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 Table of Contents  
REVIEW ARTICLE
Year : 2017  |  Volume : 7  |  Issue : 2  |  Page : 120-123

D-lightful therapy in prevention of periodontal disease


1 Division of Periodontics, Annamalai University, Chidambaram, Tamil Nadu, India
2 Division of Periodontia, RMDCH, Annamalai University, Chidambaram, Tamil Nadu, India
3 Division of Periodontics, RMDCH, Annamalai University, Chidambaram, Tamil Nadu, India

Date of Web Publication28-Dec-2017

Correspondence Address:
Dr. Ramaprabha Govindarajulu
c-13, Cavery Nagar, Mayiladuthurai, Nagapattinam - 609 003, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ijmd.ijmd_33_17

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  Abstract 


Vitamin D has been shown to regulate musculoskeletal health by mediating calcium absorption and mineral homeostasis. Studies have shown an association between alveolar bone density, osteoporosis, and tooth loss suggesting that low bone mass may be a risk factor for periodontal disease. An emerging hypothesis is that Vitamin D may be beneficial for oral health, not only because of its direct effect on bone metabolism but also due to its ability to function as an anti-inflammatory agent stimulating the production of antimicrobial peptides, thereby protecting the periodontium. Several recent reports demonstrate a significant association between periodontal health and the intake of Vitamin D. This review discusses the pharmacology behind Vitamin D supplementation, current literature concerning Vitamin D supplementation, and various supplementation options in the treatment of periodontal disease.

Keywords: Cholecalciferol; chronic periodontitis; ergocalciferol; Vitamin D deficiency; Vitamin D supplements


How to cite this article:
Govindarajulu R, Sree Shankar S L, Swaminathan S, Krishnan V. D-lightful therapy in prevention of periodontal disease. Indian J Multidiscip Dent 2017;7:120-3

How to cite this URL:
Govindarajulu R, Sree Shankar S L, Swaminathan S, Krishnan V. D-lightful therapy in prevention of periodontal disease. Indian J Multidiscip Dent [serial online] 2017 [cited 2019 Jul 21];7:120-3. Available from: http://www.ijmdent.com/text.asp?2017/7/2/120/221763


  Introduction Top


Chronic periodontitis is one of the most common chronic infectious diseases known to humans, characterized by the loss of periodontal attachment with a reported prevalence varying between 10%–60% in adults. Possible underlying mechanisms include decreased dietary quality and chronic inflammation.[1] One such dietary factor involved in periodontitis is Vitamin D deficiency. A variety of risk factors have been identified that modify the host response and thereby tip the biological balance from health to disease. These factors include genetic, environmental, and lifestyle/behavioral such as exercise, nutrition, and smoking. As Vitamin D plays a crucial role in bone maintenance and immunity, there is a biologic rationale to suspect that Vitamin D deficiency could negatively affect the periodontium.[2]

Oral epithelial cells are capable of converting inactive Vitamin D to the active form of 25-hydroxyvitamin D (25(OH)D), which has been shown to induce expression of the antimicrobial peptide LL-37 and other host defense mediators. This may represent a mechanism by which Vitamin D enhances innate immune defenses against periodontal pathogenic bacteria.[3] It also reduces the concentrations of matrix metalloproteinases and maintains oral health. Hypovitaminosis D is a risk factor for periodontal disease which meets the criteria for causality in a biological system proposed by Hill. The cross-sectional evidence for this association and for variation with Vitamin D polymorphisms supports the suggestion of causality, as do the results of the single randomized controlled trial of Vitamin D supplementation for periodontal disease. The fact that there are recognized mechanisms by which hypovitaminosis D can worsen the risks of gingival inflammation, worsen tissue destruction, increase bone loss, and reduce the efficiency of defensive mechanisms after bacterial infection and also supports the likelihood of causality.[4]

Vitamin D insufficiency affects almost 50% of the population worldwide. An estimated 1 billion people worldwide, across all ethnicities and age groups, have Vitamin D deficiency. It is also suggested to measure the serum 25(OH)D level as the initial diagnostic test in patients at risk for deficiency.[5] Treatment with either Vitamin D2 or Vitamin D3 is recommended for deficient patients to reduce periodontal problems.

