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UNIVERSIDADE FEDERAL DO CEARÁ
FACULDADE DE FARMÁCIA, ODONTOLOGIA E ENFERMAGEM
DEPARTAMENTO DE CLÍNICA ODONTOLÓGICA
CURSO DE ODONTOLOGIA
ALESSANDRA HELEN MAGACHO VIEIRA
AVALIAÇÃO DA EFICIÊNCIA DE AGENTES
ANTI-HIPERESTÉSICOS NO TRATAMENTO DA
HIPERESTESIA DENTINÁRIA
FORTALEZA
2007
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ALESSANDRA HELEN MAGACHO VIEIRA
AVALIAÇÃO DA EFICIÊNCIA DE AGENTES
ANTI-HIPERESTÉSICOS NO TRATAMENTO DA
HIPERESTESIA DENTINÁRIA
Dissertação submetida à Coordenação do Programa
de Pós-Graduação em Odontologia, da Universidade
Federal do Ceará, como requisito parcial para
obtenção do grau de Mestre em Odontologia. Área
de Concentração: Clínica Odontológica.
Orientador: Prof. Dr. Sérgio Lima Santiago
FORTALEZA
2007
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V713a Vieira, Alessandra Helen Magacho
Avaliação da eficiência de agentes anti-hiperestésicos
no tratamento da hiperestesia dentinária / Alessandra
Helen Magacho Vieira. – Fortaleza, 2007.
72f.
Orientador: Prof. Dr. Sérgio Lima Santiago.
Dissertação (Mestrado) – Universidade Federal do
Ceará. Programa de Pós-Graduação em Odontologia,
Fortaleza-CE, 2007.
1. Sensibilidade da dentina. 2. Oxalatos. 3. Lasers. 4.
Efeito Placebo. I. Santiago, Sérgio Lima (orient.). II.
Título.
CDD 617.634
À minha família.
AGRADECIMENTOS
Aos meus pais, Fátima e Erivan, pelo amor incondicional, e ao meu irmão,
Fabiano, por acreditar e impulsionar a concretização dos meus objetivos.
Ao meu grande amor, Márcio, por tornar cada dia especial.
À Prof
a
. Sandra Figueiredo e ao Prof. William Silvestre, pelo carinho e incentivo.
Ao Prof. Sérgio Santiago, pelo exemplo de dedicação, pela oportunidade e pela
orientação do trabalho. Obrigada pela confiança e por contribuir para meu crescimento
pessoal e profissional.
Ao Prof. Juliano Sartori, pela disponibilidade e realização da análise estatística.
Aos professores da Disciplina de Dentística, Haroldo Beltrão, Lidiany Karla e
Carlos Augusto, que estiveram ao meu lado em momentos importantes. Agradeço a
honestidade, o companheirismo e os conhecimentos transmitidos.
Aos meus colegas da turma de Mestrado, pela amizade, sugestões e reflexões.
Às amigas e companheiras de pesquisa, Vanara Passos e Jorgiana de Assis, pelo
apoio e por possibilitarem a realização deste trabalho.
À Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES), pela
concessão da bolsa de auxílio financeiro e à Universidade Federal do Ceará, pela realização
do Curso de Pós-Graduação.
RESUMO
A hiperestesia dentinária é um fenômeno sensorial complexo e de difícil solução
na clínica odontológica. Apesar da grande diversidade de tratamentos propostos, ainda não
existe uma terapia considerada ideal para eliminar essa situação desconfortável. Esta
dissertação, constituída por dois artigos científicos, teve por objetivos: (1) revisar criticamente
a literatura disponível sobre os principais aspectos relacionados à etiologia e ao tratamento da
hiperestesia dentinária; (2) avaliar clinicamente a eficiência de agentes anti-hiperestésicos no
tratamento da hiperestesia dentinária. No estudo 1, a literatura científica pertinente ao assunto
foi analisada através dos resultados de investigações clínicas e laboratoriais pesquisadas
usando a base de dados medline e busca manual de referências citadas em artigos científicos.
No estudo 2, um total de 164 dentes, provenientes de 30 pacientes com diagnóstico de
hiperestesia dentinária moderada ou severa, foi dividido aleatoriamente em três grupos e
avaliado clinicamente de acordo com o tratamento administrado: aplicação de laser de
arseniato de gálio-alumínio (AsGaAl), aplicação de gel de oxalato de potássio a 3% e
aplicação de gel placebo. As aplicações dos tratamentos foram realizadas em intervalos
semanais, durante o período de quatro semanas consecutivas e o grau de sensibilidade foi
mensurado para cada dente através de uma escala visual analógica em resposta aos estímulos
tátil (sonda exploradora) e evaporativo (jato de ar) antes da primeira aplicação (baseline),
imediatamente após e três meses após a última aplicação dos tratamentos. Os dados foram
submetidos à análise estatística pelo teste de Kruskal-Wallis (p=0,05) e o grau de redução da
hiperestesia dentinária foi avaliado para cada um dos períodos observacionais em relação ao
baseline. A análise crítica apresentada no artigo 1 mostrou que a literatura apresenta diversos
tipos de tratamento para a hiperestesia dentinária, que variam desde procedimentos simples,
que podem ser executados pelo próprio paciente, até procedimentos complexos, que envolvem
a combinação de diferentes terapias. Os resultados do artigo 2 demonstraram que a aplicação
dos tratamentos propostos, inclusive o placebo, proporcionou redução estatisticamente
significante, imediata e mediata, da sensibilidade em resposta aos estímulos tátil e evaporativo
(p<0,05). No entanto, não houve diferença estatisticamente significante entre os três grupos
estudados, independentemente do estímulo aplicado, tanto na avaliação imediata quanto na
mediata (p>0,05). Em conclusão, os resultados desses estudos indicam que o conhecimento
acerca do mecanismo de ocorrência da hiperestesia dentinária e dos agentes anti-
hiperestésicos disponíveis é indispensável para a elaboração de um tratamento eficiente. Além
disso, concluiu-se que os três tratamentos utilizados no estudo clínico são eficientes para a
redução da hiperestesia dentinária e que existe grande influência do efeito placebo na redução
da sensibilidade dolorosa.
Palavras-chave: Sensibilidade da Dentina. Oxalatos. Lasers. Efeito Placebo.
ABSTRACT
Dentinal hypersensitivity is a complex sensorial condition which can cause
considerable concern in the dental office. Despite the large number of different proposed
kinds of treatment, there is no product or therapy reported in literature that could be
considered ideal to eliminate this uncomfortable situation. The aim of this study, comprised
by two manuscripts, was: (1) to critically review the literature related to the main evidences
about the etiology and the management of dentinal hypersensitivity; (2) to evaluate the
clinical performance of different dentine desensitizers in the treatment of dentinal
hypersensitivity. In study 1, the scientific literature related to the issue was analyzed through
the results of laboratory and clinical investigations searched using medline and manual tracing
of references cited scientific papers. In study 2, a total of 164 teeth, from 30 patients with
clinical diagnosis of moderate or severe dentinal hypersensitivity, were randomly divided into
three groups and clinically evaluated according to the desensitizing treatment under study:
gallium-aluminun-arsenide (GaAlAs) laser therapy, 3% potassium oxalate application and
placebo gel application. Treatment sessions were performed at seven-day intervals for four
consecutive weeks and the degree of sensitivity in response to tactile (probe) and evaporative
(air blast) stimuli was assessed according to a visual analogue scale at baseline, immediately
after and three months after the last treatment session. Data scores were submitted to Kruskal-
Wallis statistical analysis (p=0.05) and were analyzed by dentinal hypersensitivity reduction
for each observational moment in relation to baseline. The critical review presented in study 1
showed that the reviewed literature points out several treatment modalities ranging from
simple procedures, which can be performed by the patient him/herself, to complex procedures
that involve the combination of therapies. The results of study 2 demonstrated that the
treatment of dentinal hypersensitivity performed with both active and control groups produced
statistically significant reduction of pain in response to evaporative and tactile stimulation
immediately after and three months after treatment (p<0.05). No significant differences
among the three groups could be detected in both immediate and mediate evaluations
irrespective of the applied stimulus (p>0.05). In conclusion, the results of these studies
suggest that knowledge about the available desensitizing products and the factors involved in
the mechanism of the dentinal hypersensitivity is indispensable in order to perform an
effective treatment. Besides, it could be concluded that the three treatments performed in the
clinical study were effective for treating dentinal hypersensitivity and that the placebo effect
plays an important role in sensitivity reduction.
Key words: Dentin sensitivity. Oxalates. Lasers. Placebo effect.
