INTRODUCTION stimuli are believed to alter the

INTRODUCTION

Dentinal hypersensitivity (DH) is a
relatively common dental clinical condition in permanent teeth caused by dentin
exposure to the oral environment as a consequence of loss of enamel and /or
cementum & commonly affecting the facial surfaces of premolar and canine.1
It afflicts perhaps 15% of the adult population world-wide2, and
possibility up to 57% in some regions.3

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An international workshop held in New
York, USA, in November 1994 defined the condition   as4 “A short, sharp pain arising
from exposed dentine in response to stimuli, typically thermal, evaporative,
tactile, osmotic or chemical and which cannot be ascribed to any other dental
defect or pathology”. A modification of this definition was suggested by the
Canadian Advisory Board on Dentine Hypersensitivity5 in 2003, which
suggested that ‘disease’ should be substituted for ‘pathology’.

Various theories have been proposed to explain the actual mechanism
responsible for DH. These include the:

1.      Odontoblastic transduction theory6

2.      Neural theory7

3.      Hydrodynamic theory8,9

Among these, the
hydrodynamic theory has ever been widely accepted. Comprehension of the
hydrodynamic theory forms the basis for successful management outcomes. Pain, caused by the movement of fluid in the
dentinal tubules, can be explained by the widely accepted “Hydrodynamic theory”
proposed by Brännström and Astron in 1964. According to this theory, certain
stimuli, allows the movement of dentinal fluid inside the tubules, indirectly
stimulating the extremities of the pulp nerves, causing the pain sensation. The
various stimuli are believed to alter the flow and pressure of the tubule fluid
and thus by hydrodynamic action any changes are evident to mechano-receptors
surrounding the odontoblast processes.

Two major approaches are commonly employed in the treatment and
prevention of DH: occlusion of tubules and nerve activity blockage. In the
tubular occlusion approach, the tooth is treated with an agent that occludes
the dentinal tubules, thus resulting in stoppage of pulpal fluid flow, leading
to reduction in DH.10,11

In the blockage of nerve activity, potassium ions cause a depolarization
of the cellular membrane of the nerve terminal by concentrating on dentinal
tubules and thus giving rise to a refractory period with decreased sensitivity.12

Various modalities which
are available for the treatment of dentinal hypersensitivity.13Nerve
desensitization, Protein
precipitation, Plugging
dentinal tubules, Dentin
adhesive sealers, Lasers

Potassium nitrate was
introduced as a desensitizing agent by Hodosh. (1974) & one of the widely
prescribed desensitizing agents. It has been used in concentrations of 1%, 2%,
5%, 10%, and 15% or as a saturated solution. Potassium salts act by diffusion
along the dentinal tubules and decreasing the excitability of the intradental
nerve fibers by blocking the axonic action.14,15 By increasing the
potassium ion concentration adjacent to the dentinal nerve terminals, there is
depolarization and activation of nerve fibres. A prolonged period of
depolarization results in inactivation of the action potential. Divalent cation
solutions stabilize the nerve membrane without changing the membrane potential.16

 Kleinberg et al., (2002) developed a system  which  
consists of 8% arginine with bicarbonate and calcium carbonate. The
arginine, on which the Pro-Arginine technology relies, is a natural amino-acid
found in small concentrations in the saliva17. The mechanisms of
action of the Pro-Argin technology have been elucidated by Kleinberg et al.
Firstly, arginine physically adsorbs onto the surface of calcium carbonate,
thereby forming a positively charged agglomerate. This agglomerate binds to the
dentinal surface and tubuled. Secondly, the pH of this agglomerate is alkaline
to allow mineral deposits of calcium and phosphate on the dentinal surface. The
new dentifrice has been clinically proven to provide both significant instant
and lasting dentin hypersensitivity relief and a whitening benefit.18  

