The Role of Nutrition in the Management of Osteoporosis and Periodontal Diseases
Explore the connection between osteoporosis and periodontal diseases, highlighting the role of nutrition in preventing bone loss.
This course was published in the October/November 2024 issue and expires November 2027. The author has no commercial conflicts of interest to disclose. This 2 credit hour self-study activity is electronically mediated.
AGD Subject Code: 150
EDUCATIONAL OBJECTIVES
After reading this course, the participant should be able to:
- Discuss the relationship between osteoporosis and periodontal diseases.
- Identify the role of nutrition in the development and management of osteoporosis.
- Describe the association between osteoporosis and osteonecrosis of the jaw.
An age-related disease, osteoporosis is highly prevalent and results in serious effects on health and quality of life. In the United States, 10 million individuals have osteoporosis and another 34 million have low bone mass (osteopenia). Approximately 80% of individuals with osteoporosis are women. One in four men older than age 50 is also affected by the disease.1
Osteoporosis usually goes undetected until pain or spontaneous fracture occurs. It has a genetic component and is characterized by decreased bone strength, causing bones to be more susceptible to fracture.1,2 The disease is associated with decreased estrogen, inadequate calcium, vitamin D, energy intake, and a lack of weight-bearing activity.1,3
Though exercise is generally known to positively impact skeletal health, if caloric intake is inadequate, exercise can further contribute to low energy availability. Low calorie intake can result in hypothalamic–pituitary–gonadal axis disturbances, altered bone metabolism, increased bone stress injury risk, and osteoporosis.3
Osteoporosis and periodontal diseases are multifactorial inflammatory chronic diseases with systemic and localized bone loss, respectively. According to existing studies, systemic loss of bone mass density (BMD) due to osteoporosis can also affect alveolar bone density, clinical attachment loss, and periodontal diseases.4,5 A literature review by Yu and Wang5 noted that osteoporosis is significantly associated with higher prevalence and severity of radiographic alveolar bone loss. In the mandible, cortical bone is concentrated at the inferior cortex, and begins to decrease in width after age 50. The thinning of mandibular cortex width is correlated with systemic BMD, and serves as a potential risk indicator for osteoporosis.5
Inflammation and its influence on bone remodeling play critical roles in the pathogenesis of osteoporosis and periodontitis and may serve as the central mechanistic link between these disorders. In post-menopausal women, a decrease in estrogen levels forms bone-resorbing cytokines and elevated inflammatory response exacerbate osteoclastic bone resorption while inhibiting osteoblastic bone formation, resulting in net bone loss.5
The risk of developing periodontal disease is increased during the menopausal transition stage (0 to 4 years after menopause) due to a decrease in BMD caused by sudden estrogen deficiency.4 For personalized therapeutic management, monitoring BMD is critical and a relationship to osteoporosis should be considered when identifying periodontal issues.1 With the connection between systemic and alveolar bone loss in mind, routine dental exams and intraoral radiographs may serve as a low-cost screening tool for low systemic BMD and increased fracture risk.5,6
Nutrition and Osteoporosis
The relationship between calcium intake and bone density indicates a protective effect in women who report a lifetime of high calcium intake but not among women who only increased calcium intake after menopause.1 Building bone during the formative years is the best assurance against osteoporosis. Adequate calcium intake is essential at all stages of life, with a daily intake of a minimum of 1,000 mg for all healthy adults and 1,200 mg for women older than age 51.7 Some calcium-rich foods, such as kale, broccoli, and watercress, contain between 100 and 150 mg of calcium per 100 g.7
Recent research suggests a significant relationship between increased dairy consumption and decreased prevalence of periodontal diseases.8 High calcium intake from dairy foods may prevent bone loss by inhibiting the secretion of parathyroid hormone, which contributes to bone resorption.8
Vitamin D is well-known for its role in calcium homeostasis and maintaining healthy bones. Vitamin D increases the efficiency of the intestinal absorption of dietary calcium, reduces calcium losses in urine, and mobilizes calcium stored in the skeleton. When absorption is insufficient to maintain calcium homeostasis, preservation of blood calcium levels is prioritized over skeletal integrity.9 In addition to vitamin D’s role in bone and calcium homeostasis, it has antimicrobial and anti-inflammatory functions.10