SUMÁRIO
1. INTRODUÇÃO GERAL ......................................................................................... 8
2. PROPOSIÇÃO ......................................................................................................... 10
3. CAPÍTULO 1 ........................................................................................................... 11
4. CAPÍTULO 2 ........................................................................................................... 37
5. CONCLUSÃO GERAL ........................................................................................... 61
6. REFERÊNCIAS BIBLIOGRÁFICAS .................................................................... 62
ANEXOS ..................................................................................................................... 68
8
1. INTRODUÇÃO GERAL
A hiperestesia dentinária, também denominada hipersensibilidade dentinária
cervical, consiste em uma resposta exagerada da dentina quando exposta a estímulos
sensoriais (táteis, térmicos, evaporativos, químicos ou osmóticos), que normalmente não
causariam resposta em um dente normal (1). É caracterizada como uma sensação dolorosa, do
tipo localizada, transitória e aguda, que pode variar em intensidade desde um leve desconforto
a uma dor extrema (2,3). Dependendo do grau de intensidade, a hiperestesia pode afetar a
alimentação, a ingestão de líquidos, a respiração, a capacidade de efetivo controle da placa
bacteriana pelos pacientes e até mesmo provocar mudanças emocionais que alteram o estilo
de vida do indivíduo (1).
Esta condição tem sido considerada uma das queixas mais freqüentes nos relatos
de odontalgia e representa um problema constante na clínica odontológica (4,5). Estudos de
prevalência, realizados em diversas partes do mundo, indicam que a hiperestesia dentinária
afeta entre 10% e 30% da população em geral (4,6-11), sendo os dentes mais comumente
acometidos os caninos e pré-molares (12-14). Adicionalmente, haverá uma crescente
demanda de pacientes incomodados com esta situação desconfortável, considerando o
aumento da expectativa de vida dos indivíduos, que mantêm por mais tempo os seus dentes na
cavidade bucal (1,2,4).
Várias teorias têm sido propostas para explicar a ocorrência da hiperestesia
dentinária (15-17). No entanto, o complexo mecanismo no qual fibras nervosas, localizadas
próximas à camada odontoblástica, são influenciadas por estímulos, que atuam na superfície
da dentina exposta, ainda não é completamente elucidado (17-20). Atualmente, a teoria da
hidrodinâmica é a hipótese mais aceita na literatura para interpretar a ativação destas fibras
em conseqüência da transmissão de estímulos sensoriais (4,17,21,22).
Em condições normais, a dentina é permeada por diversos canalículos que se
apresentam completamente protegidos do meio externo pela presença do esmalte ou do
cemento dentário (22,23). No entanto, esta cobertura pode ser facilmente perdida em
conseqüência de processos de abrasão, erosão, abfração ou pelo desnudamento da superfície
radicular por recessão gengival ou procedimentos periodontais e determinar a exposição dos
túbulos dentinários ao meio bucal (13,22,24,25).
De acordo com os princípios da hidrodinâmica, a sensação dolorosa percebida
após a aplicação de um estímulo sobre a dentina exposta ao meio bucal é conseqüência do
9
deslocamento rápido do fluido presente dentro dos túbulos dentinários (15,16). Essa
movimentação do fluido atua, portanto, como um sinalizador da presença de estímulos na
superfície dentinária (18,26). Dependendo da natureza do estímulo, o fluido dentinário pode
ser facilmente deslocado em direção à polpa ou em sentido contrário e determinar uma
variação na pressão intra-pulpar capaz de estimular fibras nociceptivas, localizadas próximas
à camada odontoblástica (15,16). A pressão aplicada sobre as terminações nervosas pode
produzir deformação na membrana dessas fibras, abertura dos canais de sódio e a conseqüente
despolarização da membrana (26,27). Após a ativação, sinais nociceptivos são transmitidos
para o complexo do núcleo trigeminal localizado na medula, que desempenha um papel
fundamental na tranferência desses sinais para regiões do córtex cerebral associadas com a
percepção da dor (26).
A literatura apresenta diversas formas de tratamento para a hiperestesia dentinária,
que variam desde procedimentos simples a terapias complexas (3-5,21,22,28-56). Levando-se
em consideração que o mecanismo da hidrodinâmica é o mais aceito para explicar a
sensibilidade dolorosa em resposta a estímulos sensoriais, os agentes anti-hiperestésicos que
reduzem a permeabilidade da dentina através da obliteração dos túbulos dentinários parecem
ser os mais adequados para a diminuição dos sintomas (19,57,58).
Historicamente, agentes anti-hiperestésicos, como óleo quente, arsênico, nitrato de
prata e formaldeído, foram utilizados para o alívio da sensação dolorosa (20,31). Atualmente,
outras opções, tais como: a aplicação tópica de oxalato de potássio ou a irradiação da
superfície dentinária com laser, surgiram e têm-se mostrado eficientes na redução da
sensibilidade (3,5,29,31-34,38,40,42-44,48,51-53). No entanto, ainda não existe um produto
considerado ideal no tratamento da hiperestesia dentinária (5,7,32,37) e, em geral, a escolha
do agente anti-hiperestésico para o completo alívio da sensibilidade dolorosa é uma decisão
difícil na clínica odontológica (4,14,24,25).
Nesse contexto, o conhecimento gerado pelos diversos estudos laboratoriais e
clínicos torna-se fundamental para o direcionamento dos profissionais em busca de um
tratamento eficiente (32,59). Entretanto, variações no planejamento e nos procedimentos
experimentais utilizados nestas investigações freqüentemente produzem resultados
contraditórios e difíceis de serem comparados (59-62). Dessa maneira, é fundamental que
novos estudos clínicos bem conduzidos sejam desenvolvidos no sentido de elucidar ou
comprovar estratégias terapêuticas eficientes para o tratamento da hiperestesia dentinária.
10
2. PROPOSIÇÃO
Os objetivos do presente trabalho foram:
a) revisar criticamente a literatura disponível sobre os principais aspectos relacionados à
etiologia e ao tratamento da hiperestesia dentinária;
b) avaliar clinicamente a eficiência do gel oxalato de potássio a 3% e do laser de arseniato de
gálio-alumínio (AsGaAl) no tratamento da hiperestesia dentinária, utilizando-se um gel
placebo como controle.
11
3. CAPÍTULO 1
MANAGEMENT OF DENTINAL HYPERSENSITIVITY: A CRITICAL REVIEW
Alessandra Helen Magacho Vieira, Sérgio Lima Santiago
Department of Restorative Dentistry, Dentistry School, Federal University of Ceará, Ceará,
Brazil
Full address of the author to whom correspondence should be sent:
Alessandra Helen Magacho Vieira
Rua Dr. José Lourenço, 781 / 201
60115-280 Fortaleza, CE (Brazil)
Tel. +55 85 9911 2446 / +55 85 3366 8426 / +55 85 3366 8410
e-mail: ale_m[email protected]
12
ABSTRACT
Dentinal hypersensitivity is a complex sensorial condition which can cause
considerable concern in the dental office. Despite the large number of available treatment
modalities, there is no current desensitizing agent considered ideal to manage this
uncomfortable situation. The choice of the right therapy is very intricate and requires a
complete understanding of the mechanism by which a stimulus applied on the exposed
dentine surface can influence the nerve fibers and produce the hyperesthesia. In this review,
the main evidences regarding the etiology and the management of dentinal hypersensitivity
are critically analyzed through the results of laboratory and clinical investigations.
Key words – Dentinal hypersensitivity; hyperesthesia; desensitizing agents.
13
INTRODUCTION
Dentinal hypersensitivity is an exaggerated response of exposed dentine when in
contact with thermal, evaporative, tactile, osmotic or chemical stimuli (1). It is characterized
by a localized, transient and sharp pain which may range from mild discomfort to extreme
pain (1,2). Depending on its intensity, the hyperesthesia can affect eating, drinking and
breathing, hinder the ability to control dental plaque effectively and, sometimes, it may even
result in emotional changes that alter lifestyle (1).
This painful condition of the dentine is considered the most frequent complaint
among reported odontalgias (3). Prevalence studies concerning the dentinal hypersensitivity
indicate that it affects 10 to 30 percent of the general population (2, 4-8). Moreover, with
teeth being retained for longer periods, there will be increasing demand by patients involved
in this uncomfortable situation (1,2,4,9,10).
Several theories have been proposed to elucidate the mechanism of dentinal
hypersensitivity (4,11-14). The Hydrodynamic Theory is considered to be the most widely
accepted to explain the relationship between the presence of stimuli on the dentine surface
and the nerve activation (11,12,14-20). According to its concept, the dentine exposure to the
oral environment and the patency of the dentinal tubules are the main factors associated with
the development of dentinal hypersensitivity (2,11,18,21). Dentine exposure usually occurs as
a result of enamel loss by erosion, abrasion, abfraction or denudation of root surfaces as a
result of gingival recession or periodontal procedures (1,3,4,17,22,23).
The reviewed literature presents a large number of treatment modalities for the
management of dentinal hypersensitivity (3,4,9,10,14,16,17,19). Local application of
desensitizing agents either by a dental professional or by the patient him/herself at home is the
commonest attempt to eliminate or reduce the painful condition (4). Nevertheless, there is no
14
product that comprises all the qualities required for it to be designated as the ideal dentine
desensitizer (3,4).
Therefore, a critical analysis with regard to the development of this hyperesthesia
and its therapeutic approach is indispensable in order to suggest an effective treatment and
control its incidence. The purpose of this review was to critically analyze the main evidences
related to the etiology and management of dentinal hypersensitivity reported in laboratory and
clinical investigations.
15
LITERATURE REVIEW
1. Peripheral and central mechanisms of dentinal pain
The mechanism of the dentinal pain reaction in response to a variety of stimuli is
very complex and not yet clearly understood (15,17,24,25). Several theories have been
proposed to explain this mechanism in the last few years (4,11-14,26).
