Noise exposure is an important health issue because of the continuous industrial growth, considered today as the second risk factor for public health–being airborne particulate matter the most significant environmental risk factor [1–3]. The World Health Organization published its most recent noise pollution guidelines for Europe in 2018 [4]. This publication states that “noise is an important public health issue; it has negative impacts on human health and well-being and is a growing concern.” The World Health Organization Regional Office for Europe has developed guidelines which provide recommendations for protecting human health from exposure to environmental noise and are essential to drive policy action that could protect communities from the adverse effects of noise.

Industrial noise is characterized by high intensity and a wide spectrum of wavelengths that includes low-frequency noise. This one is an agent of disease that often is not taken seriously in noise protection procedures due to the fact that the human ear is less attuned to the acoustic phenomena within the lower frequencies (<500 Hz), and it is not able to perceive (<20 Hz), only in the form of vibrations [5, 6].

Although the human ear cannot detect lower frequencies, noise is considered a stress factor that involves several negative effects on multiple organs and systems when exposed to it [2, 7]. Most investigations focus on auditory effects; however, the effects of sound exposure can go beyond hearing loss [8, 9]. The non-auditory effects of noise exposure can change the normal procedures of other organs and systems [10], including: degenerative cellular changes, stomach vascular injury [8], increased connective tissue in the liver [11], swelling of the renal glomerulus [12] fibrosis in the cardiac muscle [13], increased perivascular tissue of coronary arteries with significant periarterial fibrosis [14], induction of coronary perivascular fibrosis that differs under corticosteroid administration [15], increased in atrial interstitial fibrosis and a decreased in connexin 43 in rat hearts [16], increased risk of hypertension [17], increased in myocardial infarction and strokes [18] and changes in the adrenal cortex [19]. In the oral cavity, the authors described a morphological and functional change in the parotid gland [6], periodontal injury [20], and dental wear [21, 22].

Studies by Cavacas et al. [21] showed that the teeth of rats exposed to industrial noise had a band-like structure between the pulp and dentin in the upper chamber, which is probably tertiary dentin, produced in response to noise exposure by odontoblast-like cells. These changes may be related to the direct impact of sound pressure or to an adaptive response of the pulp-dentin complex related to stress, since excessive stress results in hyperactivity of the masticatory muscles, as seen in parafunctional activities, particularly bruxism [23–27].

The pulp-dentin complex is a notable symbiose: dentine and pulp are two tissues strongly related [28]. Both suffer deteriorating changes due to aging, caries, injuries, cavity preparation, adhesive techniques, and tooth wear. Nanci [28] and Daud et al. [29] describe that pulp tissue suffers a reduction in the pulp chamber by continuous formation of dentin, an obliteration of the pulp canal, which can result in reduced vascularity, structural changes in blood capillaries, presence of fibrous bundles resulting from a change in the distribution of collagen fibers and a reduction of pulp cell density. The dentine presents a complete tubule closure and an increase of sclerotic dentin formation, decreasing dentin permeability and making it more brittle. Daud et al. [29] and Murray et al. [30] state that dental aging leads to a reduction in dental pulp density and changes in cell morphology which compromise the repair capacity of the pulp during an injury.

Several researchers have described similarities between rat teeth and human teeth at the histological and physiological level in shape and function. In addition, the teeth of these animals appear to be an adequate model for the study of age-related changes in the cells of the pulp-dentin complex, since it would be difficult to obtain an adequate number of samples of human teeth from different age exposed to industrial noise [30].

There are several studies on the health impact of occupational and environmental noise exposure. However, there are still few studies that focus only on health impacts from low-frequency noise, especially industrial noise [1]. From the changes reported in the studies above, it is clear that the stomatognathic system is also affected by the effects of prolonged exposure to noise. So, with this study we intend to characterize the effect of industrial noise on circumpulpar dentin and dental pulp of Wistar rats from a morphological, specifically histological point of view, through a qualitative and quantitative analysis, by evaluating the pulp cell density.

This work was undertake following the materials used in previous studies [21, 22] and it was conducted as a pilot study.

Histological sections showed differences between the cusps of the molars exposed to industrial noise and the cusps of the molars of the control groups. The results were divided into qualitative observations and quantitative analyses. Within each of these analyses, the results at the 3^rd and 7^th months of exposure were demonstrated, as well as the corresponding controls.