A recent European consensus stated that an inadequate vitamin D status impacts periodontal health and oral functions.11 Research has shown that serum vitamin D concentrations were inversely associated with higher periodontal destruction, severe periodontitis stages, and tooth loss.11 Vitamin D supplementation combined with calcium has been shown to reduce tooth loss and improve periodontal health.12 Although adequate amounts of vitamin D may be derived from exposure to sunlight, additional food sources are necessary in most cases. Natural sources include oily fish such as salmon, sardines, and tuna, as well as cod liver oil and fish oils. The National Academy of Medicine recommends 15 mcg (600 IU) of vitamin D for ages 1 to 70 and 20 mcg (800 IU) after age 70.1
Vitamin K influences bone health through multiple mechanisms. Osteocalcin, a vitamin K-dependent protein in the bone, is synthesized by osteoblasts during the mineralization phase of the bone.13 Osteocalcin binds to calcium ions and hydroxyapatite crystals, regulating their size and shape. Vitamin K also stimulates osteoblastogenesis and inhibits osteoclastogenesis through nuclear factor-κB.2 Bacterial flora in the gut synthesizes vitamin K. Green leafy vegetables are excellent sources of vitamin K.1
Research has reported a positive association between using phytochemicals (plant chemicals) in preventing osteoporosis bone loss associated with decreased estrogen.1 Phytochemicals are natural components of foods found in soy products, flaxseed, and seaweed.1,14 The isoflavones or phytoestrogens in soybeans are structurally and functionally similar to estrogen and do not elicit adverse side effects of hormone replacement therapy, such as cancer of reproductive organs.15
Prebiotics — functional food components (primarily fibers) that serve as substrates for the gut microbiota — indirectly improve mineral absorption and bone mass. Prebiotics, by definition, are not absorbed but hydrolyzed and fermented by colonic bacteria in the lower gut.1 Proposed mechanisms of the effects of prebiotics on bone are related primarily to the production of short-chain fatty acids by colonic bacteria, which may act to enhance mineral (eg, calcium) absorption through the subsequently reduced pH environment in the gut.13
High levels of phosphorus, sodium, or caffeine increase calcium loss in the urine.1 Research suggests that the ratio of calcium-to-phosphorus intake is vital to bone status, even when calcium consumption is adequate to recommended intakes.16 Phosphorus intake above nutrient needs may disrupt hormonal regulation of phosphorus, calcium, and vitamin D, contributing to disordered mineral metabolism and bone loss.16
Some evidence shows that the addition of phosphorus to the food supply may contribute to the burden of osteoporosis in the population. Most dietary phosphorus is contained in protein-rich foods such as meat, milk, cheese, poultry, fish, and processed foods that contain phosphate-based additives to improve their consistency and appearance.17 Inorganic phosphate salts added to foods in processing dissociate easily in the gut and are rapidly absorbed and highly bioavailable.16,18 Phosphoric acid, a commonly used inorganic phosphate additive, has an absorption efficiency of almost 100% and is present in a significant number of products, ranging from carbonated soda to commercial salad dressings.16
A high salt diet is a risk factor for osteoporosis in post-menopausal women.19-22 Diets high in sodium alter calcium metabolism by increasing urinary calcium excretion, resulting in calciuria.23 To maintain homeostasis, urinary calcium losses may be compensated for by an increase in the efficiency of calcium absorption and an increase in the rate of bone resorption mediated by increased parathyroid hormone due to temporarily reduced serum calcium concentration.19,21,22,24
The published literature on sodium and calcium metabolism indicates that the average calcium loss is one mmol Ca (40 mg) per 100 mmol (2290 mg) of sodium. Without adaptive compensatory mechanisms, a daily loss of 40 mg of calcium would deplete 10% of the skeleton within a decade.19 Therefore, salt restriction may be effective in preventing osteoporosis, especially after menopause.22
One of the World Health Organization’s three pillars of sodium reduction is raising consumer awareness of the harmful effects of excessive salt intake, and about the benefits of reading food labels and of choosing healthy foods.20 The US Department of Agriculture’s Dietary Guidelines for Americans — the foundation of MyPlate (choosemyplate.gov) — also promote low sodium intake as a healthy eating pattern. Dental hygienists may want to use this site to help advise their patients on making healthy dietary choices.1
The impact of caffeine consumption on bone metabolism offers a mixed picture, with some but not all studies suggesting a potential link between caffeine intake and reduced BMD or increased fracture risk.25 Differences in methodology, selected populations, and duration/ timing of the studies may account for study outcome discrepancies.
