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 Table of Contents  
REVIEW ARTICLE
Year : 2012  |  Volume : 3  |  Issue : 4  |  Page : 257-263

Alcohol and periodontal health in adolescence


1 Department of Biochemistry, MN DAV Dental College and Hospital, Solan, Himachal Pradesh, India
2 Department of Periodontics, MN DAV Dental College and Hospital, Solan, Himachal Pradesh, India
3 Department of Pedodontics, MN DAV Dental College and Hospital, Solan, Himachal Pradesh, India

Date of Web Publication12-Jul-2013

Correspondence Address:
Ranjan Katyal
Department of Biochemistry, MN Dav Dental College and Hospital, Solan, Himachal Pradesh - 173 223
India
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DOI: 10.4103/0976-433X.114973

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  Abstract 

Alcohol is considered to be a major cause of morbidity and mortality in adults in most parts of the world. Ethanol, the most common hepatotoxin, can injure the liver cells directly or through its toxic metabolites i.e., acetaldehyde and free radicals. Its effect begins on its exposure to oral mucosa, but liver is the main site for its metabolism and not surprisingly its toxicity. Besides promoting the formation of reactive oxygen species and reactive nitrogen species, long-term ethanol ingestion might deplete the hepatocyte of some important secondary component of the antioxidant defense system. Thus, alcohol and its metabolites tip the balance between the oxidative stress and the antioxidant defense system toward the net oxidant excess, which seems to be one of the contributing factors in the pathophysiology of periodontitis, oral cancer besides alcohol-induced liver disease.

Keywords: Alcohol, alcoholic liver disease, oxidative stress, periodontitis


How to cite this article:
Katyal R, Saroch N, Bharat Bhushan A K. Alcohol and periodontal health in adolescence. SRM J Res Dent Sci 2012;3:257-63

How to cite this URL:
Katyal R, Saroch N, Bharat Bhushan A K. Alcohol and periodontal health in adolescence. SRM J Res Dent Sci [serial online] 2012 [cited 2019 Sep 21];3:257-63. Available from: http://www.srmjrds.in/text.asp?2012/3/4/257/114973


  Introduction Top


Alcohol is the most commonly used beverage worldwide and is considered a socially acceptable toxin. At present, except for the control of alcohol abuse, these are no effective modality of either prevention or treatment alcohol is one of the largest health problems in the United States. [1] There are approximately 10 million alcoholics in America and alcoholism alone leads to over 200,000 deaths per year, requiring over 12 million dollars annually in medical expenditures. [2] According to WHO statistics, mortality rates were 7.5/1,00,00 in Finland and 57.2/100,000 in France and corresponding per capita alcohol consumption were 5.1 and 16.8 g of absolute alcohol, respectively. [3] Much of this alcohol-related morbidity and mortality is due to alcohol-induced liver disease [ALD (directly)], periodontitis, and cancer (indirectly), as the association between chronic alcoholism and cirrhosis of liver is a well-established clinical manifestation. Alcohol is considered as the etiological agent in the overwhelming majority of the fatal cases. [4],[5] Periodontitis is widely occurring chronic disease. It is a bacterial infection that causes the destruction of the supporting structures of the teeth. If it is not treated, it will lead to tooth loss. [6],[7],[8] This review is intended to provide the nomenclature, mechanisms of actions, features, and sources of most common free radicals and reactive oxygen species, as well as analyzed the typical biological targets for oxidative damage and is based on a review of direct and indirect antioxidant host defenses, particularly in relation to effect of alcohol in periodontal disease.


