersensitivity in the presence
of gingival recession ≥1 mm usually requires a surgical
root coverage procedure with or without daily use of
desensitising toothpastes and/or professional applica-
tion of desensitising agents, dentine bonding materials,
or cervical restorations.
References
1. Addy, Martin. Tooth brushing, tooth wear, and dentine hypersen-
sitivity- are they associated? Int Dent J 2005 55: 261-267.
2. Brannstrom M. A hydrodynamic mechanism in the transmission
of pain producing stimuli through the dentine. In: Anderson DJ
(ed), Sensory Mechanisms in Dentine. pp 73-79. Oxford, Pergamon.
3. Curro FA. Tooth hypersensitivity in the spectrum of pain. Dent
Clin North Am 1990 34: 429-437.
4. Baker DL, Seymour GJ. The possible pathogenesis of gingival
recession: a histological study of induced recession in the rat. J
Clin Periodontol 1976 3: 208-219.
5. Hopps RM, Johnson NW. Relationship between histological degree
of inflammation and epithelial proliferation in macaque gingiva. J
Periodontal Res 1974 9: 273-283.
6. Albandar, JM, Kingman A. Gingival bleeding, and dental calculus
in adults 30 years of age and older in the United States 1988-1994.
J Periodontol 1999 70(1): 30-43.
7. Gorman WJ: Prevalence and etiology of gingival recession. J Peri-
odontol 1967 38: 316-322.
8. Kassab MM, Cohen, RE. The etiology and prevalence of gingival
recession. JADA February 2003: 134.
9. Daprile G, Gatto MR, Checci L. The evolution of buccal gingival
recessions in a student population: a 5-year follow-up. J Periodontol
2007 78: 611-614.
10. Trott JR, Love B. An analysis of localized gingival recession in 766 Win-
nipeg High School Students. Dent Pract Dent Rec 1966 16: 209-213.
11. Tezel A, Varol C, Canakci V et al. Evaluation of gingival recession in
left-and right-handed adults. Intern J Neuroscience 2001 110: 135-146.
12. Litonjua LA, Andreana S, Bush PJ et al. Toothbrushing and gingival
recession. Int Dent J 2003 53: 67-72.
13. Budtz-Jørgensen E, Mohon P, Rentsch A et al. Caries prevalence
and associated predisposing conditions in recently hospitalized
elderly persons. Acta Odontol Scand 1996 54: 51-56.
14. Susin C, Haas AN, Oppermann RV et al. Gingival recession: epi-
demiology and risk indicators in a representative urban Brazilian
population. J Periodontol 2004 75: 1377-1386.
15. Müller HP, Stadermann S, Heinecke. Gingival recession in smokers
and non-smokers with minimal periodontal disease. J Clin Periodontol
2002 29: 129-136.
16. Rees JS. The prevalence of dentine hypersensitivity in general
dental practice in the UK. J Clin Periodontol 2000 27: 850-865.
17. Lost C. Depth of alveolar bone dehiscences in relation to gingival
recessions. J Clin Periodontol 1984: 11: 58-59.
18. Staufer K, Landmesser H. Effects of crowding in the lower
anterior segment-a risk evaluation depending upon the degree of
crowding. J Orofac Orthop 2004 65: 13-25.
19. 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 1: 32-36.
409
20. Stoner JE, Mazdaysna S. Gingival recession in the lower incisor
region of 15-year-old subjects. J Periodontol 1980 51: 74-76.
21. Parfitt GH, Mjör JA. A clinical evaluation of local gingival reces-
sion in children. J Dent Child 1964 31: 257.
22. Akpata ES, Jackson D. The prevalence and distribution of gingi-
vitis and gingival recession in children and young adults in Lagos,
Nigeria. J Periodontol 1979 50: 79-83.
23. Vehkalahti, M. Occurrence of gingival recession in adults. J Peri-
odontol 1989 60: 599-602.
24. Addy M, Griffiths G, Mostafa P et al. Dentine hypersensitivity: the dis-
tribution of recession, sensitivity and plaque. J Dent 1987 15: 242-248.
25. Chabansky MB, Gillam DG, Bulman JS et al. Clinical evaluation
of cervical dentine sensitivity in a population of patients referred
to a specialist Periodontology department: a pilot study. J Oral
Rehabil 1997 24: 666-672.
26. Bernimoulin, J, Curilovie Z. Gingival recession and tooth mobility.
J Clin Periodontol 1977 4: 107-114.
27. Wennstrom JL, Lindhe, J, Sinclair F et al. Some periodontal tis-
sue reactions to orthodontic tooth movement in monkeys. J Clin
Periodontol 1987 14: 21-29.
28. 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.
29. Kocht A, Simon G, Person P et al. Gingival recession in relation to
history of hard toothbrush use. J Periodontol 1993 64: 900-905.
30. Gunsolly JC, Quinn SM, Tew J et al. The effect of smoking on individuals
with minimal periodontal destruction. J Periodontol 1998 69: 165-170.
31. Niemi ML, Sandhoom 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: 254-261.
32. Robinson PG, Deacon SA, Deery C et al. Manual versus powered
toothbrushing for oral health. [Update of Cochrane Database Syst
Rev. 2003 (1)CD002281 PMID: 12535436]. [Review] [345 refs].
