Lasers and Desensitizing Agents in Dentinal Hypersensitivity Therapy: History
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Contributor:
Francesca Cattoni
,
Lucrezia Ferrante
,
Sara Mandile
,
Giulia Tetè
,
Elisabetta Maria Polizzi
,
Giorgio Gastaldi

Lasers represent a means of treating dentin hypersensitivity, used alone and/or in conjunction with specific products for the treatment of such a pathology. The selected articles that examined diode lasers were divided according to the wattage (w) used: low-level laser therapy protocols, i.e., those using a wattage of less than 1 W, and high-level laser therapy protocols, i.e., those using a wattage of 1 W or more. Laser therapy was found to be effective in the treatment of dentin hypersensitivity. However, the level of effectiveness depends on the laser used. Both the Nd: YAG laser and the diode laser (high and low power) are effective in the treatment of dentin hypersensitivity. However, the high-power laser appears to be more effective in combination with fluoride varnish and the Nd: YAG laser achieved greater long-term benefits than the diode laser.

  • hypersensitivity and diode laser
  • hypersensitivity and Nd-Yag laser
  • dentin exposure
  • sensitive dentine

1. Introduction

Dentine is very sensitive to touch, heat, cold, sweet food, etc., as nerve fibres are found almost everywhere. Nerve fibres are found in the peri odontoblastic space of the predentin and in most mineralised dentin, on the pulpal side. The hydrodynamic theory of pain induction is based on the movements of the dentin tubule contents, which stimulate nerve endings in the odontoblast layer. Another theory is based on the possible conduction property of the pain stimulus by the odontoblasts themselves. Indeed, it has been suggested that, in certain animals, odontoblasts may originate from the neural crest cells: it would therefore be possible that they also possess properties that enable them to transmit sensory stimuli. In this respect, the serrating or communicating junctions (gap junctions) between the various cellular elements of the odontoblastic and subodontoblastic regions may be particularly important [1].
These junctions allow the exchange of fluids and ions and have low electrical resistance, which allows action potentials to diffuse without delay. The pain that originates from dentin is sharp, stabbing, and short-lasting, and would be typical of A-fibre activity. Dentinal hypersensitivity is a condition characterized by the appearance of short, intense pain that persists until the stimulus is removed, and is not related to any dental pathology other than the anatomical exposure of the cervical dentine to the oral environment, leading to the exposure of the open dentinal tubules and the reactivity of the dental pulp nerve to the external environmental stimuli. Dentin hypersensitivity is a treatable condition, and its management involves, as a first step, a differential diagnosis to ascertain that the dental pain is not related to other problems and pathologies. As far as aetiology is concerned, Brännstrom’s hydrodynamic theory is the most accredited in the aetiopathogenesis of dentin hypersensitivity [2].
The evocative stimulus (e.g., cold) can cause a rapid displacement of pulpal fluid within the dentinal tubule system (contraction, expansion, displacement). The direction of this flow can be centrifugal (i.e., from the pulp outwards) or centripetal (i.e., from the oral environment towards the pulp). The displacement of pulpal fluid induces changes in the shape of receptors (mechanoreceptors) that accompany the odontoblast extension inside the dentinal tubule for a short distance. These receptors are said to be able to transduce the ‘deformation’ signal into a pain nerve impulse that is conducted to the pulpal nerve plexus (Raschow’s plexus) via myelin fibres with a high conduction velocity called A-delta ‘Aδ’ fibres. Stimulation of the ‘Aδ’ fibres appears to be correlated with acute pain symptoms of odontogenic origin, including dentinal hypersensitivity. Hypersensitivity is due to the opening of the dentinal tubules (very small and very numerous tunnels that connect the outside with the inside of the tooth), making it possible for stimuli to pass through to irritate the dental pulp. In particular, thermal lowering, dehydration obtained by means of an air jet, evaporation, and the application of an osmotic stimulus (sugar, acid, salt, etc.) induce the centrifugal displacement of the tubular fluid and are able to activate the nerve endings more effectively than tactile and thermal stimuli of the temperature increase that produce the displacement of the fluid in the direction of the pulp [3]. It has been said that for the painful manifestation of dentin hypersensitivity to occur, it is necessary to have the dentin exposed to the evocative stimuli of the oral environment. Painful symptoms only appear if there is a flow of pulpal fluid through the dentine and it is therefore necessary for the two ends of the dentinal tubule to be pervious both to the pulpal tissues and to the oral environment; therefore, the concept that must be considered is that of dentinal permeability. The diagnosis of dentinal hypersensitivity requires an accurate anamnestic, dental, and radiological examination. A differential diagnosis is necessary to exclude existing carious pathologies, pulpal pathologies, current prosthetic, or conservative therapies that may be the cause, and it is also necessary to investigate each patient’s vicious habits. Hypersensitivity testing should form part of the initial objective examination and be performed by a direct air jet on the dental elements to be evaluated [4].
Physical, chemical, pathological, biological, and/or developmental problems that result in dental and/or periodontal damage or defects cause dentin exposure. Various clinical conditions believed to play a role in the development of dentin hypersensitivity include erosion, abrasion, corrosion, and enamel abrasion [5]. Dentin hypersensitivity is one of the most common causes of discomfort among patients [6].
In patients with dentinal hypersensitivity, the affected teeth become sensitive to generally harmless environmental stimuli. Cold, heat, chemicals (acidic or sweet fruit, food, drinks, etc.), and airflow can induce a short, sharp pain that may impair daily activities such as eating, drinking, talking, and brushing teeth. This severe disorder can last more than 6 months and become a constant nuisance, attacking the emotional and psychological sphere of the individual [7][8][9][10].
Dental hypersensitivity can be a result of:
−
Gingival recession, an important predisposing factor as it exposes the cervical dentine and the root
−
Aging
−
Dehiscence of soft tissue
−
Brushing that is too aggressive
These issues often lead to the apical displacement of the gingival margins, resulting in exposure of the dentine, which can then lead to dentinal hypersensitivity [11][12][13][14]. There is still no single treatment for dentin hypersensitivity, and the market offers such a wide range of products that orientation around them appears complex. Various substances and even machines such as lasers can be used to treat dentin hypersensitivity [10]. The proposed products are divided into chemical agents (e.g., potassium salts, fluoride, sodium citrate, corticosteroids, silver nitrate, strontium chloride, formaldehyde, and calcium hydroxide) and physical agents (composites, microfilled and unfilled resins, sealants, dentin adhesives, glass ionomer cements, etc.) [15][16][17].
The specific machines for treating dentin hypersensitivity are lasers. Protocols that can be defined as specific for such treatment are low and medium power and have been reported to be effective in hypersensitivity treatment. These machines can act either by reducing pulpal nerve excitability or by inducing the occlusion of the dentinal tubules [18][19]. Laser therapy, however, is costlier than the therapies commonly used with the various desensitizing agents. Therefore, to ‘justify’ the expense to the patient, it is important that the doctor is able to demonstrate the validity of this treatment and guarantee, as far as possible, that this treatment offers more benefits than desensitizing agents and is, above all, longer lasting.