Physiology of Vitamin D

Vitamin D is a group of fat-soluble secosteroids synthesized in the skin under the influence of ultraviolet (UV) light of the sun, or it is obtained from food, especially fatty fish. After hydroxylation in the liver into 25(OH)D and kidney into 1,25-dihydroxyvitamin D (1,25(OH)2D), the active metabolite can enter the cell, bind to the Vitamin D-receptor, and subsequently to a responsive gene such as that of calcium-binding protein. Vitamin D is primarily responsible for regulating the intestinal calcium absorption. With inadequate Vitamin D levels, calcium and phosphorus homeostasis becomes impaired. The body then responds by increasing the production and release of parathyroid hormone into the circulation. The increase in parathyroid hormone restores calcium homeostasis by increasing renal tubular reabsorption of calcium in the kidney, increasing calcium mobilization from the bone, and enhancing the production of 1,25(OH)2D.

Low intake of Vitamin D and calcium may lead to a negative calcium balance, thus causing a secondary release of calcium from bone, including the alveolar bone. In addition to its effect on skeletal homeostasis, Vitamin D has anti-inflammatory and antimicrobial effects, through modulation of inflammatory cytokine production by immune cells and by stimulation of secretion of peptides with antibacterial action, by cells of the monocyte-macrophage lineage.[6]

The inflammatory response leads to tissue destruction either by direct action of bacterial products or by activation of host defense cells and secretion of inflammatory mediators. These locally produced factors eventually result in connective tissue breakdown and bone loss through activation of osteoclast-mediated bone resorption. Vitamin D reduces the risk of periodontal disease and gingivitis by the induction of LL-37 and defensins. Polymorphisms of the Vitamin D receptor gene are also associated with periodontitis, alveolar bone loss, clinical attachment loss, and/or tooth loss.[7]

Causes of Vitamin D deficiency

Vitamin D deficiency are more common in children and aged persons, pregnant and nursing women, Obesity and due to lack of sun exposure, malabsorption, antiseizure medications, glucocorticoids, AIDS drugs, or antifungal drugs, reduced skin synthesis, sunscreen usage, traditional clothing, urbanization, reduced exercise.

Sources

  • Sunlight gives 90% of Vitamin D between 10 am to 3 pm. Exposure of the body in a bathing suit to 1 minimal erythemal dose (MED or the dose of radiation that causes a slight pinkness of the skin 24 h after exposure) equaling about 20,000 units. Thus, exposure of arms and legs to 0.5 MED approximates ingesting 3000 units of Vitamin D3
  • Dietary sources of vitamin D are milk, yogurt, butter, mushroom, fatty fish such as tuna, mackerel, and salmon. Foods fortified with Vitamin D, like some dairy products, orange juice, soy milk, and cereals, beef, liver, cheese, egg yolk
  • Vitamin D supplements: It is believed that for optimal health, in general, serum 25-hydroxyvitamin levels should be 75 nmol/L or higher and that likely a diet containing a minimum of 1,000 IU (25 ug) Vitamin D per day is required to achieve this level. Hence, if aiming for 1000 IU (25 ug) of Vitamin D through dietary sources, many glasses of milk and multiple servings of fish need to be consumed each day. Thus, supplements are warranted to help achieve these levels of Vitamin D.


Ideally, the desirable concentration of 25(OH)D for general health is ≥30 ng/ml and 20–30 ng/ml is considered as Vitamin D insufficiency. Level <20 ng/ml is generally considered as Vitamin D deficiency.

A recent meta-analysis by the Cochrane Database that Vitamin D comes in two forms:

  1. Ergocalciferol (Vitamin D2)
  2. Cholecalciferol (Vitamin D3).


According to the latest research, D3 is approximately 87% more potent in raising and maintaining Vitamin D concentrations and produces 2- to 3-fold greater storage of Vitamin D than does D2.

