Nanoemulgel (NEG) of Ketoprofen with eugenol as oil phase for the treatment of ligature-induced experimental periodontitis in Wistar rats

Abstract

Aim: The aim of the novel study was to check the efficacy of a locally applied 2%w/w nanoemulgel (NEG) of Ketoprofen (KP) in preventing the periodontitis, and was also checked NEG without KP to ensure the effect of eugenol in NEG as an oil phase. Design: For experimentally induced periodontitis, sterile silk ligatures (3/0) were placed around the crevices of the first left lower molar teeth of the male Wistar rats. During 8 weeks, all rats were fed with 10%w/v sucrose solution. The experimental assessment was carried out at 11 d after treatment of experimental periodontal disease (EPD) rats by various clinical parameters like gingival index (GI), tooth mobility (TM), alveolar bone loss (ABL), histological analysis, detection of TNF-a, and IL-1b in gingival tissue by ELISA and the roughness were measured by atomic force microscopy (AFM) in tapping modes. Results: After treatment, comparison studies with EPD were performed. NEG loaded with KP prevents significantly (p50.05) various parameters (GI, TM, and ABL), which were responsible for periodontitis. The histopathology of the periodontium showed that Group 3 (NEG loaded with KP) had a more significant reduction in inflammatory cell infiltration, alveolar bones resorption, and cementum (p50.05). In the topographical images, significant reduction in roughness of NEG loaded with KP was observed in comparison with EPD without treatment. Conclusion: The study revealed the great synergistic potential of the combined NEG of an antiinflammatory drug KP along with eugenol as the oil phase, which have potential antibacterial, analgesic, and anesthetic properties to combat periodontal disease.

Periodontal disease may induce liver fibrosis in an experimental study on Wistar rats

“…Periodontal disease is an inflammatory disease characterized by gingival bleeding, destruction of the connective tissues, formation of the periodontal pockets, and alveolar bone loss . The pathogenesis of periodontitis involves bacterial communities forming on the subgingival surfaces of the tooth and initiation of an inflammatory reaction on host …”

“…Rat models can be used to study periodontal disease, due to the anatomical and histological similarities with the human cohort . An easy and fast model to induce periodontal disease consists on placing a silk ligature around incisors or molars .…”

“…An easy and fast model to induce periodontal disease consists on placing a silk ligature around incisors or molars . The bacterial inoculation and the ligature placed increase plaque retention and produce gingival injuries, which causes a notable inflammatory response . These changes result in breaking the periodontal tissue, and enables easy transfer of periodontal pathogens to the blood stream …”

Denervation effectively aggravates rat experimental periodontitis

“…A ligature‐induced periodontitis model has been used quite frequently in animals such as mice, rats and dogs . Most rat experimental periodontitis models are established successfully at 6‐8 weeks after ligature . Obvious alveolar bone loss should be observed in these rats.…”

Towards the nano‐control of periodontal inflammation?

“…Various anti‐inflammatory agents acting on different pathways of inflammation were also tested: 15d‐PGJ2 (Napimoga et al, ), ketoprofen (Srivastava, Neupane, Kumar, & Kohli, ), thymol (Botelho et al, ), redox injectable gel (Saita et al, ), risedronate (Khajuria, Zahra, & Razdan, ), metformin hydrochloride (Pereira et al, ), curcumin (Zambrano et al, ), L‐cysteine (Ni et al, ), auranofin (ARN) (Valerio, Alexis, & Kirkwood, ) and N‐phenacyl‐thiazolium bromide (Lin, Feng, Yu, Wang, & Chang, ). Inflammatory response was evaluated by the analysis of many cells, such as neutrophils, lymphocytes, macrophages and mediators, such as IL‐1β, IL‐6, tumour necrosis factor (TNF) α, CCL‐22 and forkhead box (FOX) P3.…”