Bite Force and Its Correlation with Periodontal Status and Salivary IL-1β Levels: A Comparative Study.

Chronic periodontitis

One of the most prevalent long-term bacterial infections that damages the tooth's supporting tissues and causes tooth loss and attachment apparatus destruction is chronic periodontal disease (1).  There are genetic variables associated with chronic periodontitis (CP) that affect the various disease phases.  It is yet unclear, though, if these genetic predispositions could affect the relationships between these conditions.  The hallmark of periodontitis is host-mediated inflammation linked to microbes, which damages periodontal supporting tissues.  It is regarded as one of the main reasons why adults lose their teeth (2).

 

The bacteria and/or microbiota linked to the disease have been investigated as red-complex bacteria (Porphyromonas gingivalis, Treponema den4cola, and Tannerella forsythia) in chronic periodontitis. The polymicrobial infection causes the inflammation of periodontal disease. (3). Tannerella forsythia was suggested as a potential keystone pathogen among chronic periodontal bacteria that cause illness. Tannerella forsythia, is an anaerobic, Gram-nega3ve microorganism closely related to chronic periodontal disease. Different factors such as diabetes, smoking, gene3c predisposi3on, poor dental hygiene, fixed orthodon3c appliances can cause dysbiosis in the bacterial community (4). The goals of periodontal therapy are to lower the amount of bacteria and inhibit inflammation. The two main elements of non-surgical periodontal therapy (SRP) are subgingival debridement and oral hygiene instruction (OHI). Periodontal therapy has a high success rate in enhancing clinical parameters such as plaque index (PI), bleeding on probing (BOP), probing pocket depth (PPD), clinical attachment level (CAL), and, ultimately, decreased tooth loss. Risk factors may have an impact on treatment results. These can include smoking, obesity, poor oral hygiene, tooth-related parameters, compliance, and non-modifiable variables like heredity or acquired disorders (5).

 

 A crucial indicator of how well the masticatory system is working is the biting force. The ability to bite is derived from the muscles of the jaw elevator involved in mastication. Certain features of craniomandibular biomechanics, including as muscular contraction and adaptation to the texture and density of food, modify the biting force that is generated (6).

 

Bite force is a gauge of the functioning of the masticatory system, and dentists frequently assess a patient's bite force. The primary purpose of this is to evaluate the therapeutic advantages of prosthetic devices through an understanding of mastication mechanics (7).

 

Maximum biting force, or MBF, is an objective indicator of chewing that takes into account the conditions of the stomatognathic system and provides information on tooth occlusion, muscle efficiency, and the development of masticatory function (8).

 

 During mastication, the loading forces produced by the masticatory muscles are controlled by periodontal ligament mechanoreceptors (9).

 

The threshold level at which mechanoreceptor function is lowered may so result from decreased periodontal support. Biting force variations could result from this circumstance (10). The polypeptide interleukin-1 has a multiplicity of functions and roles in inflammation, immunology, tissue disintegration, and tissue homeostasis. After activation, it is produced by a variety of cell types, including monocytes, macrophages, T lymphocytes, fibroblasts, vascular cells, brain cells, and skin cells. IL-1 is essential to the pathogenesis of periodontitis because it controls bone resorption and the host's inflammatory response. Although other cell types can also make it, monocytes and macrophages are the main producers. IL-1α and IL-1β are the two subtypes of IL-1. The genes responsible for producing IL-1 have thus attracted the greatest interest lately as possible indicators of the advancement of periodontal disease (11).

 

Detecting of IL-1 β:

After washing the unconnected components out of each well, the substrate solution was added. Both the hue of the Avidin HRP conjugate and the biotinylated detection antibodies would be blue. An enzyme-substrate interaction's color changes to yellow upon the addition of a sulphuric acid solution (15).

 

Figure (1): - IL-1B variations in saliva samples

The total sample was 40 healthy subjects divided into two groups equally (20 periodontitis and 20 non periodontitis) with age range 40-50 years. Table (1) shows the demographic data for both groups. In this table the age in years categorized into two groups with the older age group of 45-50 of highly percentage of patients than the other with higher percentage of male however no significant association was found concerning all variables with both groups. A seen in Table (1): 

 

Table (1): Demographic description of the sample.

 

Two indicators of periodontal conditions were used, periodontal pockets PD1and PD2. According to the data, the periodontitis group's mean periodontal pocket PD1 value was not significantly higher than that of the non-periodontitis group (p>0.05). The periodontal pocket PD2 showed the same image, however there was a statistically significant difference (p≤0.05). Regarding bite force measurement, the data analysis revealed that the periodontitis group had significantly lower maximum bite force readings (p≤0.05). Regarding Interleukin-1β, the opposite outcome was noted, with statistically significant differences (p≤0.05), as shown in Table (2).