  Biochemical Alterations Top


[Table 1]

The metabolic and cellular effects of ethanol and its metabolites include impairment of mitochondrial oxidative phosphorylation, enzyme inhibition, impairment of microtubular protein export, enhanced free radical production and lipid peroxidation, interference with removal of toxic lipid aldehydes due to decreased glutathione (GSH) functions. [9] Biochemically, increased levels of γ-glutamyl transferase, carbohydrate deficient transferrin, immunoglobulin IgA, lactate, acetate, uric acid, and triacylglycerol and reversal of ALT to AST ratio are observed in ALD. There are other markers with considerable potential for more accurate reflection of recent alcohol intake such as urinary ratio of serotonin metabolites i.e., 5-hydroxytryptophol, 5-hydroxyindol-3-acetic acid, β-hexoaminidase, plasma levels of very low-density lipoproteins-cholesterol and high-density lipoprotein cholesterol. [10] Chronic alcohol consumption also increases cholesterol content of liver plasma membrane fractions due to adaptations. [11] In addition, changes in cytochrome a and b, succinic dehydrogenase and cytochrome oxidase may also be observed. [12] Alteration of the hepatocytes redox homeostatis gives rise to a number of metabolic disorders that include lactic acidosis, hyperlipidemia, hyperuricemia, and hyperinsulinemia. It is well documented, that ethanol metabolism impairs the regenerative capacity of the liver. Therefore, it appears that ethanol oxidation not only results in hepatotoxicty, but also impairs the ability of liver to respond to the toxic assault. Alcohol consumption is associated with impaired barrier function of the intestinal mucosa in nutrients with ALD. Increased concentration of lipopolysaccharide (LPS) in the blood and its decreased clearance is considered a good marker of intestinal mucosal dysfunctions. People with gingivitis had low levels of prostaglandin E2 in gingival crevicular fluid (CF-PGE2), while people with periodontitis had higher CF-PGE2 levels. Gingivitis is a precursor to periodontitis. PGE2, an inflammatory biomarker, can differentiate between these two conditions. [13]
Table 1: ALD: Biochemical alterations and clinical manifestations

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  Risk Factors Top


The individual susceptibility to develop ALD also depends on many other factors like consumption of alcohol, genetics, and nutrition. [14] It has been well documented that ALD results from the dose-dependent and tissue-dependent consumption of alcohol. The disease process is characterized by early steatosis, inflammation, and necrosis (often knows as steatohepatitis), as in some individuals ultimately it progresses to fibrosis and cirrhosis. The assertion that women are more susceptible to ALD is supported by several studies. This is partly due to lower body weight and to their higher body fat content which results in lower body water distribution and consequently in a higher level of blood and organ alcohol compared to males. [15] Only 10-30% of heavy persistent drinkers develop cirrhosis, although well over 50% may have fatty liver. Under-nutrition and direct alcohol toxicity are also known to synergistically increase the likelihood of liver damage. Nutritional deficiencies of protein may promote toxic effects of alcohol by depleting hepatic amino acids and enzymes. Alcohol may also increase the minimum daily requirements of choline, folic acids, and other vital nutrients. [16] Amaral et al. after identifying 1530 papers concluded that alcohol consumption can be considered a risk indicator for periodontitis. [17] Studies on alcohol dependence have been reported to have positive associations between alcohol intake and periodontitis, where confounding effect of dental plaque was taken into account. There is evidence to suggest alcohol consumption is a risk indicator for periodontitis. Occurrence of periodontitis among alcohol users was found to be high and the frequency of alcohol consumption increased the odds of periodontitis incrementally mainly in smokers. [18] Alcohol may increase periodontal-disease risk in several ways: By decreasing the ability of neutrophils to fight infection; interfering with the clotting mechanism; decreasing the formation of new bone, and causing deficiencies in vitamin B complex and protein, components necessary for healing. [19] Factors that influence the progression of periodontitis, include individual characteristics, social and behavioral factors, genetics, tooth factors, bacterial composition of the biofilm around the tooth, and excessive alcohol intake. [20]

Metabolism of alcohol

Hepatocytes possess three pathways for ethanol metabolism situated in different subcellular compartments [Figure 1]. The oxidation of ethanol (low ethanol concentration) to acetaldehyde by ADH is the major pathway resulting in increased the formation of NADH. The rate of NADH production exceeds its rate of oxidation leading to an increase in NADH/NAD + ratio [Figure 1]: Step 1], thereby, resulting in reduction of hepatic gluconeogenesis, the decrease in citric acid cycle activity and impairment of fatty acid oxidation.
Figure 1: Alcohol metabolism and its subsequent effects