According to the Transducer Theory, the odontoblastic processes can be directly
excited by a variety of sensorial stimuli and release neurotransmitters which are responsible
for conducting impulses to the nerve endings (4,15,24). The Neural Theory is based on the
hypothesis that an applied stimulus can directly influence the nerve terminals within the
dentinal tubules through direct communication with nerve fibers from the dental pulp
(4,11,15,24). However, there was no solid evidence capable of supporting the statements of
these theories (4,11,14,24).
The most widely accepted hypothesis about how the stimuli influence nerve fibers
is the Hydrodynamic Theory (11,12,14-20). It states that the painful sensation that arises from
exposed dentine after sensorial stimulation is a result of rapid fluid movement inside the
dentinal tubules (11,12,14,17-19). The presence of tube-like structures in hypersensitive
dentine plays an important role in maintaining the patency of the tubules which may prevent
physicochemical processes from occluding the tubules, thereby maintaining the fluid flow
across dentine structure. It was observed that biopsies from hypersensitive regions exhibited
hollow, tube-like structures within the lumina of dentinal tubules in approximately 75.8% of
the tubules, whereas in biopsies of non-sensitive areas of the same teeth, these tube-like
structures were only seen in about 20.4% of the tubules. (27). According to the hydrodynamic
mechanism, the fluid movement inside the tubules elicited by hydrodynamic stimuli is
16
thought to serve as a fluid transducer, signaling the presence of stimuli at the outer opening of
the dentinal tubules (25,26). Depending on the nature of the applied stimulus, the fluid within
the tubules can be easily displaced in either an inward or outward direction and determine a
variation in the intra-pulpal pressure that stimulates nociceptive nerve fibers located on the
pulpal side of the dentinal tubules (11,12). The pressure on the nerve endings of the
subodontoblastic plexus produces deformation on the nerve membranes and opens the
channels permeable to sodium (13). Due to the concentration gradient and negative charge in
extracellular fluid, these ions enter the fiber by means of these channels and depolarize the
membrane (13). Following nerve activation, nociceptive signals are transmitted to the
trigeminal nuclear complex located in the medulla. This site plays an important role in
processing and transferring these signals to higher brain regions. The perception of pain is
thought to occur primarily within the cerebral cortex (26) (Figure 1).
Nevertheless, the complete mechanisms of odontogenic pain are complex and
incompletely understood (28). The pain system can undergo dramatic changes in response to
certain peripheral stimuli, leading to the development of two hallmark features of many
clinical pain conditions: allodynia and hyperalgesia (26). Hyperalgesia is defined as an
increase in the perceived magnitude of a painful stimulus and allodynia is defined as a
reduction in pain threshold so that previously non-noxious stimuli are perceived as painful
(26,28,29,30).
Considering that dentinal pain in hypersensitive teeth is classically defined by an
exaggerated painful response to innocuous sensory stimulus, the altered pain state of
allodynia, which is also experienced during inflammation of pulpal or periradicular tissue,
may be designated as an essential feature in the mechanism of dentinal hypersensitivity (29).
Moreover, dentinal hypersensitivity is not an invariant sensation as pulpal inflammation may
predispose a tooth to enhanced dentinal hypersensitivity by reducing the threshold for
17
activation presumably because of peripheral or central mechanisms (26). Although the
development and maintenance of mechanical allodynia in teeth with pulpal inflammation has
yet to be elucidated, some potential hypotheses have been suggested. These hypotheses
propose that mechanical allodynia in teeth with pulpal inflammation could be generated by
either sensitization of mechanoreceptors (pulpal or periradicular) or a result of central
sensitization (29,30).
During pulpal inflammation, activation or sensitization of nociceptors can be
obtained by the concentration or deposition of inflammatory mediators that leads tissue levels
to be sufficiently high to permit binding and activation of the receptor (26). There are many
mediators, receptors, channels, enzymes, and transcription factors involved in pain signaling
pathways (26,31). Peripheral afferent fibers respond to mediators such as nerve growth factor
by increasing protein synthesis of substance P and calcitonin gene-related peptide (CGRP)
and by sprouting terminal fibers in the inflamed tissue (26). While glutamate, substance P and
CGRP are released as excitatory neurotransmitters from central terminals of primary afferent
sensory neurons, γ-amino butyric acid (GABA) and glycine are released from interneurons
and bind to their receptors in the dorsal horn, and act as inhibitory neurotransmitters.
Adenosine triphosphate (ATP) is believed to cause significant membrane Ca
2
+ permeability
and can elicit pain via ATP-gated ion channels of the P2X receptor family. There have been
seven P2X subunits identified so far (31). Other important receptor involved in pain signaling
pathway in the primary sensory neurons is the transient receptor potential (TRP). The
vanilloid receptor TRPV1 is known as the receptor for capsaicin and shows high Ca
2
+
permeability and is also activated by temperatures over 43ºC (32). TRPV1 can be sensitized
by ATP and bradykinin, and the threshold for heat activation of the sensitised TRPV1
becomes as low as 30ºC. Additionally, several channels and receptors expressed in
18
nociceptive sensory neurons have been recently identified, thus many of these molecules and
pathways are attractive therapeutic targets for the treatment of pain (31).
2. Management of dentinal hypersensitivity
The management of dentinal hypersensitivity should be first based on the correct
diagnosis of the condition and its causative factors (33). In addition to the desensitizing
approach, the treatment plan for dentinal hypersensitivity should include identifying and
eliminating predisposing etiologic factors, such as endogenous or exogenous acids and
toothbrush trauma, in order to prevent or minimize further damage on the exposed dentine
surface (33,34). Otherwise, the treatment is likely to provide only short-term success (20).
In fact, the achievement of an effective treatment for dentinal hypersensitivity has
been a challenge for clinicians over the years (4). Historically, several desensitizing agents
have been used for treating this problem, including, hot oil, arsenic, silver nitrate and
formaldehyde (23). Now, other types of treatment, such as oxalates and calcium phosphate
solutions, have emerged and shown significant effectiveness in reducing the hyperesthesia
(3,14,17,19,23,35-38).
Dentine desensitizers can be usually assigned to three large groups: the anti-
inflammatory, therapeutic occlusive agents and those with effect on nerve fibers
depolarization (19). Since the hydrodynamic mechanism is the most accepted to explain the
dentinal pain, the products that interfere with dentinal permeability seem to be more
appropriate for desensitization (3,6,23,24,26). The occlusion of dentinal tubules promotes
reduction in dentinal permeability, and proportionally decreases the degree of pain
(3,6,24,35,39). This occlusion can be obtained through protein precipitation, particles
deposition, application of laser beams or restorative procedures (18,19).
19
There are several requirements for considering a therapeutic occlusive agent as
being ideal (40). Among others, it should be effective for a long period, easy and practical to
apply, well tolerated by the patient and not irritating to the pulp (3,40). However, no current
agent incorporates all these requirements and, therefore, an ideal treatment technique still has
to be developed (3,19,40). Considering the need for a better approach to the management of
dentinal hypersensitivity, the products that produce obliteration of dentinal tubules (oxalates,
fluorides, laser beams, calcium phosphate solutions) have been intensely tested through
laboratory and clinical studies (3,10,14,17-19,23,24,36-38,41-49). Laboratory studies are
summarized in Table 1 and clinical studies are summarized in Table 2.
3. Laboratory investigations
Most of laboratory investigations are based on measuring the permeability of
dentine discs obtained from extracted teeth (23,24,41,44,48,50). In these studies, a hydrostatic
pressure gradient is applied to the specimens and the bulk fluid movement occurring through
dentine is quantified (23,24,41). The measurement of dentine hydraulic conductance provides
a convenient measurement of dentine permeability and allows the researcher to evaluate in
vitro the efficacy of desensitizing agents in obliterating dentinal tubules (23,24,41,50).
Greenhill, Pashley (24) evaluated the ability of some dentine desensitizers to
reduce the rate of fluid flow through dentine discs. The specimens treated with 30%
potassium oxalate presented the largest reduction (98.4%) in the hydraulic conductance of
dentine. This probably happens as a result of the deposition of insoluble calcium oxalate
crystals on the dentine surface that consequently control the permeability of the exposed
dentine.
20
The reduction in dentine permeability after dentine surface treatment with
potassium oxalate was also experienced by Pashley, Galloway (41) through the application of
different potassium oxalate formulations – 30% neutral dipotassium oxalate and acidic 3%
monopotassium-monohydrogen oxalate – in different experimental groups of dentine discs.
Pereira et al. (48) observed in vitro that potassium oxalate-based agents were able
to reduce filtration to values similar to those obtained with a smear layer with a mean flow
reduction of 83%. In this study, the reduction in hydraulic conductance obtained with fluoride
gel ranged from 41.47 to 77.47%.
According to Santiago et al. (23), the formulations based on potassium oxalate are
considered an excellent option for the treatment of the dentinal hypersensitivity. A decrease in
dentine permeability of about 75% was obtained with different potassium oxalate
formulations, which indicates the obstructive effectiveness of these products.
