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      Evaluation of Co-Q10 anti-gingivitis effect on plaque induced gingivitis: A randomized controlled clinical trial

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          Abstract

          Background:

          Deficiency of Co-Q10 has been found to be responsible for periodontal destruction; therefore, this study was undertaken to evaluate the anti-gingivitis effect of Co-Q10 on plaque induced gingivitis.

          Materials and Methods:

          Thirty subjects with plaque induced gingivitis were enrolled in a split mouth randomized controlled trial. For each subject, scaling was randomly performed for any two quadrants, followed by the topical application of Co-Q10 randomly in a previously scaled and as an unscaled quadrant for a period of 28 days. Four treatment options were planned: option A: scaling only; option B: Co-Q10 along with scaling; option C: Co-Q10.

          Results:

          Marked reduction in gingival, bleeding, and plaque scores were recorded at the sites where C0-Q10 was applied. Mean±S.D of aforementioned periodontal parameters at 28th day showed significant reduction for option A, B, and C when compared with baseline.

          Conclusion:

          Promising results were obtained after the solitary application of Co-Q10 as well as when it was used as an adjunct to scaling and root planing for treatment of plaque induced gingivitis.

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          Most cited references13

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          Biochemical, physiological and medical aspects of ubiquinone function.

          This presentation is a brief review of current knowledge concerning some biochemical, physiological and medical aspects of the function of ubiquinone (coenzyme Q) in mammalian organisms. In addition to its well-established function as a component of the mitochondrial respiratory chain, ubiquinone has in recent years acquired increasing attention with regard to its function in the reduced form (ubiquinol) as an antioxidant. Ubiquinone, partly in the reduced form, occurs in all cellular membranes as well as in blood serum and in serum lipoproteins. Ubiquinol efficiently protects membrane phospholipids and serum low-density lipoprotein from lipid peroxidation, and, as recent data indicate, also mitochondrial membrane proteins and DNA from free-radical induced oxidative damage. These effects of ubiquinol are independent of those of exogenous antioxidants, such as vitamin E, although ubiquinol can also potentiate the effect of vitamin E by regenerating it from its oxidized form. Tissue ubiquinone levels are regulated through the mevalonate pathway, increasing upon various forms of oxidative stress, and decreasing during aging. Drugs inhibiting cholesterol biosynthesis via the mevalonate pathway may inhibit or stimulate ubiquinone biosynthesis, depending on their site of action. Administration of ubiquinone as a dietary supplement seems to lead primarily to increased serum levels, which may account for most of the reported beneficial effects of ubiquinone intake in various instances of experimental and clinical medicine.
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            Functions of coenzyme Q10 in inflammation and gene expression.

            Clinical studies demonstrated the efficacy of Coenzyme Q10 (CoQ10) as an adjuvant therapeutic in cardiovascular diseases, mitochondrial myopathies and neurodegenerative diseases. More recently, expression profiling revealed that Coenzyme Q10 (CoQ10) influences the expression of several hundred genes. To unravel the functional connections of these genes, we performed a text mining approach using the Genomatix BiblioSphere. We identified signalling pathways of G-protein coupled receptors, JAK/STAT, and Integrin which contain a number of CoQ10 sensitive genes. Further analysis suggested that IL5, thrombin, vitronectin, vitronectin receptor, and C-reactive protein are regulated by CoQ10 via the transcription factor NFkappaB1. To test this hypothesis, we studied the effect of CoQ10 on the NFkappaB1-dependent pro-inflammatory cytokine TNF-alpha. As a model, we utilized the murine macrophage cell lines RAW264.7 transfected with human apolipoprotein E3 (apoE3, control) or pro-inflammatory apoE4. In the presence of 2.5 microM or 75 microM CoQ10 the LPS-induced TNF-alpha response was significantly reduced to 73.3 +/- 2.8% and 74.7 +/- 8.9% in apoE3 or apoE4 cells, respectively. Therefore, the in silico analysis as well as the cell culture experiments suggested that CoQ10 exerts anti-inflammatory properties via NFkappaB1-dependent gene expression.
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              Oxidant/antioxidant interactions of nicotine, Coenzyme Q10, Pycnogenol and phytoestrogens in oral periosteal fibroblasts and MG63 osteoblasts.

              There is a growing awareness that oxidative stress may play a role in periodontal disease. The aim of this investigation was to evaluate potential oxidant/antioxidant interactions of nicotine with antioxidants (Coenzyme Q10 (CoQ), Pycnogenol and phytoestrogens in a cell culture model. Duplicate incubations of human periosteal fibroblasts and osteoblasts were performed with 14C-testosterone as substrate, in the presence or absence of CoQ (20 microg/ml), Pycnogenol (150 microg/ml), and phytoestrogens (10 and 40 microg/ml), alone and in combination with nicotine (250 microg/ml). At the end of a 24-h incubation period, the medium was solvent extracted and testosterone metabolites were separated by thin-layer chromatography and quantified using a radioisotope scanner. The incubations of osteoblasts and periosteal fibroblasts with CoQ, Pycnogenol or phytoestrogens stimulated the synthesis of the physiologically active androgen DHT, while the yields of DHT were significantly reduced in response to nicotine compared to control values (p<0.001 for phytoestrogens). The combination of nicotine with CoQ, Pycnogenol or phytoestrogens increased the yields of DHT compared with incubation with nicotine alone in both cell types. This investigation suggests that the catabolic effects of nicotine could be reversed by the addition of antioxidants such as CoQ or Pycnogenol and phytoestrogens.
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                Author and article information

                Journal
                J Indian Soc Periodontol
                J Indian Soc Periodontol
                JISP
                Journal of Indian Society of Periodontology
                Medknow Publications & Media Pvt Ltd (India )
                0972-124X
                0975-1580
                Oct-Dec 2012
                : 16
                : 4
                : 539-542
                Affiliations
                [1] Department of Periodontics, Institute of Dental Sciences, Bareilly, Uttar Pradesh, India
                Author notes
                Address for correspondence: Dr. Anirban Chatterjee, Head of Department, Periodontics, Institute of Dental Sciences Bareilly, Uttar Pradesh, India. E-mail: dranirbanchatterjee@ 123456yahoo.com
                Article
                JISP-16-539
                10.4103/0972-124X.106902
                3590723
                23493408
                c5093fee-5d20-4eb1-b18d-bbaaa7fd15c1
                Copyright: © Journal of Indian Society of Periodontology

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 02 December 2010
                : 29 November 2011
                Categories
                Original Article

                Dentistry
                plaque induced gingivitis,coenzyme-q10,anti-gingivitis
                Dentistry
                plaque induced gingivitis, coenzyme-q10, anti-gingivitis

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