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However, ethanol oxidation at high concentration is brought about by the cytochrome P 450 (cyt P 4502E1 ) dependent microsomal ethanol oxidizing system (MEOS). After chronic alcohol consumption there is an increase in the activity of MEOS which involves specific cytochrome P 450 (CYP 4502FI ). [21] The third pathway for ethanol metabolism utilizes catalase that is capable of oxidizing ethanol in the presence of hydrogen peroxide (H 2 O 2 ). This system involves the oxidation of hypoxanthine and NADPH by xanthine oxidase and NADPH oxidase, respectively, and makes H 2 O 2 available for oxidation of alcohol. Regardless of the pathway, acetaldehyde is the first major specific oxidation product of ethanol and under normal conditions, acetaldehyde itself is oxidized rapidly by aldehyde dehydrogenase [22] to acetate [Figure 1]: Step 2]. Increased blood acetate in the presence of ethanol indicates metabolic tolerance to alcohol and can be used as a laboratory marker of alcoholism and heavy drinking. [23]

Formation of peroxidants

Although there is clear evidence that the pro-oxidant formation is dependent on the production of O 2.- ; however, the presence of this radical alone is not sufficient to explain the oxidative damage caused by alcohol. Of the superoxide-derived pro-oxidants that can be formed in vivo, O 2.- is believed to play a central role in alcohol-induced liver injury. The reason for this assumption are two-fold first, O 2 .- is a product of normal cellular metabolism; second, many other oxidants in vivo are derived from O 2 .- . Instead of being a direct oxidant, O 2 .- is more likely to react through many catalytic pathways in the cell to produce more potent oxidants. For instance, the reduction of O 2 .- by the two isoforms of superoxide dismutase (SOD) forms H 2 O2. H 2 O2 can lead to the formation of hydroxyl-free radicals (OH . ) via transition metal catalyzed Fenton reaction or via Haber Weiss reaction with O2 .- . Alternatively, H 2 O2 can react Cl - via myeloperoxidase in neutrophils to produce hypoclorous acid (HOCl - ). An additional pathway of O2 .- dependent oxidative stress involves the enzyme-independent reaction of O2 .- with nitric oxide (NO) to form peroxynitrite (ONOO - ). [Figure 1] is a schematic depiction of these potential pathways of oxidant formation in liver after alcohol consumption. All of the above-mentioned pathways form pro-oxidants with the sufficient redox potential to lead to the formation of L-hydroxyethyl radical. Furthermore, because radicals often imitate chain reaction in vivo, other pro-oxidants that are not derived directly from O2 .- may nevertheless be dependent on O2 .- production (e.g., peroxyl radicals). Therefore, it is reasonable to speculate that O2 .- appears to be a key starting point of oxidative stress during alcohol exposure.

Acetaldehyde is a reactive compound that readily forms covalent bonds with functional groups of biologically important compounds. Formation of acetaldehyde adducts with proteins, amino acids, nucleotides, and phospholipids in liver and blood has been demonstrated [Figure 1]: Step 3]. Such adducts may provide a marker for past drinking activity of an individual, just as hemoglobin A1c has proved useful as an index of blood glucose control in diabetic patients. [24] It has been documented that ethanol-specific CYP4502E1 generates higher amounts of reactive oxygen species (ROS) than the other forms. The NADPH-dependent electron transfer in microsomes is associated with the generation of O 2 and H 2 O2 . radicals. Both these radicals in presence of iron, produce other ROS such as hydroxyl (OH . ) and other oxidants capable of producing lipid per-oxidation. [25],[26] The increased NADH/NAD + ratio favors the formation of ROS as a result of (i) increased electron flow in mitochondria, (ii) increased production of super oxide and H 2 O 2 , (iii) increased release of iron from the cellular reservoir resulting in iron-catalyzed free-radical generation, and (iv) increase the relative activity of xanthine oxidase and myeloperoxidases with subsequent increase capacity to generate toxic oxygen species. The oxidative stress thus produced results in the per-oxidation of accumulated free fatty acids and lipid in alcoholics. [27],[28] There is an additional pathway of O 2 -dependent oxidative stress which involves the enzyme-dependent reaction of O 2 with nitric oxide (NO) to form peroxynitrite (ONOO . ) another strong oxidizing and nitration species. Similar to O 2 for ROS, it is likely that NO serves as the parent molecule for other RNS in vivo e.g., 3-nitrotyrosine and nitrosation reactions (e.g., nitrosorthiol formation) during alcohol exposure. Reactive intermediates formed during ONOO . degradation also causes one electron oxidation reaction with ethanol leading to the promotion of hydroxyethyl radicals.

