Zinc is transformed into oral health products to control plaque, reduce malodor, and retard calculus formation. The zinc elevated concentrations can be sustained for prolonged periods in plaque and saliva following delivery from mouthrinses and toothpastes. Although low concentrations of zinc can both reduce enamel demineralisation and modify remineralisation, the anticariogenic efficacy is yet disputable and not supported by various researches [ 44 ].
Iodine, Iodine metabolism and Iodine deficiency disorders revisited
Taste disorders: the role of zinc in taste functions is appreciable at various levels of organization such as taste buds, the taste sense nerve transmission, and brain. Zinc plays an important role in cell structure architecture, maintaining the cell membrane integrity, and functions of various cytoplasmic and membrane enzymes.
Early researchers concluded that zinc deficiency secondary to any etiology leads to taste disturbances and thus still zinc depletion is corrected for patients reporting with taste imbalances [ 45 ].
A study conducted on rodents concluded that zinc-deficient diet can result in parakeratosis of normally orthokeratinized oral mucosa. Hence, zinc deficiency can be a potential risk factor for oral and periodontal diseases. The parakeratotic changes in cheek, tongue, and esophagus are a sign of zinc deficiency.
Thickening of the buccal mucosa is a common manifestation along with loss of filiform papillae [ 46 ]. As stated above, zinc is a cofactor for superoxide dismutase enzyme and various studies have shown lower levels of serum zinc in patients with potentially premalignant disorders like oral leukoplakia. This may be due to consumption of zinc in counter reaction to high content of copper in areca nut or oxidants released during tobacco usage [ 47 ]. Similarly, concentration of zinc in serum is significantly decreased in oral squamous cell carcinoma and oral submucous fibrosis patients with history of tobacco consumption when compared to the control group and gradually decreased with the duration of the habit.
The serum level of zinc was reportedly lower in oral squamous cell carcinoma patients than in oral submucous fibrosis patients [ 25 , 48 ]. As transferrin transports both iron and zinc, the level of zinc increases as the level of iron decreases in iron deficiency patients. Thus, patients of OSMF also suffering from iron deficiency anemia show higher serum levels of zinc [ 25 , 48 ]. Superoxide dismutase which is a natural antioxidant of the body is a Cu-Zn protein complex that has an anticarcinogenic effect in OSMF. Secondly, zinc decreases the activity of copper containing lysyl oxidase enzyme and thus causes inhibition of cross linkage of collagen peptides.
It also plays a significant role in promoting collagen degradation through collagenase and matrix metalloproteinase. Zinc thus bears an inverse relationship with copper and thereby interferes with the mucosal absorption of copper. Excess zinc particularly impairs copper absorption as both metals are absorbed through metallothioneins. The ratio of copper to zinc is also believed to be a reliable biomarker in the development and progression towards carcinogenesis [ 48 ].
On the contrary to the popular belief of protective function of zinc, limited literature suggests carcinogenic effect of zinc [ 49 ]. Iron is the most abundant essential trace element in the human body. Iron is absorbed in the gut from diet in case of depletion and transported in the form of ferritin. Hemosiderin is a golden brown pigment which is a byproduct of metabolism of ferritin and is deposited in the cells of the reticuloendothelial system [ 51 ].
Homeostasis of iron maintains the iron levels in serum within normal range only by upregulation or downregulation of absorption mechanism of iron which is unique because it maintains homeostasis by regulating the absorption and never excretion.
Heme is the major iron containing substance in ferrous or ferric state which is present in hemoglobin, myoglobin, and cytochrome. There are numerous enzymes associated with iron, namely, cytochrome a-c, p, cytochrome c reductase, catalases, peroxidases, xanthine oxidases, tryptophan pyrrolase, succinate dehydrogenase, glucosephosphate dehydrogenase, and choline dehydrogenase. Heme forms covalent bonds with the globin protein to form hemoglobin which is the major oxygen carrying pigment in RBCs of mammalians.
It takes part in a myriad of metabolic cycles such as in the energy producing reactions the cytochromes of the Krebs cycle in all the cells and activates the energy producing oxidizing enzymes. Apart from participation in maintaining innumerable physiological and metabolic processes, it is also necessary for DNA, RNA, collagen, antibody synthesis, and so forth [ 52 ]. The biological roles of iron in the human body are beyond the scope of this paper and only few important ones have been listed.
The roles of iron in oral health and diseases are summarized as follows:. Iron deficiency anemia is the most common manifestation of low serum levels of this important trace element. Microcytic hypochromic RBCs, fatigue, achlorhydria, atrophy of epithelium, loss of attention, irritability, dyspnea, and lowered memory are some of the features of iron deficiency anemia [ 25 ]. The oral manifestations of iron deficiency anemia can be summarized as angular cheilitis, atrophic glossitis, generalised oral mucosal atrophy, candidal infections, pallor, and stomatitis.
Plummer-Vinson syndrome or Paterson-Kelly syndrome or sideropenic dysphagia is a rare condition characterized by iron deficiency anemia, dysphagia, and koilonychia with women being affected more than men. Dysphagia results from the presence of abnormal esophageal webs which have predisposition towards malignant transformation [ 53 ]. Oral premalignant lesions and conditions: a significant decrease in serum iron concentrations with elevated total iron-binding capacity has been found in OSMF patients.
The decreased iron levels in OSMF patients might be due to utilization of iron in collagen synthesis. In addition, deficient iron in the oral tissues results in decreased vascularity which further facilitates percolation of arecoline byproduct of areca nut. Further damage is caused by increased arecoline percolation which enhances fibroblastic proliferation and collagen formation [ 25 ]. Though majority of the literature suggests that OSMF leads to iron deficiency due to impaired dietary habits, Bhattacharya et al. Similarly, low serum levels of iron have been assessed in patients suffering from oral leukoplakia.