Suge et al. (44) observed reduction in the hydraulic conductance of dentine discs
treated with calcium phosphate precipitation method and of dentine discs treated with
potassium oxalate, sodium fluoride and strontium chloride. The treatment by calcium
phosphate precipitation method produced immediate reduction in dentine permeability to 6%.
This permeability remained low even seven days after the discs were immersed in artificial
saliva. The potassium oxalate treatment reduced dentine permeability to 8%. However, in this
case, the permeability gradually increased with the immersion time.
Other laboratory studies evaluated the effects of desensitizing agents on dentine
discs by verifying the morphology of dentine treated with different substances by scanning
electron microscopy (SEM) (16,18,43,46). In this context, Oda et al. (16) evaluated the
formation of an impermeable layer on dentine surface when glutaraldehyde, potassium
oxalate and fluoride were applied to dentine discs after acid etching. The results showed that
no uniform impermeable layer was formed when glutaraldehyde and oxalate were used.
21
However, when the treatment with sodium fluoride was performed, this layer could be
observed, but it was fragile and easily removed by washing the dentine surface. It must be
noticed that, in this study, the specimens were not fractured and, therefore, the effects of the
desensitizing agents were analyzed only at the dentine surface. In addition, the desensitizing
agents were applied after acid etching and this may have limited the reaction of these agents
with the dentine surface as a result of calcium and phosphate removal.
Arrais et al. (46) verified the occurrence of intra-tubular precipitation and sub-
superficial tubule occlusion of these three desensitizing agents, by means of analyzing their
corresponding effects on fractured specimens. The SEM examination demonstrated the
precipitation of crystal-like deposits extending up to 15µm inside the tubules of dentine
treated with potassium oxalate; formation of a 1µm thick layer that covered the surface and
infiltrated into tubules of discs after application of glutaraldehyde; and deposition of
precipitates that occluded the dentine surface with no attachment to the tubules walls after
phosphate fluoride treatment.
Ishikawa et al. (43) observed longitudinally sectioned specimens to investigate the
occlusion of dentinal tubules by dentine treatment with an acidic solution that contains both
calcium and phosphate. The dentine discs showed tubules occluded by a calcium phosphate
precipitate up to a distance of approximately 15µm from the surface after the treatment with
the solution.
These findings are in agreement with the results of an in vitro investigation
developed by Pereira et al. (18). In this study, impressions and resin replicas of three dentine
discs treated with potassium oxalate, calcium phosphate or glutaraldehyde were obtained and
submitted to SEM analysis. Partial occlusion of dentinal tubules by crystal precipitation,
usually below the surface, was observed after treating the dentine disc with potassium oxalate.
The disc treated with the calcium phosphate solution originated a thick smear of precipitated
22
amorphous calcium phosphate that covered most of the tubules. The impressions of both of
these discs presented short silicone tags, indicating little penetration of the impression
material into the tubules. The treatment with glutaraldehyde also resulted in partial
obliteration of the dentinal tubules. However, in this situation, the corresponding impression
showed that the impression material penetrated deeply into some open tubules.
4. Clinical studies
The clinical trials on dentinal hypersensitivity are studies of great interest to
produce scientific evidence about the effectiveness of therapeutic procedures
(3,10,14,17,19,36-38,41,45,47,50). However, the lack of standardization of the methods used
for the clinical treatment can yield contradictory findings and lead to results that are difficult
to compare (51). Furthermore, the physiologic and the emotional aspects are important factors
that influence these studies, thus the patient’s response is very subjective and largely
dependent upon the individual’s pain threshold (4,50).
Pillon et al. (14), through a controlled clinical study, verified that a single
application of a 3% potassium oxalate gel immediately after subgingival scaling and root
planing resulted in greater reduction in dentinal hypersensitivity when compared with placebo
gel application on the homologous contralateral teeth. This was observed 7, 14 and 21 days
post-treatment. The highest percentage reduction for test (81%) and control (34.7%) groups
was observed 21 days after the application.
Kishore et al. (36) evaluated the effectiveness of strontium chloride, potassium
nitrate, sodium fluoride and formalin solutions for the treatment of dentinal hypersensitivity.
It was verified that only the strontium chloride, the sodium fluoride and the formalin solutions
significantly reduced the symptoms.
23
Pereira et al. (17) studied the immediate and mediate clinical responses of
hypersensitive teeth after the application of three different potassium oxalate-based
formulations (experimental groups) and after the application of a placebo gel (control group).
The degree of sensitivity was assessed before (baseline), after four applications at seven-day
intervals (immediate results) as well as after 6 months and 1 year (mediate results). The
results demonstrated that all the substances applied, including the placebo, irrespective of the
time period, resulted in an immediate reduction in dentinal hypersensitivity, which could also
be observed after 6 months and 1 year.
The advent of laser technology and its growing use in dentistry included an
additional therapeutic option for the treatment of dentinal hypersensitivity (3,9). The lasers
used for this purpose may be divided into two groups: the low output power (low-level) lasers
and the middle output power lasers (19,40).
Low-level laser therapy causes a photobiomodulating effect that increases the
cellular metabolic activity of the odontoblasts and obliterates dentinal tubules as a result of
the intensification of tertiary dentine production (52). On the other hand, the middle output
power laser application promotes occlusion of these tubules through melting the dentine
structure (38).
Ladarlado et al. (3) compared the therapeutic effects of a 660nm wavelength red
diode laser and an 830nm wavelength infrared diode laser on the treatment of adult
individuals with dentinal hypersensitivity and observed a higher level of desensitization with
the 660nm red diode laser.
Corona et al. (19) evaluated the use of low-level laser therapy and the sodium
fluoride varnish application for the treatment of dentinal hypersensitivity. Both treatments
were effective in decreasing the painful condition. Nevertheless, the laser therapy showed
improved results for treating teeth with a higher degree of sensitivity.
24
Schwarz et al. (37) observed the effects of an Er:YAG laser and an aqueous
solution (22.5% polyurethane-isocyanate; 77.5% methylenechloride) on hypersensitive
dentine. The therapies resulted in significant reduction in discomfort immediately after and 1
week post-treatment. After 2 months, the discomfort in the group treated with the
desensitizing solution increased up to 65% and even up to 90% after 6 months, whereas the
effect of the laser remained at the same level achieved immediately after the treatment.
Compared with an untreated control group, both treatment forms resulted in a significant
reduction in the hyperesthesia at both examination periods.
Lan et al. (38) evaluated the morphologic changes of hypersensitive dentine after
Nd:YAG laser irradiation by taking an impression of the dentine surface before and after laser
treatment and then examining it by SEM. The presence of protrusive rods on the impression
indicates the penetration of the material inside dentine structure and, therefore, it is a measure
of open dentinal tubules. The impression obtained after the laser treatment showed no
protrusive rods, in comparison with the presence of numerous rods before the irradiation.
Because of protrusive rods on the impression material is related to open tubules in
hypersensitive areas, these authors supported the hypothesis that Nd:YAG laser irradiation
can be used to seal exposed dentinal tubules of hypersensitive teeth.
Some clinical studies have reported the influence of the placebo effect on the
treatment of dentinal hypersensitivity (10,17,42,45,47). This effect is described as a complex
physiological and psychological interaction that depends to a large extent on the relationship
between the patient and the professional (10,40). A positive and motivated emotional
behavior may activate the central system pain inhibition, which controls the painful stimulus
of the periphery by releasing endorphins. In studies on dentinal hypersensitivity, the trust in
the professional and the will to obtain relief undoubtedly contribute to this effect (17).
25
Another possible phenomenon which can occur in clinical trials is the Hawthorne
effect (10,50). It is related to non-intervention procedures, such as frequent examinations,
improved oral hygiene or compliance with the treatment regimen. In dentinal hypersensitivity
clinical studies, better oral hygiene may allow greater saliva access to patent dentinal tubules
and, therefore, may enhance tubule occlusion through the deposition of salivary calcium,
phosphate and proteins (10). In addition, it must also be taken in consideration the possibility
that, in clinical investigation that evaluate different desensitizing agents, the saliva could
dissolve and carry the agents under study, leading to the desensitization of non-treated teeth
(carryover effect) (50).
The positive response with the use of the placebo was verified by Lier et al. (45).
The results of a test group, treated with Nd:YAG laser, and a control group, in which the laser
device was positioned but not activated, were compared and a similar reduction in the painful
sensation was obtained in both groups.
Gentile et al. (47) observed reduction in dentinal hypersensitivity in 32 patients
distributed into two groups: a treated group, exposed to six laser applications (gallium-
aluminum-arsenide diode laser), and a control group that received applications of a curing
light, as placebo. There was no statistically significant difference in pain reduction between
treated and control groups between the beginning and end of treatment.
Similar results were obtained by Pereira et al. (17) after the application of three
different potassium oxalate-based formulations in patients of experimental groups and after
the application of a placebo gel in a control group. All the experimental groups and the
placebo group resulted in an immediate statistically significant reduction in dentinal
hypersensitivity, which continued after the periods of 6 months and 1 year.