NovaMin® is the branded
ingredient that is found in a number of professional use and over-the-counter
dental products designed to give immediate and long-lasting relief from tooth
sensitivity. In the treatment of dentinal hypersensitivity the physical
occlusion of Novamin® particles begins when the material is subjected to an
aqueous environment. Sodium ions (Na+) in the particles immediately begin to
exchange with hydrogen cations (H+ or H3O+). This rapid release of ions allows
calcium (Ca+) ions in the particle structure, as well as phosphate (PO4 3-)
ions to be released from the material. This initial series of reactions occurs
within the seconds of exposure, and the release of the calcium and phosphate
ions continues so long as the particles are exposed to an aqueous environment.19
A localized, transient increase in pH occurs during an initial exposure of the
material due to the release of sodium. This increase in pH helps to precipitate
the calcium and phosphate ions from the Novamin® particle, along with the
calcium and phosphorus found in saliva, to form a calcium phosphate (Ca-P)
layer. As the particle reactions continue and the deposition of Ca and P
complexes continue, this layer crystallizes into hydroxycarbonate apatite,
which is chemically and structurally equivalent to biological hydroxyapatite.
The combination of the residual Novamin® particles and the hydroxycarbonate
apatite layer results in the physical occlusion of dentinal tubules, which will
relieve the hypersensitivity.20

A different treatment
modality for reducing DH involves the use of laser technology. The word
”laser” is an acronym derived from “Light Amplification by the Stimulated
Emission of Radiation”.  The first laser
use for the treatment of dentine hypersensitivity was reported by Matsumoto et
al. in 1985 using the Nd: YAG laser.21 The lasers used for the
treatment of dentine hypersensitivity are divided into two groups: low output
power (low level) lasers helium-neon (He-Ne, 6mW) and
gallium/aluminum/arsenide (GaAlAs) (diode) lasers (30-100mW) , and middle
output power lasers (Nd: YAG, CO2, Er:YAG, GaAlAs & Er,Cr:YSGG) (0.3-10W).
The rationale for laser-induced reduction in DH is based on two possible
mechanisms. The first mechanism implies the direct effect of laser irradiation
on the electric activity of nerve fibers within the dental pulp, whereas the
second involves modification of the tubular structure of the dentin by melting
and fusing of the hard tissue or smear layer and subsequent sealing of the
dentinal tubules.

The purpose of this study
was to evaluate the effectiveness of Diode Laser 810nm & various
desensitizing agents i.e. potassium nitrate , 8% Arginine & calcium
carbonate (Pro-Arginin)  & calcium
sodium phosphosilicate (Novamin) in the treatement of dentinal hypersensitivity
.

 

 

MATERIAL AND METHODOLOGY

This
study was conducted in the Department of
Periodontology,   Sardar
Patel Post Graduate Institute of Dental & Medical Sciences, Lucknow. 80
subjects including 45 males and 35 females in the age range 25-55 years were
recruited for the study. Subjects in good general health and presenting with
symptoms of dentinal hypersensitivity were considered for enrolment.

Inclusion Criteria

·       
Abrasion due to faulty tooth brushing

·       
Abfraction

·       
Parafunctional habits

·       
Occlusal disequilibrium

·       
Erosions

·       
Gingival recession

·       
No history of desensitizing dentifrice use in last 3
months  

 

Exclusion Criteria:

·       
Teeth with carious lesions

·       
Chronic or debilitating diseases

·       
Active periodontal diseases

·       
Pulpitis

·       
Dental fractures

·       
Ingestion of daily medication (Analgesics,
Anticonvulsive, Antihistaminic, Sedative Tranquilizers,  Antidepressants )

 

Dentinal
hypersensitivity was assessed by:

Air
blast stimulation:

After
phase I therapy   dentinal
hypersensitivity was  evaluated with a
blast of air from a three way syringe connected to an air compressor at a
pressure of 60 psi under room temperature of about 20–25°C. This air jet
lasting for 5 sec at a distance of 3 mm from the tooth surface was directed at
the patient’s tooth, and any uncomfortable feeling caused by the air stimuli
was recorded.

