Abstract
Objectives: Isatis tinctoria L., clary, is an herbal plant traditionally used in folk medicine for the treatment of various diseases and conditions. Although it has been primarily used as an antimicrobial and antifungal, there are data on traditional use of I. tinctoria as an agent against antiallergic, anti-thrombocytosis. The aim of the study was to examine the effect of the I. tinctoria root extract on the lipopolysaccharide (LPS)-induced periodontitis in rats on osteoclast associated bone resorptive activity, cell death including apoptosis, and inflammation in a rat of disease model of periodontitis. Materials and Methods: Periodontitis, acute or chronic inflammatory status in periodontal tissue in rats could be induced by repeated injections of LPS from Escherichia coli into the periodontal pocket area between the first and second right maxillary molars. Eighteen male rats were distributed among the following treatment groups: 1) I. tinctorial root extract (Antifect) 200 mg/kg body weight, 2) acetylsalicylic acid (ASA), 20 mg/kg body weight and 3) Phosphate buffered saline (PBS) treatment used as a control. After 15 days, maxilla, alveolar bone, molar teeth and associated periodontal tissues were harvested. Inflammatory alveolar bone resorption was analyzed by microcomputerized tomography (μCT) (microcomputer tomography). Tissues fixed with paraformaldehyde and formalin for 2 days, after that paraffin embedded histological sections were stained with haematoxylin and eosin (H/E) for the assessment of histopathological changes or tested to immunohistochemistry for detecting TRAP (tartrate resistant acid phosphatase) positive cells and caspase 3. Cell death and Apoptosis were analyzed in the periodontal tissues by tunnel assay. The inflammatory status was assessed by the measurements of proinflammatory cytokines interleukin-Iβ (IL-Iβ), interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) of gingival tissues and descriptive analysis of histological sections of periodontal. Results: Treatment with Antifect, compared to the control group, significantly diminished the process of inflammation decreasing the levels of IL-Iβ, IL-6 and TNF-α, reducing the gingival tissue lesions and preserving bone alveolar resorption. Considerably a smaller number of inflammatory cells and a larger number of fibroblasts were noticed. Also, μCT analysis showed that only Antifect treated group reduced bone resorption and the number of TRAP-positive multinucleated cells (osteoclasts), also, significantly reduced the number of apoptotic cells in the gingival tissues and of osteocytes in the alveolar bone crest. Conclusion: Antifect manifested anti-inflammatory elect and reducing alveolar bone resorption in LPS-induced periodontitis suggest that it may have a role as a therapeutic agent in periodontal diseases.
Highlights
One major actor of the oral ecosystem is the dental plaque which develops naturally on hard and soft tissues of the mouth
Eighteen male rats were distributed among the following treatment groups: 1) I. tinctorial root extract (Antifect) 200 mg/kg body weight, 2) acetylsalicylic acid (ASA), 20 mg/kg body weight and 3) Phosphate buffered saline (PBS) treatment used as a control
Recent investigations have shown that the gingival tissue from the inflamed area contains increased levels of some cytokines, primarily interleukin-lβ (IL-Iβ), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), implying that these cytokines mainly participate in the pathogenesis of periodontitis [6] [7] [8]
Summary
One major actor of the oral ecosystem is the dental plaque which develops naturally on hard and soft tissues of the mouth. This biofilm has a very complex organization that remains relatively stable with time despite regular environmental changes [1]. Subgingival Gram-negative organisms containing lipopolysaccharides (LPS) cause inflammation of the periodontal tissues inducing a local response, which implies a polymorphonuclear leukocyte infiltration, a production of reactive oxygen species (ROS) and inflammatory mediators such as cytokines and prostaglandins, amplification of lytic enzymes and activation of osteoclasts, edema and vascular dilatation [4] [5]. The culminating stadium of damaging effects of the produced cytokines and ROS is destruction of tooth-supported tissues including connective and mineralized tissue [9]
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