The placebo effect was also reported by Cooley, Sandoval (42) in a clinical study
that involved 28 individuals with hypersensitive teeth in two different areas of the mouth. The
26
teeth in one of these areas were treated with distilled water and the teeth in the other location
received treatment with potassium oxalate. The results demonstrated an initial decrease in
sensitivity in both groups. However, it was observed that the sensitivity of the water-treated
teeth remained approximately the same for three months, while the sensitivity of the oxalate-
treated teeth progressively increased over this period.
The results revealed by both laboratory and clinical research are extremely
important to support the development or improvement of therapeutic procedures (3,10,14,16,-
19,23,24,36-38,41-48,50). Consequently, the critical analysis of different studies with regard
to current desensitization methods is of great interest to provide essential information and
direct clinicians towards an effective treatment of dentinal hypersensitivity.
27
CONCLUSION
It could be concluded that dentinal hypersensitivity is a complex condition and its
management in the dental office is very intricate. The reviewed literature points out several
treatment modalities ranging from simple procedures, which can be performed by the patient
him/herself, to complex procedures that involve the combination of therapies. Therefore,
knowledge about the available desensitizing products and the factors involved in the
mechanism of the dentinal hypersensitivity is indispensable in order to perform an effective
treatment.
28
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43. Ishikawa K, Suge T, Yoshiyama M, Kawasaki A, Asaoka K, Ebisu S (1994) Occlusion of
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44. Suge T, Ishikawa K, Kawasaki A, Yoshiyama M, Asaoka K, Ebisul S (1995) Duration of
dentinal tubule occlusion by calcium phosphate precipitation method: in vitro evaluation
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45. Lier BB, Rösing CK, Aass AM, Gjermo P (2002) Treatment of dentin hypersensitivity by
Nd:YAG laser. J Clin Periodontol 29, 501–506
46. Arrais CAG, Chan DCN, Giannini M (2004) Effects of desensitizing agents on dentinal
tubule occlusion. J Appl Oral Sci 12, 144-148
47. Gentile LC, Greghi SLA (2004) Clinical evaluation of dentin hypersensitivity treatment
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agents: clinical and laboratorial methods. J Appl Oral Sci 9, 157-166 (in Portuguese)
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52. Tate Y, Yoshiba K, Yoshiba N, Iwaku M, Okiji T, Ohshima H (2006) Odontoblast
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34
FIGURE 1
Figure 1. Peripheral and central mechanisms of dentinal pain and the fluid
movement after the application of hydrodynamic stimuli at exposed dentine surface.
35
TABLE 1
Table 1. Summary of laboratory studies on dentinal hypersensitivity.
Authors Dentine desensitizer Assessment
Greenhill, Pashley 1981 30% potassium oxalate HC
Pashley, Galloway 1985 30% dipotassium oxalate; 3% monopotassium-monohydrogen oxalate HC
Pereira et al. 2005 Potassium oxalate-based agents; fluoride gel HC
Santiago et al. 2006 Potassium oxalate formulations HC
Suge et al.1995 Calcium phosphate; potassium oxalate, sodium fluoride, strontium chloride HC
Oda et al. 1999 Glutaraldehyde; potassium oxalate; fluoride SEM
Arrais et al. 2004 Glutaraldehyde; potassium oxalate; fluoride SEM
Ishikawa et al. 1994 Solution containing both calcium and phosphate SEM
Pereira et al. 2002 Potassium oxalate; calcium phosphate; glutaraldehyde SEM
HC -Hydraulic conductance and SEM - Scanning electron microscopy.
36
TABLE 2
Table 2. Summary of clinical studies on dentinal hypersensitivity
Authors Dentine desensitizer Assessment
Pillon et al. 2004 3% potassium oxalate gel; placebo gel VAS
Kishore et al. 2002 Strontium chloride; potassium nitrate; sodium fluoride; formalin solutions VRS
Pereira et al. 2001 Potassium oxalate-based formulations; placebo gel VRS
Ladarlado et al. 2002 660nm wavelength diode laser; 830nm wavelength diode laser NS
Corona et al. 2003 GaAlAs laser; sodium fluoride varnish VRS
Schwarz et al. 2002 Er:YAG laser; aqueous solution VRS
Lan et al. 2004 Nd:YAG laser SEM
Lier et al. 2002 Nd:YAG laser; control group VAS
Gentile et al. 2004 GaAlAs laser; curing light VAS
Cooley, Sandoval 1989 Potassium oxalate; distilled water Q
VAS - Visual Analogue Scale; VRS - Verbal Rating Scale; NS - Numeric Scale; SEM -
Scanning electron microscopy and Q - Questionnaire.
37
4. CAPÍTULO 2
CLINICAL EVALUATION OF A 3% POTASSIUM OXALATE GEL AND A GaAlAs
LASER FOR THE TREATMENT OF DENTINAL HYPERSENSITIVITY
Alessandra H M Vieira, DDS,
*
Vanara F Passos, DDS,
*
Jorgiana S Assis,
*
Juliano S Mendonça, PhD,
†
and Sérgio L Santiago, PhD
*
* Department of Clinical Dentistry, Federal University of Ceará, Fortaleza, Ceará, Brazil
† Department of Dentistry, University of Fortaleza, Fortaleza, Ceará, Brazil
Author responsible for correspondence (fax number and e-mail can be published):
Name: Sérgio Lima Santiago
Address: Rua Bento Albuquerque, 685 ap. 702
Fax number: +55 85 3249 4336
E-mail: [email protected]
Word count (excluding abstract and references): 3,118
Number of tables: 2
Running title: Clinical evaluation of desensitizing agents.
One-sentence summary: Both active and control groups under study provided similar
immediate and mediate reduction in dentinal hypersensitivity.
38
ABSTRACT
Background: The present study aimed at verifying the immediate and mediate
clinical performance of a low-level Gallium-Aluminum-Arsenide (GaAlAs) laser and a 3%
potassium oxalate gel for the treatment of dentinal hypersensitivity, using a placebo gel as a
control.
Methods: A total of 164 teeth from 30 patients with clinical diagnosis of moderate
or severe dentinal hypersensitivity were selected for this controlled clinical trial. The teeth
were randomly divided into three groups according to the desensitizing treatment under study
(GaAlAs laser, 3% potassium oxalate gel and placebo gel) and treatment sessions were
performed at seven-day intervals for four consecutive weeks. The degree of sensitivity in
response to evaporative and tactile stimuli was assessed according to a visual analogue scale
at baseline, immediately after and three months after the fourth application. The results were
analyzed by dentinal hypersensitivity reduction for each observational moment in relation to
baseline, for each group separately.
Results: Both active and control groups resulted in statistically significant
reduction of dentinal hypersensitivity in response to evaporative and tactile stimulation
immediately after and three months after treatment. No significant differences among the
three groups could be detected in both immediate and mediate evaluations irrespective of the
applied stimulus.
Conclusions: The treatments under study had similar effectiveness and both active
and placebo treatments were effective for treating dentinal hypersensitivity.
KEY WORDS: dentin sensitivity; oxalates; lasers; placebo effect.
39
INTRODUCTION
Dentinal hypersensitivity is an exaggerated response to sensory stimulus that
usually causes no response in a normal, healthy tooth.
1
It is perceived as a localized, rapidly
developing and transient pain and it is associated with dentine exposure to the oral
environment.
1,2
Dentine exposure can result from enamel loss by erosion, abrasion, abfraction
or denudation of root surfaces as a result of gingival recession or periodontal procedures.
3-10
Prevalence studies indicate that dentinal hypersensitivity affects 10 to 30 per cent
of the general population.
2,3,11-14
Moreover, with teeth being preserved and retained for longer
periods, there will be increasing demand by patients involved in this uncomfortable
situation.
1-3
It is considered the most frequent complaint among reported odontalgias.
15
Depending on its intensity, the hyperesthesia can affect eating, drinking and breathing, hinder
the ability to control dental plaque effectively and, sometimes, it may even result in emotional
changes that alter lifestyle.
1,5
The hydrodynamic theory is the most widely accepted hypothesis to explain how
stimuli applied on dentine surface influence nerve fibers.
3,4,5,10,16-20
It states that the painful
sensation that arises from exposed dentine after sensorial stimulation is a result of rapid fluid
movement in either an inward or outward direction inside the dentinal tubules.
16,17
The fluid
displacement within the tubules determines variation in the intra-pulpal pressure that
stimulates nerve endings located at the pulp/dentin interface and, therefore, results in
generation of pain impulses.
16,17,20
Historically, several desensitizing agents have been used for treating this problem,
including, hot oil, arsenic, silver nitrate and formaldehyde.
8,21
Now, other types of treatment,
such as oxalate gels and application of laser beams, have emerged and shown significant
effectiveness in reducing the hyperesthesia.
8,10,15,20-44
40
Potassium oxalate formulations have been intensely tested through laboratory and
clinical studies.
7,8,21,22,26,29,32,34,35,38-41,44
The application of oxalates on hypersensitive surfaces
mainly results in precipitation of insoluble calcium oxalate crystals that obliterate patent
dentinal tubules and consequently control the permeability of exposed dentine.
8,21,22,26,34,35,37-
39,45
Reduction in fluid movement within dentine by the crystal deposition, according to the
hydrodynamic mechanism, proportionally decreases the degree of pain.