Various forms of Vitamin D

Depending on the disease status, age, and severity of the deficiency, Vitamin D dosage is calculated and various forms are provided. Traditional multivitamins contain about 400 IU of Vitamin D, but many multivitamins now contain 800–1000 IU. A variety of options are available for individual Vitamin D supplements, including capsules, injections, chewable tablets, liquids, drops, granules, and transdermal cream.

A randomized controlled pilot study using oral Vitamin D3 cream found that it is as effective as capsule supplementation at increasing total 25(OH)D concentrations in the healthy, adult population.[8] Single annual “megadose” or stoss therapy of Vitamin D (e.g., 100,000, 300,000, 600,000 IU) also normalizes Vitamin D in deficient patients. Diamond et al. showed that an annual IM injection of 600,000 IU cholecalciferol was safe and resulted in the normalization of 25(OH)D levels in all the participants and remained above 50 nmol/L throughout the study.[9]

Marwaha et al. mentioned that based on the results of studies, a regular supplementation of at least 2000 IU/day Vitamin D is required to maintain normal Vitamin D levels. This study also highlighted the inadequacy of a daily Vitamin D intake of 200–400 IU in normalizing serum 25(OH)D. Recent clinical practice guidelines also recommend 50,000-70,000 IU/week Vitamin D oral supplementation for 8 weeks in case of Vitamin D deficiency. The guidelines also recommend maintaining 25(OH)D blood levels with daily 1500–2000 IU Vitamin D supplementation.[10]

Recommended daily dietary allowance for Vitamin D level of Vitamin D intake for men and women over age 30 are the following:

  • 31–50 years 200 IU (5 ug)
  • 51–70 years 400 IU (10 ug)
  • >70 years 600 IU (15 ug).


Vitamin D toxicity is rare and occurs at levels of 500 nmol/L or higher. Toxicity is associated only with excessive supplemental intake (usually well above 20,000 IU/day). Vitamin D hypersensitivity syndromes are often mistaken for Vitamin D toxicity. The most common is primary hyperparathyroidism. Granulomatous diseases, such as sarcoidosis, granulomatous TB, and some cancers also cause Vitamin D hypersensitivity as the granuloma or the tumor may make excessive amounts of calcitriol, thus raising serum calcium levels.

Drug interactions

Aluminum or magnesium-containing antacids, anticonvulsants (e.g., carbamazepine), antiretrovirals (AIDS therapies), barbiturates (e.g., phenobarbital, phenytoin), cholestyramine and colestipol (anticholesterol agents), St. John's wort, corticosteroids and glucocorticoids, hydroxychloroquine, and digitalis/digoxin interact with Vitamin D metabolism and care should be taken while prescribing these drugs.[11]


  Vitamin D Supplements and Periodontal Health Top


Krall et al. conducted 3-year, randomized, placebo-controlled trial of the effect of calcium and Vitamin D supplementation on bone loss in 145 healthy participants aged 65 years and older and concluded that calcium and Vitamin D intake has a beneficial effect on tooth retention.[12]

Bischoff-Ferrari et al. concluded that Vitamin D intake above current recommendations may be associated with better health outcomes. For all end points, the most advantageous serum concentrations of 25(OH)D begin at 75 nmol/L (30 ng/mL), and the best are between 90 and 100 nmol/L (36–40 ng/mL). A comparison of Vitamin D intake with achieved serum concentrations of 25(OH)D for the purpose of estimating optimal intake suggested that, for bone health in younger adults and all studied outcomes in older adults, an increase in the currently recommended intake of Vitamin D is warranted. An intake for all adults of >1000 IU (25 μg) is needed to bring Vitamin D concentrations in no <50% of the population up to 75 nmol/L.[13]

Miley et al. conducted a cohort study in 51 participants receiving periodontal maintenance therapy. Of these, 23 were taking Vitamin D (≥400 international units/day) and calcium (≥1000 mg/day) supplementation and 28 were not taking such supplementation. Relative to participants who did not take Vitamin D and calcium supplementation, supplement takers had shallower probing depths, fewer bleeding sites, lower gingival index values, fewer furcation involvements, less attachment loss, and less alveolar crest height loss.[14]

