Does thyroid dysfunction influence inflammatory mediators in experimental periodontitis?

Abstract

Objective. The aim of the present study was to investigate the presence of inflammatory mediators in rats with only periodontitis and periodontitis in a setting of hyper- and hypo-thyroidism and to analyze the correlative linkages between inflammatory mediators and thyroid hormones. Methods. White male 12–14 weeks old inbred rats (n=48) weighing 180–200 g were employed in the experiment. They were randomly divided into the following groups: Group I – control group, Group II – group with a model of periodontitis, Group III – group with a periodontitis in a setting of hyperthyroidism, and Group IV – group with periodontitis in a setting of hypothyroidism. The presence of tumor-necrosis factor-α (TNF-α) and interleukins IL-1β and IL-10 in the periodontal homogenate supernatant was studied by a solid-phase enzyme-linked immunosorbent assay. Results. It was shown that experimental lipopolysaccharide (LPS)-induced periodontitis is accompanied by hyperproduction of pro-inflammatory cytokines (TNF-α, IL-1β) and reduction of anti-inflammatory cytokines (IL-10), whereas TNF-α underwent to maximum changes. Thyroid dysfunction exacerbates cytokine imbalance and severity of inflammation in experimental LPS-induced periodontitis, especially pronounced at hyperthyroidism, as evidenced by the predominance of TNF-α and IL-1β levels in the periodontal homogenate supernatant by 38.5% (р<0.01) and 75.6% (p<0.001), respectively, hyperthyroid over the euthyroid, and by 20.1% (p<0.05) and 24.1% (p<0.05), respectively, over the hypothyroid rats. Conclusions. Thyroid dysfunction, especially hyperthyroidism, may play an important role in the pro-inflammatory response in periodontitis. Hyperproduction of inflammatory mediators in thyroid dysfunction can induce a noticeable damage in the whole apparatus of the periodontium, thereby causing progression of periodontitis.

Transcriptomic Analysis Reveals Genetic Cross-Talk between Periodontitis and Hypothyroidism

“…In this context, it is not surprising that patients with HT show a pronounced destruction of respective connective tissues [ 8 ]. The second approach is the influence of HT on the PD-related immune response; in experimental PD, thyroid dysfunction was found to foster cytokine imbalance and severity of inflammation [ 14 ]. In addition to that, a potential role of vitamin D in the interplay between PD and HT was reported [ 15 ].…”

“…Moreover, thyroid autoimmunity was also found to be related to psoriasis [ 23 ]. Considering this, the potential role of LCE family as cross-talk genes between PD and HT would most likely indicate an increase of (auto-) immunity; this is supported by the upper mentioned fact that the thyroid dysfunction would foster cytokine imbalance and severity of periodontal inflammation [ 14 ]. Furthermore, the biological processes immune system process and complement, which were identified as potentially relevant in the current study, would be in line with this hypothesis.…”

The influence of chronic hyper-homocysteinemia on characteristics of peripheral neutrophils’ programmed death in lipo-polysaccharide-induced periodontitis

“…Rats were randomly divided into four groups (n = 12 per group): group 1 -control, group 2 -rats with a model of periodontitis. For two weeks, the animals were injected with 40 μl (1 mg/ml) of E. coli lipopolysaccharide (LPS) (Sigma-Aldrich, USA) into gingival tissues every other day [6]. Group 3 included rats with HHcy (n = 12).…”

“…For instance, in European countries, the incidence of severe periodontitis in the cohort of 35-44 year old adults ranges from 5 to 20%, increasing to 40% in older population groups [4,5]. At the same time, the frequency of periodontal disease among an adult population in Ukraine reaches 85-95% [6].…”

Osteoporosis and Alveolar Bone Health in Periodontitis Niche: A Predisposing Factors-Centered Review

“…It was reported that thyroid disorders are associated with an increased prevalence rate of periodontal inflammation and tissue destruction, measured by clinical parameters and inflammatory markers. This correlative relationship is more evident in hyperthyroidism populations than in those with hypothyroidism [ 95 , 96 ]. The results of animal studies corroborate clinical findings.…”