8,26,35,39,45
An additional therapeutic approach for dentinal hypersensitivity came up with the
advent of laser technology and its growing use in dentistry.
15,23-25,28,30,31,33,42
The low-level
laser therapy can occlude dentinal tubules by increasing the cellular metabolic activity of
odontoblasts which promotes intensification on tertiary dentine production.
46
Review of literature presents a great number of treatment modalities for dentinal
hypersensitivity, which suggests that none of them is totally efficient.
3,4,7,23,28,45,47
There is no
current desensitizing agent considered ideal to manage this complex sensorial
condition.
5,12,15,23,28
Clinical trials have supported different standpoints and the results have
proved to be mostly contradictory.
45,48,49
Besides, the placebo effect has to be taken into
consideration for its significant role often reported in clinical investigations.
7,21,24,31,47
Therefore, reports on controlled studies with emphasis on the effectiveness of
desensitizing agents are important and well-recognized.
6,23
The purpose of this study was to
assess, at different examination periods, the clinical performance of a low-level gallium-
aluminum-arsenide (GaAlAs) laser and a 3% potassium oxalate gel for treating hypersensitive
teeth, using a placebo gel as a control.
41
MATERIALS AND METHODS
A total of 164 teeth from 30 patients (7 males and 23 females, aged between 24
and 68 years) with clinical diagnosis of moderate or severe dentinal hypersensitivity were
selected and enrolled for the study on March 2007. To participate in the trial, patients should
present good oral hygiene and at least three hypersensitive teeth, especially canines and pre-
molars. Patients who presented severe systemic and/or psychological diseases, constant use of
analgesic and/or anti-inflammatory drugs or allergic response to dental products were
excluded. Besides, during the previous six months, the individuals should not have used any
desensitizing agent and/or have been submitted to periodontal surgery or scaling. The selected
teeth should not present carious lesions, defective restorations, cracks or fractures, premature
contact, prosthesis or orthodontics appliances, periodontal pockets, mobility or evidence of
pulpits. Participants were informed about the purpose and design of the investigation and
signed an appropriate informed consent form. Standard dentifrices, toothbrushes and
instructions were given to all subjects. The research protocol was approved by the Committee
of Ethics in Research of Federal University of Ceará (protocol number 36/07).
The experimental model was split-mouth, controlled and double-blinded. The
equipment and substances used in the study included a low-level GaAlAs diode laser device,
‡
a 3% potassium oxalate gel
§
and a placebo gel
║
containing the same composition of the
potassium oxalate gel except for the active substance. Both gels had the same color and
texture characteristics. The 164 teeth (23 incisors, 20 canines, 77 pre-molars, 44 molars) were
randomly divided into three groups according to the desensitizing treatment under study: laser
treatment, potassium oxalate gel treatment and placebo gel treatment. This randomization was
performed by placing all the selected teeth in a list and assigning its treatment according to a
predefined sequence: (1) laser; (2) potassium oxalate gel; (3) placebo gel. Moreover, the three
42
different treatments were designated to the same patient to permit data correlation regarding
his/her sensitivity threshold.
The degree of sensitivity was determined for each tooth in response to tactile
(probe) and evaporative (air blast) stimuli. The probe stimulus was applied under slight
manual pressure in mesiodistal direction on the cervical area of the tooth. The air blast was
performed with an air syringe for one second at the distance of 1cm of the tooth surface.
Dentinal hypersensitivity was assessed by patient’s indication of the amount of pain related to
each tooth, immediately after each stimulus, according to a visual analogue scale (VAS). The
VAS was 10cm long and, on the left and right ends, contained an indication of “no pain” and
“severe pain”, respectively. The participants were instructed to place a mark on this 10cm line
that corresponded to the pain severity of each tooth elicited by the hydrodynamic stimuli. The
sensitivity patterns were recorded at baseline, immediately after and three months after
treatment by an examiner previously calibrated for applying the stimuli. Neither the examiner
nor the patients knew which type of treatment corresponded to each tooth.
The treatments were applied under relative isolation by one experienced operator
other than the examiner. The diode laser device was used on contact mode with the following
parameters: continuous emission, 30mW output power, wavelength of 660nm and 4Jcm
-2
energy density. Laser beam was applied with the laser tip positioned perpendicularly to the
tooth surface at four points to the apex (apical point) and the cervical area (mesio-buccal,
disto-buccal and lingual points) of the tooth. Potassium oxalate gel was applied according to
manufacturer’s instructions: passive application, using a brush, for 2 minutes. During this
period, the laser device was positioned, but not activated. The placebo gel application
followed the same procedure. The treatment was repeated at seven-day intervals for four
consecutive weeks. Three months after the fourth treatment session, patients were recalled for
reassessment of dentinal hypersensitivity.
43
Statistical Analysis
The mean values of the clinical parameters were calculated for the three groups
according to the different stimuli. Scores obtained immediately after and three months after
the fourth treatment session were considered, respectively, the immediate and the mediate
results of the treatment. The data was submitted to Kruskal-Wallis test with significance level
of 5% (p=0.05) and analyzed by dentinal hypersensitivity reduction for each observational
moment in relation to baseline.
44
RESULTS
A total of twenty-four patients completed the three-month study period, which
corresponded to 80% of the patients and teeth involved in the investigation. No complications
such as detrimental pulpal effects or allergic reactions were observed during this period. All
teeth remained vital after treatment, with no adverse reactions reported or clinically detectable
complications.
Table 1 shows the VAS scores (means and standard deviations) recorded after
application of each of the stimuli for active and control groups at baseline, immediate and
mediate periods. No statistically significant differences in VAS scores existed between the
three groups at baseline following application of any of the stimuli (p>0.05). All groups
provided significant overall reduction in dentinal hypersensitivity in response to evaporative
and tactile stimulation (p<0.05). As presented in Table 1, the three treatment forms resulted in
statistically significant reduction of VAS scores between baseline and immediate results
(p<0.001). This could also be observed between baseline and mediate results (p<0.05).
Additionally, the laser treatment tended to result in greater reduction of sensitivity between
immediate and mediate results when considering the evaporative stimulation (p<0.05),
whereas the effectiveness of the oxalate and placebo treatments remained at the same level
achieved immediately after treatment (p>0.05). However, statistically significant differences
were not detected among the three groups at both immediate and mediate results irrespective
of the stimulus (p>0.05).
The pain severity elicited by the two different stimuli irrespective of the treatment
is presented in Table 2. The VAS scores recorded at baseline demonstrate that the evaporative
stimulus was more effective for detecting sensitivity (p<0.05). Three months after treatment,
45
percent reduction of sensitivity in response to tactile and evaporative stimuli was 65.5% and
62.5%, respectively, compared to baseline scores.
46
DISCUSSION
The present study evaluated the clinical performance of an oxalate gel and a
GaAlAs laser, using placebo gel as control, for treating hypersensitive teeth. The degree of
pain was recorded following tactile and evaporative stimulation, according to a VAS, in the
following periods: baseline, immediate and mediate. It was observed that the three groups
were very similar with respect to the degree of pain recorded at baseline in response to any of
the stimuli. During the period of this study, all treatments resulted in statistically significant
reduction in discomfort immediately after and three months after treatment. However,
statistical analysis demonstrated no significant differences among the three groups in the
decrease of dentinal pain observed in the immediate and mediate periods irrespective of the
stimulus.
Potassium oxalate formulations have become well accepted for treating dentinal
hypersensitivity as many laboratory and clinical studies have supported its ability in
obliterating dentinal tubules.
7,8,21,22,26,29,32,34,35,38-41,44
It has been demonstrated, by scanning
electron microscopy, that topical application of oxalates on dentine discs results in
precipitation of insoluble calcium oxalate crystals on dentine surface and inside patent
tubules.
22,26,34,38,44
The crystal deposition reduces fluid movement within dentine and,
consequently, decreases dentinal sensitivity according to the hydrodynamic
principles.
8,26,35,39,45
Reduction in dentine hydraulic conductance over 75% after application of
different potassium oxalate formulations on dentine discs surfaces has been observed in vitro
by Greenhill and Pashley,
26
Pashley and Galloway,
35
Pereira et al.,
39
Santiago et al.
8
and Suge
et al.
44
Previous clinical studies about potassium oxalate effects on dentinal hypersensitivity
developed by Cooley and Sandoval,
21
Kishore et al.,
29
Merika et al.,
32
Pereira et al.
7
and Pillon
et al.
40
also support the results of the present investigation. However, an extensive comparison
47
with the findings of these studies may be limited due to variations in clinical trial design and
experimental procedures.
45,48,49
Pereira et al.
7
obtained significant clinical reduction in sensitivity scores with
application of three different potassium oxalate formulations and with application of a
placebo gel (control group) immediately after, 6 months and 1 year after four treatment
sessions at seven-day intervals. In addition to the occluding effects, potassium oxalate neural
action was mentioned for explaining the relief on dentinal hypersensitivity observed
immediately after treatment. Similarly to the present study, these authors used tactile and
evaporative stimulation for eliciting pain sensation. According to Holland et al.,
49
these
stimuli are recommended for quantifying dentinal pain in clinical trials as they are both
physiological and controllable. Nevertheless, the degree of pain severity was recorded in
accordance to a verbal descriptor scale, while in the present investigation a VAS was adopted.