Bashutski et al. assessed outcomes of periodontal surgery in Vitamin-D-sufficient and insufficient individuals and concluded that Vitamin D deficiency at the time of periodontal surgery negatively affects treatment outcomes for up to 1 year. Analysis of these data suggests that Vitamin D status may be critical for postsurgical healing.[15]

McMahon et al. conducted studies and found human gingival epithelial cells produce peptides, such as β-defensins and the cathelicidin LL-37, that are both antimicrobial and that modulate the innate immune response. In myeloid and airway epithelial cells, the active form of Vitamin D3(1,25(OH)2D3) increases the expression and antibacterial activity of LL-37. Incubation of three-dimensional cultures with 1,25(OH)2D3 led to an increase in antibacterial activity against the periodontal pathogen aggregatibacter actinomycetemcomitans when the bacteria were added to the apical surface. This study was the first to demonstrate the effect of Vitamin D on antibacterial defense of oral epithelial cells, suggesting that Vitamin D3 could be utilized to enhance the innate immune defense in the oral cavity.[16]

Boggess et al. conducted a case–control study and examined the relationship between maternal Vitamin D status and periodontal disease. Vitamin D insufficiency (serum 25(OH)D <75 nmol/l) is associated with maternal periodontal disease during pregnancy. Vitamin D supplementation represents a potential therapeutic strategy to improve maternal oral health.[17]

A pilot study done in Puerto Rican adults confirms that low Vitamin D status strongly associated with periodontitis.[18] Dietrich et al. found that optimal ranges of serum Vitamin D may reduce susceptibility to gingival inflammation and that gingivitis may be a useful clinical model to evaluate the anti-inflammatory effects of Vitamin D. More recent randomized clinical trial of Hiremath showed that Vitamin D has a dose-dependent anti-inflammatory effect on gingivitis.[19]

Antonoglou et al. in a prospective study showed a positive association between the serum 1,25(OH)D and periodontal health in type I diabetic patients.[20]


  Conclusion Top


Vitamin D insufficiency is a common problem in especially those who have chronic illness and who are malnourished, limited geographically to the amount of sun exposure, as well as those with darker skin, and on chronic medications. Hypovitaminosis D resulting from lack of UVB exposure is not easily corrected by dietary intake alone in the absence of supplementation. Supplementation with 800–1000 IU/d of Vitamin D or 50,000 IU monthly is safe for most people and can ensure levels of Vitamin D within the optimal range. This intake is within the currently recommended safe upper tolerable limit for Vitamin D of 2000 IU/d for those aged 1 year and older. Dr. Vieth, an Vitamin D researcher and scientist, points out, “Worrying about Vitamin D toxicity is like worrying about drowning when you are dying of thirst. He and his colleagues have expressed frustration with the currently recommended intakes of Vitamin D and stated that there is a need to recommend intakes that are effective in reducing disease. However, more research is needed concerning the goals of Vitamin D therapy and dosing and to evaluate the efficacy of Vitamin D supplementations in prevention of periodontal disease.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Chapple IL. Potential mechanisms underpinning the nutritional modulation of periodontal inflammation. J Am Dent Assoc 2009;140:178-84.  Back to cited text no. 1
    
2.
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3.
Diamond G, Yim S, Rigo I, McMahon L. Measuring antimicrobial peptide activity on epithelial surfaces in cell culture. Methods Mol Biol 2010;618:371-82.  Back to cited text no. 3
    
4.
Grant WB, Boucher BJ. Are hill's criteria for causality satisfied for Vitamin D and periodontal disease? Dermatoendocrinol 2010;2:30-6.  Back to cited text no. 4
    
5.
Holick MF. Vitamin D deficiency. N Engl J Med 2007;357:266-81.  Back to cited text no. 5
    
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Bikle DD. Vitamin D and the skin: Physiology and pathophysiology. Rev Endocr Metab Disord 2012;13:3-19.  Back to cited text no. 6
    
