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What Is The Role Of Vitamin C
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Vitamin C, Calcium, And Oral Health
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What Is The Role Of Vitamin C In Collagen Synthesis?
Łukasz Ustianowski Łukasz Ustianowski Scilit Preprints.org r Ostrowski Scilit Preprints.org Google Scholar and Andrzej Pawlik Andrzej Pawlik Scilit Preprints.org Google Scholar *
Received: 27 February 2023 / Revised: 31 March 2023 / Accepted: 3 April 2023 / Published: 5 April 2023
(This article is from a new issue of a special issue on the health benefits of vitamins, minerals and probiotics)
Periodontitis is a common disease that affects the bone and soft tissues of the Periodontal complex. If left untreated, it can lead to severe mobility or tooth loss. The pathogenesis of periodontitis is complex, with important factors being chronic inflammation in tooth and periodontal tissues and changes in the oral microbiome. However, recent studies suggest a role for vitamins such as vitamin C (VitC) and vitamin D (vitD) in the development of the disease. VitC regulates many biochemical reactions, but is primarily involved in collagen synthesis. VitC deficiency has been reported to damage periodontal ligaments. VitC supplementation improves postoperative outcomes in patients with periodontitis. VitD is a steroid product that can be produced in the skin under UV light and then converted to an active form in other tissues such as the kidney. VitD is designed to reduce the effects of certain cytokines found in teeth and to maintain proper tooth mineral density. Additionally, VitD supplementation was associated with better outcomes in surgical treatment of periodontitis. In this review, we summarize the latest knowledge on the role of vitamins C and D in the pathogenesis and treatment of periodontitis.
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Periodontitis is a common disease characterized by the growth of the alveolar bone complex and the soft tissues of the periodontal complex. It occurs in about 47% of the population. Periodontitis can lead to mobility and loss of teeth or implants [1]. The overall pathogenesis of the process is the interaction of dysbiotic bacteria that creates a plaque biofilm and normal immune responses in the dentin and periodontal tissues [2]. Persistent inflammation, including supra- and subgingival biofilm dysbiosis, is important in the initiation and progression of periodontitis [3]. Continuous inflammation in periodontal tissue leads to destruction of connective tissue and alveolar bone structure. In addition, oral bacteria and pathobionts play an important role in contributing to periodontitis by interfering with key pathogens such as P. gingivalis, T. forsythia and A. actinomycetemcomitans [4]. Periodic inflammation and dysbiosis of the microbiota is caused not only by lack of oral hygiene, but also by environmental components, for example, poor nutrition and psychological stress [5, 6].
Periodontitis is a disease caused by local immunity against microbial infection occurring in the periodontal tissue, which aims to eliminate the causative agents. In periodontal tissues, which are physiological defenses against pathogens, initial inflammation can develop into a chronic inflammatory process that leads to activation of the immune system. However, the formation of plaque reduces the immunity of the bacteria, creating favorable conditions for other anaerobic bacteria and increasing the pathogenicity of the micro-organisms in the plaque. This results in the release of several mediators, including inflammatory cytokines, chemokines, and metalloproteinases, that damage periodontal tissues. If left untreated, gradual resorption leads to tooth weakening and even tooth loss.
Recent studies suggest that oxidative stress is also involved in the pathogenesis of periodontal disease. Oxidative stress appears to contribute to the development of chronic inflammation in the periodontal tissues of patients with periodontitis. An increase in oxidants associated with antioxidant stress leads to damage to cellular components. In the cell, proteins are damaged and lipids are oxidized. High levels of reactive oxygen species (ROS) have been found in damaged periodontal tissues; In addition, levels of reactive oxygen metabolites and biomarkers of lipid peroxidation such as malondialdehyde were elevated in patients with periodontal disease. Thus, oxidative stress appears to be one of the possible causes of periodontal disease [5, 6]. Recent studies suggest a role for various nutrients and vitamins, including vitamin C (VitC) and vitamin D (VitD), in the development of periodontal disease.
VitC, also known as L-ascorbic acid, is a substance that cannot be synthesized by humans; therefore, it should be given a proper diet [7]. About 90% of the daily requirement comes from vegetables and fruits, which are excellent sources of this vitamin [8]. The National Institutes of Health recommends a daily intake of VitC for adults: 75 mg for women and 90 mg for men. Scurvy, which can kill, is caused by a deficiency of VitC [9]. Its symptoms include weakened collagen and connective tissue, poor wound healing, weakened teeth, decreased immunity, and increased risk of serious infections such as pneumonia [10]. It is associated with the synthesis of collagen, which is an important agent that provides structural strength to connective tissues [11]. Common symptoms of disability include muscle weakness, petechial hemorrhage, spontaneous ecchymosis, hemorrhage, restlessness, lethargy, and irritability. It can lead to death due to dangerous complications such as stroke or myocardial hemorrhage [12]. As for the periodontal tissues, symptoms include gingival pain, swelling, and bleeding from vascular fragility, which can eventually lead to tooth loss [12]. Stabilization of collagen tertiary structure depends on the action of VitC [13].
Source Naturals Vitamin C Ascorbic Acid Crystals (8 Oz)
The immune system is modulated by many VitC activities. As this substance is a very effective antioxidant, it can protect important biomolecules from toxins, pollutants and oxidants by donating electrons [14]. In addition, VitC has a significant effect on neutrophil function, stimulating their migration toward infection and enhancing phagocytosis and killing of microbes. It also promotes neutrophil apoptosis and destruction by macrophages [15].
VitC is also involved in synthesizing catecholamine hormones and amidated peptides such as vasopressin by being a cofactor for hydroxylase enzymes. These hormones are important for the cardiovascular effects of severe infection [16].
VitD is synthesized from 7-dehydrocholesterol during a photochemical reaction and is hydroxylated in the liver to 25-hydroxyvitamin D3 (25(OH)D3). It is the major plasma VitD, a biologically active metabolite that balances calcium and phosphorus concentrations in the blood by regulating intestinal absorption and renal reabsorption. VitD is present in fatty fish meat and fish oil, although its prevalence is relatively low in other food types [17]. VitD has many important physiological functions [18]. In addition, VitD has been shown to directly and indirectly affect bone turnover, which is important in preventing osteoporosis, rickets, and fractures in the elderly [19, 20]. A meta-analysis by Bischoff-Ferrari et al. showed an association between VitD supplementation and fracture prevention [21]. In addition, it is an important factor in the prevention and treatment of diseases caused by disturbances in immune homeostasis [22]. VitD receptors have been found on monocytes, macrophages, neutrophils, and dendritic cells. They have been shown to be involved in the secretion of compounds with antimicrobial activity. It affects the function of the immune system and is an important part of the defense mechanisms against bacterial infections in the oral cavity [22].
VitD
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