After the formation of first stable product of ethanol metabolism, acetaldehyde, an imbalance between its production and disposition, results. This leads to tremendous increase in hepatic venous blood reflecting its high tissue levels. [29] Metabolism of excess acetaldehyde by alternative pathway such as aldehyde oxidase and xanthine oxidase may play a role in ethanol-induced free-radical injury by generating H 2 O 2 and O 2 radicals. [30] Besides, acetaldehyde also promotes lipid peroxidation and GSH depletion, probably by inhibiting its synthesis [Figure 1]: Step 5].

Metabolism of ethanol and acetaldehyde is associated with the generation of neutrophiles chemoattractants [Figure 1]: Step 4]. Activated tissue neutrophiles further contribute to tissue oxidative injury by releasing O 2 radicals. The membrane vesicles, altered by the exposure to acetaldehyde, lead to increased O 2 production by neutrophiles suggesting immunological activation in periodontitis. [31] Electron transport in the respiratory chain (mitochondria), where 1-2% of O 2 is consumed, is relatively univalent to O 2 radical. Generation of ROS in the cells can be either deliberate or accidental and are also known to be generated during auto-oxidation of thiols, impact of irradiation, Fenton and Haber-Weiss reactions catalyzed by loosely bound transition metals, xenobiotics metabolism, prostaglandin and leukotrine synthesis via cyclooxygenase and lipoxygenase pathway. [32],[33] Another important factor in the development of ALD is over production of tumor necrosis factor (TNF-α), a cytokine that results in cytotoxicity. [34] During its cytotoxic effects, there is over production of free radicals and uncontrolled ROS along with IL-1, IL-6, and chemokines. Studies demonstrate that production of ROS by TNF-α originated from mitochondria and they participate and cause the imitation and propagation of peroxidative phenomena [35] escalating damage to parenchyma cells. This results in the expression of genes including TNF and other promoting factors such as cytokine-induced neutrophiles chemoattractant and IL-8 through activation of oxidative stress responsive transcription factor (NF-κB) that accelerates cell damage. The existence of pro-inflammatory state is characterized by increase in inflammatory mediators such as TNF-α, which then leads to increase in oxidative stress. [36] Oxidative stress was also observed in patients with periodontitis which could be closely linked to biomarkers of inflammation that may be mediated by C-reactive protein levels. An alternative mechanism could be an association between measures of periodontitis, systemic dissemination of bacteria, and subsequent oxidative damage at various sites in the host, resulting in oxidative stress. [37] Experimental evidence was emerged to implicate bacterial plaque deposits as the primary factor initiating periodontitis. Specific bacteria and immunoinflammatory mechanisms were differentially implicated in the disease. [8] In the mid-1990s, early insights about complex diseases, such as periodontitis, led to new conceptual models of the pathogenesis of periodontitis. Those models included the bacterial activation of immunoinflammatory mechanisms, some of which targeted control of the bacterial challenge and others that had adverse effects on bone and connective tissue remodeling. Such models also acknowledged that different environmental and genetic factors modified the clinical phenotype of periodontal disease. Thus, there are multiple processes promoting the formation of toxic oxygen and nitrogen species, suggesting that oxidative stress contribute significantly to the pathophysiology of periodontitis, cancer, and ALD. [25],[26],[27],[28]

