Use of Lasers in Dentistry

Laser was put in or introduced in dentistry in 1960s. Then, a persistent range of studies were made on various applications of laser in dental practice. The two major types of lasers were came in terms of clinical implementations: hard lasers such as (CO2) carbon dioxide, neodymium–yttrium aluminum garnet (Nd:YAG), and erbium–yttrium aluminum garnet (Er:YAG) with both hard and soft tissue employments. For the sake of a potential for thermal tissue damage, and high-cost, hard lasers have some limitations. Furthermore, cold or soft lasers have been predominantly utilized for biostimulation or low-level laser therapy (LLLT). Lasers are utilized in different disciplines in dentistry such as restorative dentistry wherever they are utilized for improving the resistance of dental enamel, diagnosis of caries and photopolymerization of composite resin; endodontics for bactericidal cleansing of root canal; periodontics for gingivectomy, frenectomy, gingivoplasty, and vestibuloplasty; pedodontics to get ready tooth surfaces for sealant application; and oral and maxillofacial surgery to handle and treat vascular malformation.

Dental lasers are assorted and classified with regard to the lasting medium used such as solid laser, gas laser or application in various tissues such as hard tissue or soft tissue lasers, the risk of laser usage and the range of wavelength. The literature about the inadvertent impacts or effects of laser irradiation on orodental structures is restricted and insufficient or scanty to provoke readers’ worries and concerns regarding the prospective hazards of laser therapy. Scanty and insufficient knowledge about undesirable effects of laser might give rise to sweeping and overwhelming therapeutic pitfalls; as a consequence; for this reason, a functional and an efficient treatment alternative would provide or supply as a potentially destructive modality.

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The goal of the current paper was to dispute and debate laser effects on orodental soft and hard tissues during dental processes. General provisions and precautions regarding banning and prevention of laser damage to the operator and the patient have been examined and discussed several times. The side effects of the dental laser are also analyzed.

Methods

We accomplished an electronic search utilizing specialized a structured set of data held in a computer (databases) such as PubMed, Google Scholar, Science Direct, PubMed Central, and Scopus to explore relevant studies by utilizing various keywords such as, ‘dentistry’, ‘laser’, ‘side effect’, and ‘adverse effect’.

Laser Side Effects

The laser energy is turned into or converted into heat when absorbed by tissue components, such as chromophores, DNA/RNA, proteins, water, and enzymes. The tissue damage because of the thermal effects of laser is broadly and largely attributable to the degree of heating in a way that growing and increasing temperature causes or leads to more cruel and severe changes; hyperthermia begins at 42–45°C, which performs and results in shrinkage of collagen and structural alteration. Mitigation or reduction of enzymatic activity occurs or takes place at 50°C. Temperature of 60°C gives rise to or causes coagulation of collagens, protein denaturation, and membrane permeabilization. The tissue drying and formation of vacuoles happen at 100°C. Starting of vaporization and tissue carbonization is the outcome of heat over 100°C. The temperature of 300–1000°C causes or leads to thermoablation of tissues, disruption and photoablation.

The study related to the thermal impacts of Nd:YAG, argon, and CO2 laser beams on dentin, enamel, and dental pulp explained and demonstrated the potency of Nd:YAG laser beam to perforate and penetrate deeply through the dentin and enamel to the pulp. In spite of the fact that the impacts of argon laser were closely connected with the degree of enamel surface cleanliness, the superficial and deep temperatures were notified to be low even after surface cleaning. With respect to CO2 laser, very high temperatures were produced on the enamel and dentin surfaces; whilst, pulp chamber reached low temperatures.

Laser Effects on Dental Pulp

An excess in temperature of 6°C can give rise to irreversible pulpitis, whilst pulpal necrosis happens when temperature rises higher (11°C). There is no general agreement or consensus in the literature about pulpal damage made by laser thermal impacts. Some studies notified different grades of pulpal damage whilst others displayed no sign of pulpal changes in terms of laser type and power setting. In a paper by von Fraunhofer et al., the impact of Nd:YAG laser at ≤240 J on third molars within 3 minutes after extraction was explained or demonstrated that if the residual or remaining dentin thickness was greater than 1 mm, irradiation makes no significant pulpal response. Inequality, thermal harm or insult of CO2 laser at 5 × 103 J/cm2 was notified and reported to give rise to calcification in the pulp chamber and an intention or increase in pulpal volume by approximately one third. Bader and Krejci in another study, explained that laser cavity preparation rose and caused overheating of teeth leading to pulpitis. Furthermore, various temperatures were recorded according to the anatomic site of cavity preparation; Class I preparations yielded the highest values, followed by Class V cavities in enamel. Furthermore, preparation in cementum or caries removal caused the lowest temperature raise or increase.

Laser Impacts on Tooth Surface

The tooth surface maybe affected by laser irradiation likewise; for example, sufficiently great or important to be worthy of attention or significant decrease in shear bond strength of brackets to the teeth following bleaching with carbamide peroxide and diode laser has been notified or reported. In spite of the fact that Er-YAG laser irradiation with water and 35 μs pulse duration did not effect, or result in surface visible cracks, it made a 20% reduction in the bending strength of the dentin.

Histopathological Changes of Laser

The dental laser therapy makes or causes some histopathological changes also. Cell necrosis in the periodontal ligament (generally due to thermal impact) was notified 1 day after laser treatment, whilst teeth under conventional preparation elaborated or developed no evidence of cell necrosis. 15 days following treatment, increased size and number of osteocytes and osteoclasts were clear and evident in the periradicular bone in both laser and conventionally-treated teeth. Furthermore, initial bone resorption was discovered and detected in laser-treated teeth. Conventionally-treated teeth started to return to normal morphology within 30 days posttreatment. Furthermore, the laser-treated teeth exhibited cemental lysis, ankylosis, and serious or significant bone remodeling. Laser can make or cause pulpal vasodilation, and high-power lasers cause edema and occasional inflammation.

Conclusion

Regardless of many advantages of dental lasers, this method can be potentially dangerous and hazardous due to effects on dental pulp, subcutaneous and submucosal tissues, tooth surface, and risk of infection transmission. Thus, dental practitioners must be aware of laser adverse impacts or effects during therapeutic processes to minimize the potential risks for patients.

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