In vitro and animal studies indicate that caffeine’s biological effects may adversely affect BMD.26 A limited number of population-based studies suggest that in individuals at increased risk for osteoporosis and fractures, such as older adults and post-menopausal white women, caffeine consumption at levels equivalent to two or more cups of coffee daily may affect bone metabolism and modestly raise the risk for osteoporosis and fractures.25,27
High doses of caffeine may damage bone metabolism, bone healing, and osteoblastic activity.8 Caffeine can also reduce calcium absorption and increase its elimination.27 One proposed effect of caffeine on bone metabolism is its ability to increase the urinary excretion of calcium, which may be secondary to bone resorption, resulting in decreased stores available for bone deposition. Furthermore, caffeine may suppress vitamin D function by altering the vitamin D receptor expression on human osteoblasts and a marker of osteoblast activity, suggesting that caffeine impairs osteoblast activation.25,28,29
Acid production by a high-protein diet negatively impacts bone by increasing urinary calcium excretion and osteoclastic activity.30 Adequate intake of other nutrients — such as calcium, vitamin D,31 and rich plant-source foods, including green leafy vegetables, stalks, roots, tubers, and fruit — is essential in maintaining acid-base homeostasis. These foods provide a source of dietary alkali and a wide variety of micronutrients with potential effects on bone.30,32
Combining a net base-producing alkaline diet (fruits and vegetables) and a high-protein diet might optimize peak bone mass achievement during development and significantly mitigate or eliminate age-related decreases in bone mass.32 Research demonstrates that a high-protein diet combined with a low-calcium intake is detrimental to bone, leading to an elevated fracture risk.33 This particular nutritional profile is rare, but its negative impact should be known. Research on protein intake and bone health indicates little benefit of increasing protein intake beyond 0.8 to 1.3 g/kg body weight/day in healthy adults.34
Osteoporosis and Osteonecrosis of the Jaw
Osteonecrosis of the jaw (ONJ) is defined as exposed necrotic bone in the maxillofacial region that does not heal after 8 weeks in patients with no history of craniofacial radiation, who receive chronic bisphosphonate therapy for the treatment of post-menopausal osteoporosis, and in subjects not using bisphosphonates.35,36 The incidence is estimated to be 0.7 per 100,000 patients.35 Risk factors for ONJ include invasive dental procedures and preexisting periodontal diseases, cancer, anticancer therapy, severe immunosuppression, intravenous bisphosphonates, duration of exposure to bisphosphonate therapy, glucocorticoids, and smoking.36
A causal link between bisphosphonate use and ONJ has not been established, although it appears to be likely. Periodontal diseases, low-grade inflammatory conditions that necessitate tooth extraction, can be considered underestimated risk factors for the onset of medication-related ONJ. This finding highlights the need to manage periodontal diseases in patients taking bisphosphonates.37
Despite a number of potential mechanisms, including over-suppresion of bone turnover, the pathophysiology of ONJ remains poorly defined. The guidelines from the American Dental Association state that the benefit provided by antiresorptive therapy outweighs the low risk of developing ONJ and that discontinuing bisphosphonate therapy may not lower the risk since bisphosphonates stay in bone for years but may negatively effect low bone mass treatment outcomes.35 Patients considering dentoalveolar surgery while taking bisphosphonates should be advised of the risks and alternatives.35
The American Dental Hygienists’ Association “Standards for Clinical Dental Hygiene Practice” state that one of the dental hygienist’s responsibilities is assessing nutrition history and dietary practices and integrating nutrition counseling into comprehensive dental hygiene care. By providing nutritional counseling, dental hygienists educate patients on the role of nutrition not only in the prevention of oral disease but also in the prevention of systemic diseases.39,40
References
- Stegeman, C.A., Davis, J.R. (2018) The Dental Hygienist’s Guide to Nutritional Care. 5th edition. Elsevier.