Several studies have pointed out noise as an aggressive agent that causes several changes in biological tissues, namely at the level of the stomatognathic system [6, 8, 10–18, 20–22]. Exposure to noise pollution has increased, in contrast to other pollution factors [31]. Thus, it becomes important to determine and understand the possible effects of these on health, especially in the pulpo-dentin complex.

Our qualitative analysis corroborates the results of previous studies of our group that showed an apparent increase in tertiary dentin and a decrease in the pre-dentin layers [21, 22]. Moreover, tertiary dentin is found near the pulp chamber because it is formed by odontoblastic cells as a response to the stimulus (industrial noise) to protect the pulp [32, 33].

The odontoblastic layer appears to suffer a decrease in its density, maybe because odontoblasts suffer a reduction in size and reorganization, leading to a less capacity for an aggression response [32–35].

Near to this layer, we can find the Weill zone that seems to decrease in thickness, when related to the pulp cells rearrangement due to the stimulus [22].

Subodontoblastic cells also appear to suffer a density decrease due to the differentiation into odontoblast-like cells, which have restored activity [29, 32–34].

Fibroblasts seem to decrease their number on the 3rd month [29, 32]. However, on the 7th month it appears that they suffer an increase, maybe related to their function: these pulp cells are responsible for pulp matrix maintenance with the production and turnover of collagen, which is important to the dental tissue repair [32, 33].

In this investigation, there was a decrease in cell density in teeth exposed to noise compared to control teeth. However, it was observed that this decrease is not constant over the months. According to the results obtained, there appears to be a marked decrease in cell density in the first 3 months. Between the 4^th and the 7^th month, there is a gradual increase in similarity between the control group and the exposed group.

This decrease in the number of cells may be related to a response of the organism to industrial noise-which may occur due to psychological stress and/or to the physical vibration of tissue structures-or to an adaptive response of the organism and the pulp-dentin complex to adapt to the narrowing of the pulp chamber, which occurs through the deposition of tertiary dentin [33]. This narrowing has been associated with environmental influences (such as industrial noise) and aging.

In the literature, several age-related changes in the pulp-dentin complex are described. The dental pulp decreases in volume, becomes more fibrous, less vascularized, and less innervated, and cell density decreases [33, 34], corroborating studies that show a reduction in the total number of dental pulp cells with increasing age [29, 32–34].

According to the results obtained through statistical analysis, there are significant differences in pulp cell density between the exposure and control groups on the 3rd month (p = 0.01). The decrease in cell density verified is in line with several studies that showed that the tooth responds to aggressive agents through the pulp-dentin complex [30, 32–35]. However, on the 7th month of exposure, there were no statistically significant differences between the exposed group and the control group (p = 0.66). These results can be explained by the adaptive response of the pulp tissue of the tooth to the aggressor or to stressful conditions, as well as by the pulp physiological aging of the control tooth.

As a limitation of the study, we can point out the fact that it was aimed as an exploratory study, so it was not supported by an a priori sample size calculation. Also, the fact that we limited our observations to the histological modifications induced by industrial noise in the pulp-dentin complex and dental pulp (its density and cell morphology) and can only extrapolate these results to humans with limitations. In an identical but prospective study, it will be interesting to differentiate the quantification of dental pulp cell populations.

The main purpose of this study was to evaluate the changes in pulp cell density in teeth exposed to an external aggressor. As reflected in the general objective of the present investigation, there were qualitative and quantitative changes in the pulp-dentin complex of Wistar rat teeth exposed to industrial noise, especially a decrease in pulp cell density.

In summary, we found a relationship between exposure to industrial noise and teeth morphological changes. This study places industrial noise as an aggressive stimulus capable of causing a reaction of the pulp-dentin complex, with morphological changes compatible with premature aging of the tooth.

Although there are several histological and physiological similarities between rat and human molars, these results can only be extrapolated to humans with limitations.

The original contributions presented in the study are included in the article/supplementary material, further inquiries can be directed to the corresponding author.

The animal study was reviewed and approved by the animals were treated in accordance with the EU Commission on Animal Protection for Experimental and Scientific Purposes (86/609/EEC) and with the Portuguese legislation for the same purpose (Decree-Law No. 197/96).

MC: conceived and designed the analysis, collected the data, performed the analysis, and wrote the paper. AL and CD: collected the data and analysis tools, performed the analysis, and wrote the paper. VT: review paper. All authors contributed to the article and approved the submitted version.

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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