The VAS is considered an objective method for assessing dentinal pain in which each tooth
can act as its own control.
49
It also offers the advantage of being a continuous scale and its use
for assessing sensitivity degree in clinical studies has been intensely reported by many other
investigators.
24,25,31,32,40,48,49
Besides, this method is considered preferable to the use of
numerical rating or verbal descriptor scales as these may be restrictive and not offer enough
descriptions that could be placed in a continuous order of pain severity.
45,48,49
Pillon et al.
40
verified that a single application of a 3% potassium oxalate gel
immediately after periodontal procedures resulted in an increasing percent reduction in
dentinal hypersensitivity at 7 (29.4%), 14 (64.6%) and 21 days (81.0%) post-treatment.
Conversely, in the present investigation, the effectiveness of the oxalate treatment observed
three months after the application sessions tended to remain at the same level achieved
immediately after treatment. The results obtained in the previous study may have been
strongly influenced by the spontaneous decrease of dentinal pain due to periodontal
48
procedures. According to Orchardson et al.,
2
the sensitivity tends to self-heal in a period of
three to four weeks that follows periodontal treatment. It must also be considered that in the
investigation developed by Pillon et al.,
40
though a VAS have been used for estimating the
pain severity, the evaluation of dentinal hypersensitivity was performed by asking each
participant about pain sensation during routine activities and not in response to sensorial
stimulation. Nevertheless, it is suggested that at least two hydrodynamic stimuli should be
used for assessing dentinal pain in clinical trials and the least severe stimulus should be
applied first.
45,49
In order to contribute to this standardization, the results of the present study
were analyzed irrespective of the treatment and demonstrated more pronounced painful
response to evaporative stimulus when compared to tactile stimulus and it was also confirmed
by Gentile and Greghi
24
. This may be attributed to the relatively greater number of dentinal
tubules that are potentially stimulated by an air blast compared to probe stimulus.
32,48
It must
also be mentioned that the air blast may produce three combined different physical effects:
evaporation, thermal effect and physical compression of the air to the dentinal fluid.
Recent studies on dentinal hypersensitivity are beginning to focus on the use of
lasers to manage dentinal pain since it emerged as a promising treatment modality
15,23-
25,28,30,31,33,42
This study demonstrated that the GaAlAs low-level laser therapy is an effective
method for reducing the degree of sensitivity in response to hydrodynamic stimuli
immediately after and three months after treatment. Similar results in which GaAlAs laser
irradiation provided decrease in dentinal pain elicited by thermal, tactile and evaporative
stimulation were further reported.
15,23-25,33
The clinical effect of low-level lasers on dentinal
hypersensitivity relies upon an immediate analgesic effect, as a result of laser-induced
changes in neural transmission networks, and a mediate obliteration of dentinal tubules by
tertiary dentine, due to intensification in the metabolic activity of odontoblasts.
15,23,25,28
49
Gerschman et al.
25
investigated the result of four applications of GaAlAs laser
using the wavelength of 830nm to both the apex and the cervical area of hypersensitive teeth
at one-week, two-week and eight-week intervals. It was observed that the decrease in pain
severity became more evident over time and that at eight weeks the percent reduction in
sensitivity recorded to probe and air stimuli, in accordance to a VAS, was 65% and 67%,
respectively.
25
These results differ from the findings of Gentile and Greghi,
24
that using
GaAlAs laser with the wavelength of 670nm in six applications with intervals from 48 to 72
hours, verified more accentuated reduction of pain to tactile instead of evaporative stimulus
immediately after the last application. In the present study, laser treatment was performed
with the wavelength of 660nm at seven-day intervals and the pain relief immediately after the
fourth application was also more pronounced to tactile than to evaporative stimuli. However,
it was observed that the sensitivity degree to evaporative stimulation continued to reduce
between the immediate and mediate evaluation, whereas sensitivity to tactile stimulus
remained at a similar level achieved immediately after treatment. Comparatively, laser
irradiation was performed by Gerschman et al.
25
to both the apex and cervical area of the
teeth, similarly to this study, while laser application by Gentile and Greghi
24
was directed
only to the cervical area. It is claimed that application of laser beams to the cervical area
affects A-delta fibers while irradiation on the apex area is related to C-fibers.
25
Although the
dentinal pain is said to be sharp and fast (A-delta fibers) whereas pulpal pain is slow and dull
(C-fibers), in many cases the symptoms and aetiology are mixed.
20,25
Despite promising outcomes have been reported, there is still a need for
clarification regarding the specification of laser irradiation parameters for dentinal
hypersensitivity treatment since the tissue response may be different after applications
performed with distinct active medium, wavelength, power density, emission mode or
application method.
15,28
In this context, Ladalardo et al.
15
compared the effectiveness of four
50
applications of a 660nm and an 830nm wavelength performed with GaAlAs laser in the
cervical area of hypersensitive teeth at seven-day intervals and concluded that the laser
application with the former wavelength was more effective for desensitization than the latter.
The present study supported the effectiveness of the GaAlAs laser used with the wavelength
of 660nm for treating dentinal hypersensitivity.
Although the present investigation demonstrated decrease in sensitivity scores for
both the oxalate and the laser groups, a significant immediate and mediate reduction was also
observed for the control group treated with placebo gel, and no differences could be detected
among the three groups during the period of this study. However, Gerschman et al.
25
and
Pillon et al.
40
, through controlled studies, verified significant higher decrease in dentinal
hypersensitivity for active than placebo group and also observed that the differences between
these groups increased further in the subsequent evaluations. On the other hand, Pereira et al.
7
and Gentile and Greghi
24
, in accordance to the results of the present investigation, obtained no
statistically significant difference between the results of active and control groups in reducing
the pain condition of hypersensitive teeth. Moreover, positive results involving the use of
placebo in clinical trials have also been reported by other investigators.
7,21,24,31,47
This may me
attributed to the so called placebo effect. It is described as a complex physiological and
psychological interaction that depends to a large extent on the relationship between the patient
and the professional.
21,28,47
Besides, the patient’s response to sensorial stimulation is very
subjective and largely dependent upon the individual’s pain threshold, what may influence the
results obtained in clinical trials.
3,28,48,49
It is possible that studies with longer observational periods could enhance the
differences between active and placebo groups. Therefore further clinical investigations are
needed in order to evaluate long-term stability of the positive results obtained with these
desensitizing agents. It could be concluded that all treatment modalities under study (GaAlAs
51
laser, potassium oxalate gel and placebo gel) showed similar overall performance and
provided statistically significant reduction in dentinal hypersensitivity immediately after and
three months after treatment was performed.
52
FOOTNOTES
‡ Bio Wave LLLT Dual
®
, Kondortech Equip Odontológicos Ltda., São Carlos, SP, Brazil
§ Oxa-Gel
®
, Kota Import’s Ltda., São Paulo, SP, Brazil
║ ARTPELE Farmácia com Manipulação Ltda., Fortaleza, CE, Brazil
53
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13. Rees JS, Addy M. A cross-sectional study of dentine hypersensitivity. J Clin Periodontol
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14. Von Troil B, Needleman I, Sanz M. A systematic review of the prevalence of root
sensitivity following periodontal therapy. J Clin Periodontol 2002;29:173-177.
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20. Hargreaves KM. Pain mechnisms of the pulpodentin complex. In: Hargreaves KM,
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60
TABLES
Table 1. Means and standard deviations of VAS scores recorded at baseline, immediate and
mediate periods after application of each stimulus.
Stimulus Period Laser group Oxalate group Placebo group
Baseline 6.20 ± 2.48 A,a 6.41 ± 2.43 A,a 6.30 ± 2.44 A,a
Immediate 2.66 ± 3.22 B,a 2.79 ± 3.48 B,a 2.70 ± 3.28 B,a
evaporative
Mediate 2.11 ± 2.69 C,a 2.53 ± 3.03 B,a 2.46 ± 2.93 B,a
Baseline 3.85 ± 3.26 D,d 3.67 ± 3.31 D,d 3.68 ± 3.29 D,d
Immediate 1.33 ± 2.54 E,d 1.06 ± 2.19 E,d 1.25 ± 2.50 E,d
tactile
Mediate 1.28 ± 2.19 E,d 1.31 ± 2.35 E,d 1.29 ± 2.17 E,d
¶ Different uppercase letters in the same column indicate statistically significant differences
for each stimulus (p<0.05) and different lowercase letters in the same row indicate statistically
significant differences for each stimulus (p<0.05).
Table 2. VAS scores (means and standard deviations) of sensitivity elicited by tactile and
evaporative stimuli irrespective of the treatment.
Period Evaporative stimulus Tactile stimulus
Baseline 6.30 ± 2.43 A 3.74 ± 3.27 B
Immediate 2.72 ± 3.31 C (56.8%) 1.21 ± 2.40 E (67.7%)
Mediate 2.36 ± 2.87 D (62.5%) 1.29 ± 2.22 E (65.5%)
# Different uppercase letters indicate statistically significant differences (p<0.05). The values
in parenthesis represent the percent reduction of sensitivity compared to baseline scores.