- Dempster DW, Cauley JA, Bouxsein ML, Cosman F. Marcus and Feldman’s Osteoporosis. 5th ed. Elsevier Science & Technology; 2021:1679-1693. doi:10.1016/B978-0-12-813073-5.00084-8
- Popp KL, Cooke LM, Bouxsein ML, Hughes JM. Impact of Low Energy Availability on Skeletal Health in Physically Active Adults. Calcified Tissue International. 2022;110(5):605-614. doi:10.1007/s00223-022-00957-1
- Lee Y. Association between osteoporosis and periodontal disease among menopausal women: The 2013-2015 Korea National Health and Nutrition Examination Survey. PloS one. 2022;17(3):e0265631-e0265631. doi:10.1371/journal.pone.0265631
- Yu B, Wang C. Osteoporosis and periodontal diseases – An update on their association and mechanistic links. Periodontology 2000. 2022;89(1):99-113. doi:10.1111/prd.12422
- Preda SA, Comanescu MC, Albulescu DM, et al. Correlations between periodontal indices and osteoporosis. Experimental and therapeutic medicine. 2022;23(4):254-. doi:10.3892/etm.2022.11179
- Shkembi B, Huppertz T. Calcium Absorption from Food Products: Food Matrix Effects. Nutrients. 2021;14(1):180-. doi:10.3390/nu14010180
- Lee K, Kim J. Dairy Food Consumption is Inversely Associated with the Prevalence of Periodontal Disease in Korean Adults. Nutrients. 2019;11(5):1035-. doi:10.3390/nu11051035
- Janoušek J, Pilařová V, Macáková K, et al. Vitamin D: sources, physiological role, biokinetics, deficiency, therapeutic use, toxicity, and overview of analytical methods for detection of vitamin D and its metabolites. Critical reviews in clinical laboratory sciences. 2022;59(8):517-554. doi:10.1080/10408363.2022.2070595
- Li Y, Wang J, Cai Y, Chen H. Association of Serum Vitamin D with Periodontal Disease. International dental journal. 2023;73(5):777-783.
- Botelho J, Machado V, Proença L, Delgado AS, Mendes JJ. Vitamin D Deficiency and Oral Health: A Comprehensive Review. Nutrients. 2020;12(5):1471-. doi:10.3390/nu12051471
- Chapple ILC, Bouchard P, Cagetti MG, et al. Interaction of lifestyle, behavior or systemic diseases with dental caries and periodontal diseases: consensus report of group 2 of the joint EFP/ORCA workshop on the boundaries between caries and periodontal diseases. Journal of Clinical Periodontology. 2017;44(S18):S39-S51. doi:10.1111/jcpe.12685
- Curiel MD, Rodriguez CRO. Vitamin K and Bone Health: A Review on the Effects of Vitamin K Deficiency and Supplementation and the Effect of Non-Vitamin K Antagonist Oral Anticoagulants on Different Bone Parameters. Journal of osteoporosis. 2019;2019:2069176-2069178.
- Hefft DI, Adetunji CO, eds. Applications of Seaweeds in Food and Nutrition. 1st ed. Elsevier; 2024: 101-113.
- Kim IS, Kim CH, Yang WS. Physiologically Active Molecules and Functional Properties of Soybeans in Human Health-A Current Perspective. International journal of molecular sciences. 2021;22(8):4054-. doi:10.3390/ijms22084054
- Calvo MS, Tucker KL. Is phosphorus intake that exceeds dietary requirements a risk factor in bone health? Annals of the New York Academy of Sciences. 2013;1301(1):29-35. doi:10.1111/nyas.12300
- Takeda E, Yamamoto H, Yamanaka‐Okumura H, Taketani Y. Dietary phosphorus in bone health and quality of life. Nutrition Reviews, 2012;70(6), 311–321. https://doi.org/10.1111/j.1753-4887.2012.00473.x
- Calvo MS, Uribarri J. Contributions to Total Phosphorus Intake: All Sources Considered. Seminars in dialysis. 2013;26(1):54-61. doi:10.1111/sdi.12042
- Teucher B, Dainty JR, Spinks CA, et al. Sodium and Bone Health: Impact of Moderately High and Low Salt Intakes on Calcium Metabolism in Postmenopausal Women. Journal of bone and mineral research. 2008;23(9):1477-1485. doi:10.1359/jbmr.080408
- Ghimire K, Mishra SR, Satheesh G, et al. Salt intake and salt‐reduction strategies in South Asia: From evidence to action. The journal of clinical hypertension (Greenwich, Conn). 2021;23(10):1815-1829. doi:10.1111/jch.14365
- Kwon SJ, Ha YC, Park Y. High dietary sodium intake is associated with low bone mass in postmenopausal women: Korea National Health and Nutrition Examination Survey, 2008–2011. Osteoporosis International, 2017;28(4), 1445–1452. https://doi.org/10.1007/s00198-017-3904-8
- Takase H, Takeuchi Y, Fujita T, Ohishi T. Excessive salt intake reduces bone density in the general female population. European journal of clinical investigation. 2023;53(10):e14034-e14034. doi:10.1111/eci.14034
- Humalda, Jelmer K et al. Effects of Potassium or Sodium Supplementation on Mineral Homeostasis: A Controlled Dietary Intervention Study. The journal of clinical endocrinology and metabolism 105.9, 2020: e3246–e3256. Web.