Only one tooth that was found to
be most sensitive to the air-blast stimulus was selected   for
each patient. Evaluation of DH was based on the patient’s subjective answer,
using the Visual Analog Scale.22  Ordinal values from 0 to 10 located at the
opposite ends of this scale represent “pain absence” (value 0) and “intolerable
pain” (value 10). The patients were asked to indicate a value from 0 to 10 that
best represented their pain level.

To determine the efficacy of therapy on DH pain, the following
approach was used:

a)    
Excellent(absence of pain) — VAS score reached
0                                                 

b)    
Good (light
pain) — VAS score reached 1, 2, or 3

c)    
Unsatisfactory (moderate pain) — VAS score
reached 4, 5, or 6

d)    
Unsatisfactory (strong  pain) —  VAS score reached 7, 8, or 9

e)    
 Bad(intolerable)  — VAS score reached 10

The subjects were randomly divided into four groups:

1)     Group A:  20 subjects treated with Picasso diode laser 810 nm   

2)     Group B:  20 subjects treated with Potassium nitrate 5% as a paste
form

3)     Group C:  20 subjects treated with
Calcium sodium phosphosilicate as a paste form

4)     Group D:  20 subjects treated with 8%  Arginine &
calcium carbonate as a paste form

GROUP A

At
base-line after pain evaluation by VAS .The tooth was gently dried with a
cotton roll & isolated before applying diode laser. Ga Al As-diode laser
with 810nm wavelength was used in continuous mode. Both the operator and the
subjects used appropriate protective eyewear during the laser application. The
power was set at 0.5W. The exposure time per application was 1 minute. Energy per
application was 19 J with continuous emission form, application on the buccal
surface of the teeth.  The measurements were performed before each
treatment session and 15 mins after the laser application to verify the
capacity & the extent of desensitization after irradiation. This result was
called immediate effect. The laser
application was carried out in 4 sessions, with interval of 7 days between each
session. In every session, VAS score was recorded 15 mins post laser
application. Follow up was made at 2nd , 4th & 8th
week post last session & VAS score was recorded in every follow up week to
determine the delayed  effect of laser
application.

For Potassium
nitrate (Senquel F®) GROUP-B,
Calcium Sodium Phosphosilicate  (Sensodyne
repair & protective®) GROUP- C  Novamin,  8% Arginin & Calcium Carbonate  (Colgate sensitive pro-relief™) GROUP- D Pro-arginin, after pain
evaluation by VAS at base-line ,  desensitizing pastes  were provided to each  subjects with 
instructions  to be applied at
home twice a day for 2 weeks instructed to brush with allocated paste for 5 mins  & were directed  to refrain 
from any other dentifrice or mouthwash & also refrain from consuming
very hot, cold, sweet or sour foods or drinks. The VAS score were recorded at
day 7 & day 14 during the treatment. Hypersensitivity scores were also recorded
using Visual Analog Scale at all follow-up visits i.e. 2 weeks, 4 weeks & 8
weeks after the use of desensitizing paste was stopped.  

RESULTS

         The present clinical study compares diode
laser 810 nm and various desensitizing agents in the treatment of dentinal
hypersensitivity. Total 80 samples were selected and randomized equally into
four groups and treated (desensitized agents) with either diode laser 810 NM
(LASER or Group A) or potassium nitrate 5% (POTASIIUM NITRATE or Group B) or
novamin (NOVAMIN or Group C) or pro-arginine (PRO-ARGININE or Group D). The
outcome measure of the study was pain score assessed in visual analogue scale
(VAS, 0-10 mm scale). The effect of LASER on pain were assessed at pretreatment
(Pre) and 15 min post treatment (Post) on day 1 (SESSION I), day 7 (SESSION
II), day 14 (SESSION III) and day 21 (SESSION IV). The effect of POTASIIUM
NITRATE, NOVAMIN and PRO-ARGININE on pain were assessed at pretreatment
(baseline) and post treatment (day 7 and day 14). The reversal effect of all
four treatment groups on pain were reassessed at 2nd week, 4th week and 8th week post
treatments.