61
5. CONCLUSÃO GERAL
Da avaliação dos resultados obtidos neste trabalho, pode-se concluir que:
a) a literatura apresenta diversos tipos de tratamento para a hiperestesia dentinária, que variam
desde procedimentos simples, que podem ser executados pelo próprio paciente, até
procedimentos complexos, que envolvem a combinação de diferentes terapias. Dessa forma, o
conhecimento acerca do mecanismo de ocorrência da hiperestesia dentinária e dos agentes
anti-hiperestésicos disponíveis é indispensável para a elaboração de um tratamento eficiente;
b) os agentes anti-hiperestésicos utilizados no estudo clínico podem ser considerados
eficientes para o tratamento da hiperestesia dentinária, uma vez que proporcionaram redução
estatisticamente significante do grau de sensibilidade dolorosa em resposta aos estímulos tátil
e evaporativo, nos períodos de avaliação imediato e mediato;
c) tratamentos simples e pouco dispendiosos, como a aplicação tópica de gel de oxalato de
potássio, podem produzir resultados similares na diminuição dos sintomas da hiperestesia
dentinária aos obtidos através de terapias mais complexas, que envolvem o manuseio de um
aparelho de laser;
d) o tratamento da hiperestesia dentinária está sujeito a grande influência de fatores
psicológicos do paciente e da natureza subjetiva da dor. Nesse contexto, a utilização de
placebos em estudos clínicos que avaliam agentes anti-hiperestésicos é capaz de produzir
redução significativa da sensibilidade dolorosa em resposta a estímulos hidrodinâmicos e,
além disso, demonstrar resultados estatisticamente semelhantes aos observados com os
tratamentos convencionais utilizados no presente estudo clínico;
e) o efeito anti-hiperestésico dos tratamentos utilizados no presente estudo clínico pode-se
prolongar por três meses após o término do tratamento. No entanto, é importante que novas
investigações clínicas sejam realizadas no intuito de avaliar a estabilidade dos resultados
positivos obtidos com estes tratamentos, em longo prazo.
62
6. REFERÊNCIAS BIBLIOGRÁFICAS
1. BISSADA, N. F. Symptomatology and clinical features of hypersensitive teeth. Arch Oral
Biol, v. 39, p. 31s-32s, 1994.
2. ORCHARDSON, R. et al. Dentine hypersensitivity into the 21st century. Arch Oral Biol,
v. 39, p. 113s-119s, 1994.
3. KISHORE, A.; MEHROTRA, K. K.; SAIMBI, C. S. Effectiveness of desensitizing agents.
J Endod, v. 28, p. 34-35, 2002.
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2006.
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dentine hypersensitivity in a population in Rio de Janeiro, Brazil. J Dent, v. 20, p. 272-276,
1992.
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501, 1997.
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15. BRÄNNSTRÖM, M. Sensitivity of dentin. Oral Surg, v. 21, p. 517-526, 1966.
16. BRÄNNSTRÖM, M.; ÅSTROM, A. The hydrodynamics of the dentine; its possible
relationship to dentinal pain. Int Dent J, v. 22, p. 219-227, 1972.
17. GILLAM, D. G. Mechanisms of stimulus transmission across dentin - a review. J West
Soc Periodontol Periodontal Abstr, v. 43, p. 53-65, 1995.
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68
ANEXO A – Aprovação do Comitê de Ética em Pesquisa
69
ANEXO B – Termo de consentimento livre e esclarecido
Você está sendo convidado(a) a participar, como voluntário, de uma pesquisa a ser realizada na
Universidade Federal do Ceará. Após ser esclarecido(a) sobre as informações a seguir e caso aceite fazer parte
do estudo, assine ao final deste documento, que está em duas vias. Uma delas é sua e a outra é da pesquisadora
responsável. A qualquer momento, você poderá desistir de participar da pesquisa e retirar seu consentimento.
Sua recusa não trará nenhum prejuízo em sua relação com a pesquisadora ou com a instituição. Em caso de
dúvida, você pode entrar em contato com a pesquisadora responsável através do telefone e endereço que constam
neste termo ou procurar o Comitê de Ética em Pesquisa da Universidade Federal do Ceará pelo telefone (85)
3366 8338.
1. DADOS DE IDENTIFICAÇÃO DO PACIENTE E/OU RESPONSÁVEL LEGAL
Nome do paciente:
Documento de identidade nº: Gênero: Data de nascimento:
___/___/_____
Endereço: Cidade: UF:
Telefones para contato: CEP:
Nome do responsável legal:
Documento de identidade nº: Gênero: Data de nascimento:
___/___/_____
Endereço: Cidade: UF:
Natureza (grau de parentesco, tutor, curador etc):
2. INFORMAÇÕES SOBRE A PESQUISA (PROCEDIMENTOS, RISCOS E BENEFÍCIOS)
Pesquisadora responsável: Alessandra Helen Magacho Vieira.
Endereço: Rua Capitão Francisco Pedro s/n - Rodolfo Teófilo - Curso de Odontologia FFOE (UFC).
Telefone para contato: (85) 3366 8410
Título do Projeto: Avaliação da eficiência de agentes anti-hiperestésicos no tratamento da hiperestesia dentinária.
A hiperestesia dentinária é uma das mais antigas queixas de pacientes e tem sido um problema
constante na clínica odontológica, representando um número cada vez maior de pessoas que procuram o
consultório odontológico incomodadas com esta situação desconfortável. Neste estudo serão aplicados produtos
para o alívio da hiperestesia dentinária, tratando-se de um procedimento corriqueiro em clínica odontológica e
necessário ao bem estar da saúde do paciente. Os materiais utilizados encontram-se disponíveis no mercado e
foram previamente estudados através de testes de comportamento físico e estudos prévios de biocompatibilidade,
não demonstrando nenhum risco à integridade do ser humano.
Confidencialidade: Os registros individuais dos seus dados serão mantidos em sigilo (confidencial). As
informações a respeito dessa pesquisa poderão ser publicadas em revista científica. Apenas os resultados
envolvendo médias serão divulgados ou, em pequeno número e de forma ilustrativa, fotografias sem a sua devida
identificação.
3. ASSINATURAS
Eu, __________________________________________, concordo em participar da pesquisa e
declaro que fui devidamente informado(a) e esclarecido(a) sobre o tipo de pesquisa, os procedimentos nela
envolvidos, assim como os possíveis riscos e benefícios decorrentes da minha participação. Foi esclarecido que
posso retirar meu consentimento a qualquer momento, sem que isto leve a qualquer penalidade.
Fortaleza, ___ de ________________ de 2007 _________________________________________
Sujeito da Pesquisa
Confirmamos a solicitação de consentimento, esclarecimentos sobre a pesquisa e aceite do sujeito em participar:
________________________________________ ______________________________________
Pesquisadora Responsável Testemunha
Nome: Identidade nº:
70
ANEXO C – Modelo de ficha de identificação do paciente
n
o
______ Data _____/_____/_____
1. Dados gerais do paciente
Nome ________________________________________________________________
Endereço _________________________________________ n
o
________ ap.________
Bairro __________________ CEP _______________ Fone ______________________
Cidade ____________________ Estado _____________ Data nasc. ____/____/______
Idade _____ Sexo ( ) Fem. ( ) Masc. Cor ______ Nacionalidade______________
Profissão __________________ Local de trabalho _____________________________
Endereço do Trabalho _________________________ Fone ______________________
Outras informações ______________________________________________________
Relato do paciente ______________________________________________________
Já fez algum tratamento ou cirurgia periodontal? ______ quando?_________________
Se já fez, a dor existia antes deste tratamento? ________________________________
Como aparece esta dor, qual o estímulo necessário (ar, alimentos doces ou gelados, ao
escovar os dentes)? ______________________________________________________
Já fez algum tipo de tratamento para diminuir esta dor? _________________________
Se já fez, qual o tratamento utilizado? ________________ quando?________________
Qual o tipo de sua dieta (frutas ácidas, refrigerantes)? __________________________
Como escova os seus dentes? ______________________________________________
Quantas vezes ao dia? __________ Qual é o detifrício utilizado? __________________
Qual o tipo de escova de dentes utilizada (dura, macia, extra-macia)? ______________
Tem o hábito de ranger os dentes ou apertá-los durante o dia ou à noite? ____________
Tem algum problema de saúde (diabetes, hipertireoidismo, xerostomia, problemas
digestivos, acidez)?______________________________________________________
Tem algum problema psicossomático como anorexia, bulimia e outros? ____________
Faz uso de algum medicamento ou droga (psicotrópicos ou álcool)? _______________
Tem alguma alergia a cosméticos e/ou produtos odontológicos? __________________
Está em período de gestação ou amamentação? ________________________________
71
2. Dentes:
Dente Tipo de dor Rel. oclusal Fac. desg Cárie C. Period. Rest.
Dor: P – provocada E - espontânea M - momentânea I - intermitente
Intensidade: L - leve M - moderada S - severa
Percussão: V+ - vertical positiva H+ - horizontal positiva
3. Presença de lesão cervical não cariosa:
Dente Tipo de Lesão
Cunha Pires
Localização
Face Região
Tamanho e
Profundidade
72
ANEXO D – Escala visual analógica
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