The antioxidant defense systems

The body has several endogenous antioxidant (AOD) systems to combat with ROS and NOS. Primary antioxidants include enzymes such as superoxide dismutase (SOD), glutathione peroxidase (GPx), and metal-binding proteins such as ferrtin, ceruloplasmin and transferrin. They prevent the formation of new free radical species. Secondary antioxidants are tocopherol, ascorbate, beta-carotene, uric acid, bilirubin, and albumin. Tertiary antioxidants are DNA repair enzymes and methionine sulfoxide reductase. Besides, AOD include auxiliary antioxidant present in the biological systems which indirectly neutralize free-radicals and maintain the functional integrity of antioxidants systems. Glucose-6 phosphate dehydrogenase, glutathione reductase (GR), and glutathione-S transferase (GST) enzymes fit in this group. [38] In addition, there are nonenzymatic auxiliary antioxidants like sulfydryl proteins and 3-OH- anthranilic acid which alleviate oxidative stress. Metals like iron, zinc, selenium, and copper also make a major contribution to the genesis and detoxification of free radicals. [39]

VANCOUVER, British Columbia - Oral biologists from the University at Buffalo School of Dental Medicine have shown for the first time that heavy alcohol consumption or a diet low in antioxidant vitamins can increase the risk of developing gum disease. Low levels of most antioxidants are a risk factor for periodontal disease and infection. Free radicals are released as a result of bacteria clearance and killing. Periodontal tissue depends on natural antioxidants to overcome this oxidative stress and maintain homeostasis. When antioxidants are depleted, the ability of gum tissue to overcome oxidative stress, maintain normal tissue, and control the bacterial damage appears to be compromised. [19]

Oxidative stress

The various pathological changes caused by oxidative stress have been reported in diarrhea, [40],[41] smoking, [42] malnutrition, [43] aluminum toxicity with its possible role in Alzheimer's disease, [44] anti-tuberculosis therapy, [45] hyper homocystinuria-induced cardiovascular diseases, [38] and sickle cell disease. [46] Recent studies demonstrate the link between periodontitis to some of these diseases such as diabetes, rheumatoid arthritis, and cardiovascular diseases. [47],[48] There is clear evidence that pro-oxidant formation is dependent on the production of O2 during diseases. The presence of this radical alone is not sufficient to explain the oxidative stress. There is relative excess of free radicals and/or insufficient antioxidants. The most important AOD to mention here is the depletion of mitochondrial GSH. [49] There is strong correlation between injury due to O2 - and the levels of SOD, an enzyme that reduces O 2 to H 2 O 2 in ALD. Levels of SOD correlated inversely with pathological changes in the central alcohol exposure in ALD. In recent years, oxidative stress has also been implicated in the pathophysiology of periodontitis. [31] Generalized aggressive periodontitis subjects are characterized by a higher IL-1β/IL-10 ratio than are periodontally healthy subjects, suggesting an imbalance between pro- and anti-inflammatory cytokines in generalized aggressive periodontitis. IL-10 is also associated with periodontal health and seems to be a regulator of inflammation and alveolar bone loss in periodontal diseases. It might be involved in controlling the inflammatory process at periodontally healthy sites. [50]

Ethanol intoxication also leads to an increased ratio between pro-oxidants and might as well be responsible for the increased oxidative stress. [40] One of the mechanisms by which oxidative stress causes cellular injury is by chemical modification of biologic molecules. These modifications can alter and/or interfere with normal biological processes and be toxic directly to the cell. The host immune response may also be stimulated which may cause an anti-immune-like disease in human alcoholics. It is clear that pro-oxidant can mediate and/or amplify their signal by modifying signaling cascades within the cell which include intracellular Ca, stress-activated protein kinases, transcription factors (NF-κB) and modulators of apoptosis signaling (e.g., capases, Bel-2). [48] However, whether oxidative stress is the dominant pathway of activation of these kinase cascades by ethanol remains unclear and requires further study. The concept of priming and sensitization of inflammatory cells by alcohol administration may be another way to explain how oxidative stress is responsible for ALD. There may be a series of sequential events during alcohol exposure which lead to more robust cell-killing response that is exacerbated in sensitized hepatocytes. Despite plausible mechanisms, information relating alcohol consumption to periodontitis risk is sparse. Previous studies and case controlled reports have shown positive association between alcohol use and periodontal disease. [51],[52] Low levels of most antioxidants are a risk factor for periodontal disease and infection. Free radicals are released as a result of bacteria clearance and killing. Periodontal tissue depends on natural antioxidants to overcome this oxidative stress and maintain homeostasis. When antioxidants are depleted, the ability of gum tissue to overcome oxidative stress, maintain normal tissue, and control the bacterial damage appears to be compromised. [53] Physiological alteration and pathological status, directly or indirectly produced by ROS actions, depend on disequilibrium between increased free radical production and decreased antioxidant levels. Such conditions usually lead to impairment of part or all of the antioxidant defense system and to the appearance of biological damage. There is evidence that something similar takes place in periodontitis too. [54] Regarding the oxidative stress markers found in periodontitis, individuals with periodontal disease exhibit a significant increase in the activities of oxidative stress markers. The increase in glutathione peroxidase may represent possible antioxidant compensation in detoxification reactions of organic peroxides produced during oxidative stress in gingival tissue. Since glutathione S-transferase (GST) has a direct role in the neutralization of hydroperoxides derived from the lipoperoxidation processes, increases in GST activities are probably related to the oxidative stress caused by the periodontal inflammatory process. A significant increase in oxidized glutathione (GSSG) concentrations and myeloperoxidase activity have been detected in periodontitis patients, which are clear biomarkers of oxidative stress detected in inflammatory processes linked to periodontitis. Tissue lipoperoxidation, measured as thiobarbituric acid reactive substances, seems to increase in the gingival tissue of periodontitis. [55]