- Tiyasatkulkovit W, Aksornthong S, Adulyaritthikul P, et al. Excessive salt consumption causes systemic calcium mishandling and worsens microarchitecture and strength of long bones in rats. Scientific reports. 2021;11(1):1850-1850. doi:10.1038/s41598-021-81413-2
- Berman NK, Honig S, Cronstein BN, Pillinger MH. The effects of caffeine on bone mineral density and fracture risk. Osteoporosis international. 2022;33(6):1235-1241. doi:10.1007/s00198-021-05972-w
- Galindo-Zavala R, Bou-Torrent R, Magallares-López B, et al. Expert panel consensus recommendations for diagnosis and treatment of secondary osteoporosis in children. Pediatric Rheumatology. 2020;18(1):20-14. doi:10.1186/s12969-020-0411-9
- Adiguzel KT, Koroglu O. Caffeine intake and bone mineral density in postmenopausal women. Gülhane tıp dergisi. 2022;64(3):262-267. doi:10.4274/gulhane.galenos.2022.93585
- Reuter SE, Schultz HB, Ward MB, et al. The effect of high‐dose, short‐term caffeine intake on the renal clearance of calcium, sodium and creatinine in healthy adults. British journal of clinical pharmacology. 2021;87(11):4461-4466. doi:10.1111/bcp.14856
- Rapuri PB, Gallagher JC, Nawaz Z. Caffeine decreases vitamin D receptor protein expression and 1,25(OH)2D3 stimulated alkaline phosphatase activity in human osteoblast cells. Journal of steroid biochemistry and molecular biology. 2007;103(3-5):368-371. doi:10.1016/j.jsbmb.2006.12.037
- Lambert H, Huggett C, Gannon R, Lanham-New SA. Acid–Base Homeostasis and Skeletal Health: Current Thinking and Future Perspectives. In: Nutritional Influences on Bone Health. Springer London; 2013:93-98. doi:10.1007/978-1-4471-2769-7_8
- Cao JJ. High Dietary Protein Intake and Protein-Related Acid Load on Bone Health. Current osteoporosis reports. 2017;15(6):571-576. doi:10.1007/s11914-017-0408-6
- Sebastian A. Dietary protein content and the diet’s net acid load: opposing effects on bone health. The American journal of clinical nutrition. 2005;82(5):921-922. doi:10.1093/ajcn/82.5.921
- Burckhardt P, Dawson-Hughes B, Weaver CM. Nutritional Influences on Bone Health: 8th International Symposium. 1st ed. Springer London, Limited; 2013. doi:10.1007/978-1-4471-2769-7
- Dodington DW, Young HE, Beaudette JR, Fritz PC, Ward WE. Improved Healing after Non-Surgical Periodontal Therapy Is Associated with Higher Protein Intake in Patients Who Are Non-Smokers. Nutrients. 2021;13(11):3722-. doi:10.3390/nu13113722
- Diab DL, Watts NB, Miller PD. Chapter 74 – Bisphosphonates pharmacology and use in the treatment of osteoporosis. In: Marcus and Feldman’s Osteoporosis. Fifth Edition. Elsevier Inc; 2021:1721-1736. doi:10.1016/B978-0-12-813073-5.00074-5
- Van Poznak C, Reynolds EL, Estilo CL, et al. Osteonecrosis of the jaw risk factors in bisphosphonate‐treated patients with metastatic cancer. Oral diseases. 2022;28(1):193-201. doi:10.1111/odi.13746
- Kwoen M, Park J, Kim K, et al. Association between periodontal disease, tooth extraction, and medication‐related osteonecrosis of the jaw in women receiving bisphosphonates: A national cohort‐based study. Journal of periodontology, 1970; 2023;94(1):98-107. doi:10.1002/JPER.21-0611
- American Dental Hygienists’ Association. Standards for Clinical Dental Hygiene Practice. Availabel at: adha.org/wp-content/uploads/2022/11/2016-Revised-Standards-for-Clinical-Dental-Hygiene-Practice.pdf. Accessed September 21, 2024.
- Dommisch H, Kuzmanova D, Jönsson D, Grant M, Chapple I. Effect of micronutrient malnutrition on periodontal disease and periodontal therapy. Periodontology 2000. 2018;78(1):129-153. doi:10.1111/prd.12233
- Touger-Decker R, Mobley C, Epstein JB. Nutrition and Oral Medicine. 2nd ed. 2014. Springer New York; 2014. doi:10.1007/978-1-60761-490-6
From Dimensions of Dental Hygiene. October/November 2024; 22(6):40-45.