It has also been noted that serum ferritin levels are elevated and serum iron concentrations are decreased with tumor progression in head and neck carcinomas and thus heme can be used as a follow-up tool for patients along with nutritional assessment [ 47 ]. The presence of cobalt in animal tissues was first established by Bertrand and Macheboeuf in which was later confirmed by various researches using spectrographic methods [ 55 , 56 ].
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Cobalt is an essential trace element for the human body and can occur in organic and inorganic forms. In organic form, it forms an integral part of vitamin B12 and has a substantial role in the formation of amino acids and neurotransmitters. Inorganic forms of cobalt are toxic to the human body, and the longer they stay in the body, the more the detrimental effects they cause in cells. Cobalt ions are absorbed within the human body through several pathways: firstly, with food; secondly, by the respiratory system; thirdly, by the skin; and finally, as a component of biomaterials.
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The cobalt ions enter the body through any of the abovementioned routes and bind with proteins within the bloodstream and get transported with blood to be deposited in tissues and cells. Vitamin B12, also known as cobalamin, is a water soluble vitamin and contains the biochemically rare element cobalt in the center of a planar tetrapyrrole corrin ring. Cyanocobalamin, the fourth vitamer of vitamin B12, can be metabolized in the body to an active coenzyme form and used in food supplements.
Erythropoietin, essential for formation of erythrocytes, stimulation is performed by vitamin B12 containing cobalt salts, and thus the deficiency of cobalt is strongly related to disturbances in vitamin B12 synthesis resulting in anemia and hypofunction of thyroid with increased risk of developmental abnormalities and failure in infants [ 59 ]. Apart from being an important constituent of these various forms of vitamin B12, the presence of cobalt is necessary for the efficient formation of amino acids and various proteins for myelin sheath generation.
Cobalt also plays a decisive role in generating neurotransmitters, which are requisite for proper operation of an organism. On the other hand, excess of cobalt ions within the body might increase the action of thyroid and bone marrow resulting in overproduction of erythrocytes, fibrosis in lungs, and asthma [ 60 ]. Cobalt, part of vitamin B12 also referred to as extrinsic factor, is essential for formation of erythrocytes.
Thus, the most well-known manifestation of cobalt deficiency in oral cavity is pernicious anemia which is characterized by glossitis, burning sensation, beefy red tongue present in the form of patches or completely red tongue which is also referred to as Hunters' or Moeller's glossitis, and rarely shallow ulcers [ 61 ].
Mineral Supplements for Beef Cattle | UGA Cooperative Extension
Apart from erythropoiesis, vitamin B12 also plays a significant role in nerve repair and regeneration. Hence, deficiency of cobalt can have adverse effects such as peripheral neuropathy. Lichen planus and oral lichenoid reactions have been linked to their exposure to Cr, Co, Ni, and amalgam alloys that are released from metal alloys commonly used in dentistry in the oral cavity.
These trace metals when released from the metal alloys come into direct contact with oral mucosa, leading to immune mediated damage of basal epithelial keratinocytes and subsequently inducing sensitivity reactions in the form of OLR. Some studies have linked OLR to risk of malignant transformation [ 62 ].
The total body content of chromium is relatively low and is about 0. Trivalent Cr is an essential trace element and plays an important role in glucose metabolism by serving as a cofactor for insulin action. Hexavalent chromium is a toxic industrial pollutant and has been classified as carcinogen possessing mutagenic and teratogenic properties. Chromium exposure through occupation via inhalation has been associated with various lung, GIT, and central nervous system cancers.
Chromium is excreted principally in the urine and faeces and in small quantities in the hair, sweat, and bile [ 63 ]. Chromium is an important trace element for overweight people as it is one of the key minerals in controlling blood sugar and lipid levels. Chromium [Cr III ] increases the efficacy of insulin and stimulating glucose uptake from the muscles and other tissues being the main ingredient of glucose tolerance factor GFT.
In case of low serum levels of chromium, the circulating level of GFT is also less, and, consequently, insulin is less effective in reducing blood sugar. As a result, high blood sugar stimulates further release of ineffective insulin [ 64 , 65 ]. Chromium is thought to repress p53, a tumor suppressor protein, whose inactivation through mutations is associated with many types of human cancers. Chrome ulcers, corrosive reactions on the nasal septum, acute irritation dermatitis, and allergic eczematous dermatitis have been reported among individuals exposed to hexavalent chromium compounds.
Industrial workers exposed to chromates have been documented to be at excessive risk of lung cancer. As chromium is present in very low amounts in the body, it is difficult to ascertain the deficient state. It is believed that if concentrations of chromium are lower than the normal value of 0. In spite of that, elevated plasma levels can coexist with a negative tissue balance. Hyperglycemia may be concomitant with raised plasma chromium and increased urinary excretion. The concentrations of chromium in urine, hair, and body fluids could not reflect the true chromium status of the body [ 65 ].
The role of chromium in OLR has been discussed earlier [ 62 ].
LIFESTYLE CHOICES THAT CONTRIBUTE TO MINERAL DEFICIENCY
Hyperglycemic status of diabetic patients in undiagnosed chromium deficient state may lead to a wide spectrum of oral manifestations noted in diabetics such as delayed wound healing, suppurative periodontitis, various oral fungal infections, premature periodontal diseases, and hyposalivation [ 66 ]. Selenium is a vital trace element which is an important component of the antioxidant enzymes such as glutathione peroxides and thioredoxin reductase [ 67 ].
The selenium salts required for various cellular functions inside the human body are toxic in excess amounts. Microorganisms reportedly have several selenium containing enzymes, and it is most likely that selenoproteins other than glutathione peroxidase remain to be discovered in higher animals.