Antioxidant therapy

Extensive research has been done to understand the mechanisms of tissue injury, but it has yet to be translated into a universally accepted antioxidant therapy. The focus till date is on the role of oxidants in early stages of the disease. It involves simultaneous administration of antioxidants with ethanol. Data suggests that cytokines may influence lipid metabolism both in liver and periphery by inhibiting the β-oxidation of fatty acids. Treatment with antioxidants such as overexpression of SOD, polyphenolic extracts, diphenyleneinodium, triglycerides, allopurinol, and ebselen prevent the accumulation of lipid droplets in cells. [56] Antioxidants such as vitamins C and E and other agents have been used that enhance antioxidant capacity to attenuate alcohol-induced effects. [57] Drugs that prevent their formation or limit their damaging potential to the cell should be used. S-adenosyl methionine and polyenylphosphatidylcholine were used recently to replenish the GSH pools of body, correcting the alcohol-induced oxidative stress. [9] Patients with ALD are usually malnourished, so high protein and low fat intake is recommended to stop progression of periodontitis and cancer.

Severe cases of ALD have also been benefited from corticosteroids. Treatment with N-acetylcysteine significantly inhibits hepatic lipid per-oxidation, [12] TNF-α production, steatosis, and prevents alcohol-induced necrotic cell death in liver. [35] A recent advance shows that some classic antioxidants may mediate protection in vivo, not by directly scavenging pro-oxidants per se, but by stimulating intrinsic antioxidant production through activation of the antioxidant response element on genes. [58] A great number of studies have focused on molecules that can reduce oxidative stress. Tetracycline has been found to be as useful in combating oxidative stress in periodontitis and metabolic disorders. In fact, in addition to its antimicrobial effect, it shows antioxidant, anti-inflammatory, proanabolic, immunomodulatory, angiogenetic, and antiapoptotic effects. [59] Thymoquinone has also demonstrated a variety of pharmacologic properties, including antihistaminic, antibacterial, antihypertensive, hypoglycemic, anti-inflammatory, and antioxidative activities. Through its anti-inflammatory and antioxidant properties, thymoquinone seems to play an important role in preventing periodontal diseases. [60]

After reviewing the searched articles, we bring to light various risk factors in alcoholism and further how it affects periodontal health. Origin of different types of free radicals/ROS and antioxidants systems with alcohol seem to be the prime factor in etiopathogenesis of periodontitis. The disturbance in equilibrium is due to increased free radicals and decreased antioxidants which might have an additive affect, increasing the severity of periodontal tissue damage. This opens the Pandora box for researchers to come up with an appropriate diet therapy for prevention and treatment of chronic periodontitis.


  Acknowledgment Top


Assistance by Dr. Vijay Kumar, Reader, Prosthodontics, MN DAV Dental College, Solan in preparation of this review article is acknowledged.

 
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