 

To see the
reversal effect of treatments (LASER: Group A, POTASSIUM NITRATE: Group B,
NOVAMIN: Group C and PROARGININE: Group D) on pain, the post treatment (i.e.
after stopping the treatments) VAS score of four groups over the periods
(baseline, 2nd, 4th and 8th week) were further compared between
groups and periods and summarized in Table 1 and also depicted in graph 1.
Table 1 and graph 1 showed that the post treatment mean VAS score increase
linearly with time in all groups and the increase was evident highest in Group
B followed by Group D, Group C and Group A the least (Group A 0.05) VAS score at
baseline between the groups suggesting it comparable between the groups (Table 3
and graph 3). However, at 2nd, 4th and 8th
week, it was significantly (P0.05) between the
groups i.e. found to be statistically the same

 

 DISCUSSION

     Dentine
hypersensitivity (DH) is a painful response of the tooth to different stimuli
such as brushing, acid diets, occlusal overload and thermal changes.23  In the present study, a visual analog
scale (VAS) was used to assess DH because it is easily understood by patients,
it is sensitive in discriminating among the effects of various types of
treatments, and it thus is suitable for evaluating the response.24

       According to Landry & Voyer (1990)25 there is no ideal
desensitizing agent and any treatment method for dentine hypersensitivity
should be effective from the first application and must comply with the
following characteristics: does not irritate the pulp or cause pain, easy
application, effective on a permanent basis, does not discolor or stain the
teeth, does not irritate the soft tissues or the periodontal ligament and has
low cost.

     Cervical dentine hypersensitivity has
multifactorial etiology and generally more than one factor found associated and
active in this painful manifestation. According to Garone Filho (1996)26, 
the  most common etiological
factor related to clinical manifestations of dentine hypersensitivity is the
abfraction caused by occlusal overload. Studies have confirmed that the patency
of the dentinal tubules is a prerequisite for the sensitivity of exposed
dentin. It was shown using scanning electron microscopy (SEM) that teeth with
dentinal hypersensitivity have a significantly higher number of patent dentinal
tubules per millimeter and a significantly greater mean diameter per tubule
than control teeth. The wider tubules increases the fluid movement and thus the
pain response.27

      Conventional therapies for the treatment
of DH comprehend the topical use of desensitizing agents, either professionally
or at home such as protein precipitants tubule-occluding agents, tubule
sealants, and recently lasers. Two chief mechanism of treatment of dentin
hypersensitivity are tubular occlusion and blockage of nerve activity.28

 The results of the present clinical trial
demonstrated that all the four groups tested were effective in desensitizing
hypersensitive teeth at every mentioned time intervals. However, Group A
treated with diode laser 810nm was found more effective  for long term maintenance dentinal
hypersensitivity . The
result illustrate the effectiveness of GROUP A i.e. DL 810 nm which showed
immediate & delayed effect. a study conducted by Junior B et al (2000)29 in the treatment of dentine
hypersensitivity which showed immediate analgesic effect with diode laser with
an improvement index of 91.29% in 1102 treated teeth, operating in different
bands of wavelength, 780 nm and 830 nm, and different power densities of 40 mW
and 50 mW. The finding can be attributed to the fact at the cellular level,
inhibition of nociceptive signals which arise from peripheral nerves is a major
component of the therapeutic effect.30   Further, LLLT has been shown to block the
depolarization of C-fibre afferents in dental pulp.31

Ladalardo
et al (2004)32
conducted the study on the laser interaction with the dental
pulp causes a photobiomodulating effect, increasing the cellular metabolic
activity of the odontoblasts and obliterating the dentinal tubules with the
intensification of tertiary dentine production.  Villa
et al (1988) 33 observed the profiling of odontoblasts and a
large quantity of neoformed tertiary dentine in irradiated teeth, previously
eroded by high rotation. The non-irradiated group showed intense inflammatory
process and in some cases evolved to irreversible pulp degeneration and
necrosis. The laser irradiation contributed to the repair of the dentine-pulp
complex, preserving the pulpal vitality.