2. Lasers and Desensitizing Agents in Dentinal Hypersensitivity Therapy

Dentinal hypersensitivity represents a dental disease of great clinical interest. The onset of painful symptoms can affect any dental element and patients of all ages, with a higher incidence in females aged 20 to 40 years [20][21]. There is a higher incidence of dentinal hypersensitivity in patients suffering from periodontal disease [22][23], with transient onset in patients undergoing scaling and root planing and periodontal surgery [24], and during dental whitening and conservative therapies [25].
Laser-assisted treatment of dentinal hypersensitivity appears to be effective in resolving immediate and long-term pain. Compared to conventional topical desensitizing agents, laser treatment, although more expensive, provides rapid results and is, therefore, faster for the patient [26].
Despite the previously described benefits of using the laser to treat hypersensitivity, the mechanisms by which the laser acts are still unclear and the cost–effectiveness ratio is low. Furthermore, at high temperatures, the potential thermal effects can damage sensitive pulp tissues [27].
Due to the small number of studies in the literature, a meta-analysis by Sgolastra et al. did not show these benefits in the laser treatment of hypersensitivity [28]. Hollande et al. suggested that further randomized double-blind clinical trials would be needed to evaluate the effectiveness of this technology [29]. The results show that both Nd: YAG and diode lasers (high and low power) effectively treat dentinal hypersensitivity. However, substantial differences have been highlighted in the results obtained with the different lasers or protocols used.
The Nd: YAG laser influences hypersensitivity by inducing occlusion or narrowing of the dentinal tubules and direct nerve analgesia [30]. Masumeh et al. showed that the Nd: YAG laser is significantly more effective than the diode laser and a dentin-bonding agent in reducing dentin hypersensitivity [31].
The Nd: YAG laser is costly. Therefore, it would be interesting to find out whether it can be replaced by the diode laser. The results obtained suggest that even the diode laser could be an excellent treatment in dentine hypersensitivity at both low and high power. Two included studies performed better using the high-power diode laser in combination with fluorine paints [32][33]; however, no benefit has been found when using the low-power diode laser in combination with other desensitizing agents [34].
According to a study by Lopes et al. [35], this treatment is more effective if Gluma Desensitizer is associated with the Nd: YAG laser. The articles analysed showed better results with this treatment than with desensitizers such as fluorine and sodium fluoride and compared to other lasers, such as Er: YAG [34][36][37][38].
A systematic review by Rezazadeh et al. [39] attempted to analyse all of the randomized clinical trials and comparative works, to evaluate the effectiveness of laser therapy in prevention and treatment of dentine sensitivity, and explained that previous research evaluating the desensitizing effect of lasers has used different approaches, which makes it difficult to compare their effectiveness, suggesting that the laser is an effective treatment for dentinal hypersensitivity. Some studies have not reported any significant difference between the laser and other desensitizing agents, and most studies have proposed better results (both rapid and long lasting) in combined modalities. The studies analysed have all obtained positive results in terms of the efficacy and validity of the laser treatment, both Nd: YAG and high- and low-power diode, considering them valid treatments for dentinal hypersensitivity.
In conclusion, laser treatment, especially Nd: YAG laser treatment, seems to effectively address dentinal hypersensitivity. However, further studies, especially ones using diode lasers in association with fluorine-based agents, are necessary to establish their real effectiveness and evaluate which laser and protocol are the most suitable.

This entry is adapted from the peer-reviewed paper 10.3390/dj11030063

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