 

Table 2: Interleukin-1β, maximum biting force measurement, and mean value of periodontal conditions for the periodontitis group in comparison to the non-periodontitis group. *P≤0.05 indicates significant

 

When comparing the periodontitis group to the non-periodontitis group, Table (3) displays the correlation coefficients between Interleukin-1β and periodontal conditions. The periodontal pockets PD1 and PD2 among the periodontitis group showed significant positive trends (p≤0.05). The same pattern was seen in the group without periodontitis, since the relationships were not statistically significant in either direction (p>0.05).

 

 Table (3): The correlation coefficients between the periodontal conditions and Interleukin-1β for the group with periodontitis and the group without it are shown in Table (3). *P≤0.05, significant

 

Correlation coefficients between the maximum bite force measurement, periodontal conditions and Interleukin-1β for the periodontitis group compared with the non periodontitis group was revealed in Table (4). Among the periodontitis group, data analysis displayed that there were significant correlations in negative directions between maximum bite force measurement and periodontal pocket PD2 and Interleukin-1ᵦ (p≤0.05). The same picture was noticed for periodontal pocket PD1 with statistically not significant differences (p>0.05). Concerning the non periodontitis group, the same result was observed as the correlations were not significant in negative directions (p>0.05).   

 

Table (4) shows the correlation coefficients between the periodontal conditions, maximal biting force measurement, and interleukin-1β for the group with periodontitis and the group without. *P≤0.05 indicates significant

According to the study's findings, individuals were not able to produce their optimum biting force when they had decreased periodontal tissue support, as seen by higher attachment loss and decreased residual bone support. Similar outcomes were observed in patients with reconstructed crossarch bilateral end abutment bridges in Laurell and Lundgren's study. Our results are not consistent with those of the study by Kleinfelder and Ludwig (16), they proposed that there was no correlation between the area of the periodontal ligament and the maximum bite force in teeth that were not splinted, indicating that even fewer periodontal neural receptors might be sufficient for the proper input for mechanisms that limit the pressures used when biting and chewing.

 

The temporomandibular joint and/or pulp mechanoreceptors can potentially affect the generation of the maximal biting force in the current investigation since a more comfortable bite force recording device was utilized, one that makes direct contact with the tooth surface area.

 

The average maximal bite force measured across all subject categories assessed in this study is 340 N. These trials yielded mean peak biting force values ranging from 176 N to 738 N (17). These findings are consistent with the study. The bite-force feature should be regarded as a critical criterion for evaluating people with dental or periodontal diseases, particularly those who have bruxism and oral parafunctions that may be impeded by high tooth stress. A bite's force increases with the posterior transducer's placement within the dental arch (18).

 

 A jaw-lever mechanism made of metal has helped to clarify this. Further resistance to better withstand the bite force is provided by larger root surface area and the periodontal ligament around multirooted roots (19). Masticatory muscles provide loading forces during mastication, which are regulated by the periodontal ligament's mechanoreceptors. Therefore, the threshold level of mechanoreceptor activity may be lowered by diminished periodontal support (20). Alterations in the biting function may result from this illness. Individuals lacking connection exhibited reduced sensory function, according to Williams et al. Healthy subjects' ability to bite was shown to be much higher than that of people with chronic periodontitis, according to Faster et al. (21).

 

These results are in line with another study that found a clear correlation between lower periodontal support and lower biting intensity. The disparity in periodontal disease severity among the studies could be the cause of the discrepancy. According to Cheng et al., (22) sensory performance would be impacted by an inflammatory disturbance of the periodontal ligament, leading to a loss of control over an excessive amount of biting power. Numerous morphologic and physiological parameters, including age, gender, temporomandibular joint diseases, periodontal health of the teeth, and dentition status, can affect bite force (23). Considering these limitations, all other elements were regarded as constants, with the exception of the teeth's periodontal condition; as a result, the biting force varied to varying degrees (24).

 

To assess the variation in biting force values prior to and during periodontal therapy, more bite force measurement research is required, with a bigger sample size and a longer follow-up period.

 
A correlation with IL-1B was discovered, which is in line with what Mohamadit et al. found (25). Furthermore, there was a relationship between the incidence of periodontitis and IL-1B. Therefore, our findings are consistent with those of Zeng et al., who discovered that IL-1B carriage and prevalence were elevated in patients with chronic periodontitis (26).

 

Ethical approval:

The patient's verbal and analytical consent was acquired before the sample was taken. Document number 115 states that on July 18, 2023, a local ethics commission examined and approved the study protocol, subject data, and consent form.

1.      Compared to females, men have a noticeably higher bite force value.

2.      There was no discernible change in the bite force value between the participants with skeletal class II malocclusion and Angle's class I malocclusion The bite force is influenced by the vertical facial morphology, with a larger value for hypodivergent faces compared to hyperdivergent faces. 

3.   Individuals were not able to produce their optimum biting force when they had decreased periodontal tissue support, as seen by higher attachment loss and decreased residual bone support. Additionally, there was a correlation between the IL-1B and the prevalence of periodontitis. Our results stated that patients with chronic periodontitis had increased IL-1B carriage and prevalence.

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