Mezawa et al (1988)34 reported
that LLLT interferes with transmission of peripheral nerve signals to the
central nervous system, where the signals are interpreted. The maintenance of
this analgesic state of the dentine comes from sealing of dentinal tubuli,
which impedes the internal communication of the pulp with external oral fluids.
The authors concluded that LLLT was effective in 97% of the cases.

Matsumoto et al (1985)35
carried out a histological study in monkeys (64 teeth) with exposed pulps
(class V cavities) by using 704nm diode laser (CW, 30mW) for  30s 
& better degree of repair was seen 
at 14 and 30 days after laser irradiation when compared with the
non-irradiated dental pulp group. 
Histological analysis showed a significantly improved results in forms
of repair between the groups. The resolution of inflammation showed in
irradiated group than the non-irradiated.

Recent
study by Sommer AP & Gente M (1999)36
indicates that light energy density and intensity are biologically independent
irradiation parameters, suggesting that the success or failure of LLLT may be
linked to the method of irradiation. The light reaches the pulp without losing
practically any energy, thereby clearly showing that laser light is conducted
through the inter-tubular dentine and the highly orderly structure of the
dentine. It is important to note that light travels parallel to the tubuli, but
not through the tubuli .

According
to Wilchgers & Ermert (1997)37
and Kim (1986)38 the
desensitizing effect of potassium nitrate is due to the increase in
concentration of extracellular potassium around the nerve fibres which cause
their depolarization, avoids repolarization and blocks the axonic action. This
blocks the passage of nerve stimulus, resulting in inactivation of the action
potential.

Calcium
sodium phosphosilicate, originally developed as a regenerative bone material,
has been shown to be effective at physically occluding dentinal tubules. Pradeep et al (2010)39 evaluated
the efficacy of calcium sodium phosphosilicate in 110 subjects & compared
with potassium nitrate and to a placebo. The calcium sodium phosphosilicate
group, however, was found to be statistically significantly in reduction in
visual analog scale score compared to the potassium nitrate group and the
placebo group. It has been shown that the innovative bioactive glass-containing
toothpaste occludes dentinal tubules and resists acid challenge.

Favourable
results of the efficacy of Novamin in relieving DH have also been demonstrated
by in vivo studies by Pradeep et al
(2010)39 and Rajesh et al
(2012)40 In an aqueous environment, sodium ions (Na+)
from Novamin begin to exchange with hydrogen cations (H+ or H3O+),
which allows calcium ions (Ca2+) and phosphate ions (PO43-)
to be released from the filler particle structure. Ca2+ and PO4
3- ions from Novamin, along with mineral ions in saliva are able to
form a calcium phosphate (Ca-P) layer onto dentine surfaces or into tubules, resulting
in physical tubule occlusion.

The
mechanism of action of ACC was explained by Kleinberg et al (2002)17, who suggested that the
combination of arginine and calcium carbonate forms a positively charged
complex which readily binds to the negatively charged dentine surface and
within the dentinal tubules. In addition, the alkaline pH of the ACC is
sufficient to facilitate the precipitation of calcium and phosphate from saliva
and/or dentinal fluid to form plugs that seal the patent tubules.

Clinical
trials by Nathoo et al (2009)41
and Kapferer et al (2013)42   have also proven ACC to be effective in
relieving DH.

When
the VAS scores of the four groups were compared, the laser group showed a
statistically significant reduction in DH in the first week itself. The faster
desensitizing effect of laser therapy observed in the present study may be
attributed to depressed nerve transmission.43

To see the reversal effect of treatments (LASER: Group
A, POTASSIUM NITRATE: Group B, NOVAMIN: Group C and PRO-ARGININE: Group D) on
pain, the post treatment (i.e. after stopping the treatments) VAS score of four
groups over the periods (baseline, 2nd, 4th and 8th
week) were further compared between groups and periods.  The post treatment mean VAS score increase
linearly with time in all groups and the increase was evident highest in Group
B followed by Group D, Group C and Group A the least (Group A

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