33. Silverstone LM, Featherstone MJ. Examination of the end rounding
pattern of toothbrush bristles using scanning electron microscopy:
a comparison of eight toothbrush types. 1988 4: 445-462.
34. Myer-Luekel H, Rieben AS, Kielbassa AM. Filament end-rounding
quality in electric toothbrushes. J Clin Periodontology 2005 32: 29-32.
35. Drisko C, Henderson R, Yancy J. A review of current toothbrush bristle
end- rounding studies. Compendium Cont Ed Dent 1995 16: 694-608.
36. Amano K, Miyake K, Borke JL et al. Breaking biological barriers
with a toothbrush. J Dent Res 2007 86: 769-774.
37. Kusano, HirokiKusano H, Romofuji T et al. Am J Dent 2006 1917-1910.
38. Yamamoto R, Tomofuji T, Ekuni D et al. Effects of toothbrushing
frequency on proliferation of gingival cells and collagen synthesis.
J Clin Periodontol 2004 31: 40-44.
39. Tomofui T, Morita M, Horiuchi M et al. The effect of duration and
force of mechanical toothbrushing stimulation on proliferative activ-
ity of the junctional epithelium. J Periodontol 2002 73: 1149 -1152.
40. Horiuchi M, Yamamoto T, Tomofuji T et al. Toothbrushing
promotes gingival fibroblast proliferation more effectively than
removal of dental plaque. J Clin Periodontol 2002 29: 791-795.
41. Sakamaoto T, Horiuchi M, Tomofuji T et al. Spatial extent of
gingival cell activation due to mechanical stimulation by tooth-
brushing. J Periodontol 2003 74: 585-589.
42. Tomofuji T, Ekuni D, Yamamoto T et al. Optimum force and dura-
tion of toothbrushing to enhance gingival fibroblast proliferation and
procollagen type I synthesis in dogs. J Periodontol 2003 74: 630-634.
43. Lindhe J, Hyman S, Karring T. Scaling and root planing in shallow
pockets. J Clin Periodontol 1992 9: 415-418.
44. Drisko CL, Cochran DL, Blieden T et al. Position paper: sonic and
ultrasonic scalers in periodontics. Research Science and Therapy
Committee of the American Academy of Periodontology. J Peri-
odontol 2000 71: 1792-1801.
45. Claffey N, Loos B, Gantes B et al. The relative effects of therapy
Drisko: Preventing and managing dentine hypersensitivity
410
and periodontal disease on loss of probing attachment after root
debridement. J Clin Periodontol 1988 15: 163-169.
46. Alves RV, Machion L, Casati MZ et al. Clinical attachment loss produced
by curettes and ultrasonic scalers. J Clin Periodontol 2005 32: 691-694.
47. Al-Azzawi LM, Dayem RN. A comparison between the occluding
effects of the Hd: YAG laser and the desentitizing agent sensodyne
on permeation through exposed dentinal tubules of endodontically
treated teeth: An in vitro study. Arc Oral Biol 2006 51: 535-540.
48. Oates TW, Robinson M, Gunsolley JC. Surgical therapies for the
treatment of gingival recession. A systematic review. Ann Periodontol
2003 8: 303-320.
49. Taani SD, Awartani F. Clinical evaluation of cervical dentin sensitivity
(CDS) in patient attending general dental clinics (GDC) and peri-
odontal specialty clinics (PSC). J Clin Periodontol 2002 29: 118-122.
50. Miller PD Jr. A classification of marginal tissue recession. Int J
Periodontics Restorative Dent 1985 5: 9-13.
51. Endo H Rees TD, Hallmon WW, Kono et al. Self inflicted gingival
injuries caused by excessive oral hygiene practices. Texas Dent J
2006 December: 1098.
52. Addy M, Hunter ML. Can tooth brushing damage your health?
Effects on oral and dental tissue. Int Dent J 2003 53: 177-186.
53. Ozcelik O, Haytac MC, Akkaya M. Iatrogenic trauma to oral tis-
sues. J Periodontol 2005 76: 1793-1797.
54. Campbell A, Moore A, Williams E et al. Tongue piercing: Impact
International Dental Journal (2007) Vol. 57/No.6 (Supplement 1)
of time and barbell stem length on lingual gingival recession and
tooth chipping. J Periodontol 2002 73: 289-297.
55. Mlinek A, Smukler H, Buchner A. The use of free gingival grafts
for the coverage of denuded roots. J Periodontol 1973 44: 248-254.
56. Zucchelli G. Testori T, De Sanctis M. Clinical and anatomical
factors limiting treatment outcomes of gingival recession: A new
method to predetermine the line of root coverage. J Periodontol
2006 77: 714-721.
57. Paolantonio M, Dolci M, Esposito P et al. Subpedicle acellular
dermal matrix graft and autogenous connective tissue graft in
the treatment of gingival recessions: A comparative 1-year clinical
study. J Periodontol 2002 73: 1299-1307.
58. Santos AL, Goumenos G, Pascual A. Management of gingival
recession by the use of an acellular dermal graft material: A 12-
case series. J Periodontol 2005 76: 1982-1990.
Correspondence to: Dr Connie L. Drisko, Medical College of Geor-
gia School of Dentistry, 1459 Laney Walker Boulevard, Augusta GA
30912, USA. Email: cdrisko@mail.mcg.edu