7.
Wang HY, Pan YP, Teng D, Zhao J, Lin L. The relativity between chronic periodontitis and the genetic polymorphisms of Vitamin D receptor and estrogen receptor. Zhonghua Kou Qiang Yi Xue Za Zhi 2008;43:236-9.  Back to cited text no. 7
    
8.
Sadat-Ali M, Bubshait DA, Al-Turki HA, Al-Dakheel DA, Al-Olayani WS. Topical delivery of Vitamin D3: A randomized controlled pilot study. Int J Biomed Sci 2014;10:21-4.  Back to cited text no. 8
    
9.
Diamond TH, Ho KW, Rohl PG, Meerkin M. Annual intramuscular injection of a megadose of cholecalciferol for treatment of Vitamin D deficiency: Efficacy and safety data. Med J Aust 2005;183:10-2.  Back to cited text no. 9
    
10.
Pravina S, Sudhindra K, Narayani S. Prevalence study of Vitamin D deficiency and to evaluate the efficacy of Vitamin D3 granules 60,000 IU supplementation in Vitamin D deficient apparently healthy adults. Indian J Clin Pract 2013;23:827-32.  Back to cited text no. 10
    
11.
Tsai HH, Lin HW, Simon Pickard A, Tsai HY, Mahady GB. Evaluation of documented drug interactions and contraindications associated with herbs and dietary supplements: A systematic literature review. Int J Clin Pract 2012;66:1056-78.  Back to cited text no. 11
    
12.
Krall EA, Wehler C, Garcia RI, Harris SS, Dawson-Hughes B. Calcium and Vitamin D supplements reduce tooth loss in the elderly. Am J Med 2001;111:452-6.  Back to cited text no. 12
    
13.
Bischoff-Ferrari HA, Giovannucci E, Willett WC, Dietrich T, Dawson-Hughes B. Estimation of optimal serum concentrations of 25-hydroxyvitamin D for multiple health outcomes. Am J Clin Nutr 2006;84:18-28.  Back to cited text no. 13
    
14.
Miley DD, Garcia MN, Hildebolt CF, Shannon WD, Couture RA, Anderson Spearie CL, et al. Cross-sectional study of Vitamin D and calcium supplementation effects on chronic periodontitis. J Periodontol 2009;80:1433-9.  Back to cited text no. 14
    
15.
Bashutski JD, Eber RM, Kinney JS, Benavides E, Maitra S, Braun TM, et al. The impact of Vitamin D status on periodontal surgery outcomes. J Dent Res 2011;90:1007-12.  Back to cited text no. 15
    
16.
McMahon L, Schwartz K, Yilmaz O, Brown E, Ryan LK, Diamond G, et al. Vitamin D-mediated induction of innate immunity in gingival epithelial cells. Infect Immun 2011;79:2250-6.  Back to cited text no. 16
    
17.
Boggess KA, Espinola JA, Moss K, Beck J, Offenbacher S, Camargo CA Jr., et al. Vitamin D status and periodontal disease among pregnant women. J Periodontol 2011;82:195-200.  Back to cited text no. 17
    
18.
Abreu OJ, Tatakis DN, Elias-Boneta AR, López Del Valle L, Hernandez R, Pousa MS, et al. Low Vitamin D status strongly associated with periodontitis in Puerto Rican adults. BMC Oral Health 2016;16:89.  Back to cited text no. 18
    
19.
Hiremath VP, Rao CB, Naik V, Prasad KV. Anti-inflammatory effect of Vitamin D on gingivitis: A dose-response randomised control trial. Oral Health Prev Dent 2013;11:61-9.  Back to cited text no. 19
    
20.
Antonoglou G, Knuuttila M, Niemelä O, Hiltunen L, Raunio T, Karttunen R, et al. Serum 1,25(OH)D level increases after elimination of periodontal inflammation in T1DM subjects. J Clin Endocrinol Metab 2013;98:3999-4005.  Back to cited text no. 20
    




 

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