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Year : 2020  |  Volume : 10  |  Issue : 2  |  Page : 35-37

Can excessive dietary phosphate intake influence oral diseases?

Department of Pathology, Lake Erie College of Osteopathic Medicine, Erie, PA, USA; Department of Preventive and Community Dentistry, School of Dentistry, University of Rwanda, Kigali, Rwanda; Global Affairs Program, Mccormack Graduate School of Policy and Global Studies, University of Massachusetts Boston, Boston, MA, USA

Date of Submission07-Jan-2020
Date of Acceptance13-Mar-2020
Date of Web Publication13-May-2020

Correspondence Address:
Mohammed S Razzaque
Department of Pathology, Lake Erie College of Osteopathic Medicine, 2000 West Grandview Boulevard, Erie, PA 16509

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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AIHB.AIHB_3_20

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How to cite this article:
Razzaque MS. Can excessive dietary phosphate intake influence oral diseases?. Adv Hum Biol 2020;10:35-7

How to cite this URL:
Razzaque MS. Can excessive dietary phosphate intake influence oral diseases?. Adv Hum Biol [serial online] 2020 [cited 2022 Sep 25];10:35-7. Available from: https://www.aihbonline.com/text.asp?2020/10/2/35/284286

Deficiency of most of the nutrients and minerals, for example, calcium, magnesium and iron, including vitamins, usually leads to various cellular, tissue and organ damages in healthy individuals. For instance, calcium and magnesium deficiency is related to degenerative musculoskeletal disorders.[1],[2],[3] Iron deficiency is related to anaemia, and deficiency of vitamins is associated with gum bleeding, dry mouth and oral infections. Phosphate deficiency, in pre-existing diseases, can induce oral bone deformities, including rickets.[4] In healthy individuals, instead of deficiency, excessive intake of phosphate, however, is a health risk. Both human and animal studies have convincingly shown the wide-range of disorders induced by high phosphate burden, ranging from cardiovascular calcification to musculoskeletal disorders to premature ageing.[5],[6],[7],[8] In this editorial, I will briefly summarise the evidence that suggests that oral phosphate burden from abnormal phosphate homeostasis can induce oral diseases, including dental decay and gingivitis.[9],[10]

  Phosphate and Gingivitis Top

Gingivitis, causing gum swelling, redness and bleeding, is a common human disease.[11] Without preventive measures, it can progress to debilitating periodontal diseases with tooth loss.[12] Of significant medical importance, a higher number of children and younger individuals suffer from various degrees of gingival inflammation,[13] and providing adequate treatment to reduce severe complications is a clinical priority. The exact underlying cause of gingival inflammation is not yet clear; certain factors and habits, including cigarette smoking, tobacco chewing, poor oral hygiene, certain medications (steroids, chemotherapy, etc.) and bacterial infection, may facilitate the evolvement of gingivitis.[14],[15] A large number of published studies have demonstrated a correlation between sugar-sweetened beverage (SSBs) uptake and gingivitis, ranging from children to young individuals.[16],[17] Children consuming sweetened foods and beverages, as high as 50%, have shown signs of plaque formation or gingivitis.[16] Historically, such association has been linked to the excessive sugar content of SSBs; it, however, needs to be mentioned that SSBs often contain higher levels of phosphate.[18],[19]

Studies have shown that excessive phosphate intake is very common in all age groups; such excessive consumption of phosphate-rich food can create an inflammatory microenvironment in the oral cavity.[20],[21] Of importance, 700 mg/day is the recommended dietary allowance of phosphorus for adults and the elderly in the United States (US), although studies have shown that around 35% of the US adult population consume more than double the amount of phosphate than the recommended amount.[22] A similar pattern of high phosphate consumption is also noted among children.[23] In a study conducted on schoolchildren, a higher prevalence of gingivitis has been reported in association with higher daily consumption of either phosphate or sugar.[9] The study further showed that a higher amount of phosphate intake could increase the risk of gingivitis by enhancing the synthesis of interleukin (IL)-1β and decreasing the synthesis of IL-4.[9] After adjusting for age, sex, body mass index, gingival redness and region, the dietary phosphate consumption per day was strongly correlated with the salivary level of IL-1β and was inversely correlated with the salivary level of IL-4. The disproportionate salivary levels of IL-1β and IL-4 in patients with gingivitis are reflective of oral inflammatory activity, produced by gingival cells, perhaps induced by cellular phosphate burden. Of biological significance, phosphate burden has been implicated in other inflammatory conditions, including obesity.[24] Further studies are needed to explain how phosphate-induced inflammatory microenvironment can cause gingival tissue damage.

  Phosphate and Dental Decay Top

Dental caries or decay is a common worldwide oral disorder. The decay process can be slowed down or partially reversed, if it is identified in earlier stages, and treated accordingly. The precise underlying mechanism of dental decay is not fully understood. The complex process of dental decay can be largely divided into three, often overlapping events, as follows: (1) an early initiating or triggering phase that can induce tooth enamel demineralisation; (2) dentinal penetration phase accompanied with localised inflammatory reactions and (3) dental pulp destruction phase, if adequate treatment is not provided.

Studies have convincingly shown a link between dental decay and the consumption of high sugar-containing drinks.[25] As mentioned, two main components of SSBs are sugar and phosphate. In a study, conducted on 8317 schoolchildren (average age: 9.99 ± 0.68 years), the occurrence of dental decay was significantly higher among children who consumed a higher amount of phosphate;[10] the study found that after adjusting all the covariates, for every single unit increase in calorie-adjusted sugar intake, the odds of having dental decay increased by 12%, and for 1 unit increase in phosphate, the odds of having any dental decay increased by 33%.[10] In a subgroup analysis, compared to children who consumed low sugar and low phosphate (n = 413), a significantly increased occurrence of dental decay could be noted in children who consumed low sugar but high phosphate (n = 661), again implicating that excessive phosphate consumption alone can propagate dental decay, even when sugar consumption is low [Figure 1].[10]
Figure 1: The effect of sugar and phosphorus intake on the occurrence of dental decay, modified from earlier published figure.[10] Low S/Low P: Low sugar and low phosphorus intake (n = 413); Low S/High P: low sugar and high phosphorus intake (n = 661); High S/High P: high sugar and high phosphorus intake (n = 314); in which low refers to the 1st quartile and high refers to the 4th quartile in the study population. Values at the bottom are the percent of decayed teeth (±standard error) in individual groups. *A significant difference (P < 0.05) as compared to the baseline value in low/low, based on Tukey's range test for multiple comparisons. Please note that compared to the low sugar and low phosphorus intake, significantly increased occurrence of dental decay is noted even in low sugar- and high phosphorus-consumed child, implicating an adverse role of high phosphorus intake in the evolvement of dental decay.

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An association between salivary phosphate level and inflammatory biomarkers, including salivary C-reactive protein, was recently reported. Furthermore, a statistically significant correlation was noted between increased salivary matrix metalloproteinase (MMP)-9 level and the occurrence of dental decay.[10] It is important to know whether an increased amount of salivary MMP-9 in dental decay patients is partly regulated by high phosphate intake; although additional investigational proof is needed, the potential exists for such causal relationships. Adiponectin is a product of adipose cells and can induce anti-inflammatory effects.[26] A statistically significant association is noted between higher salivary levels of adiponectin and the occurrence of dental decay. Moreover, studies have also found an association between salivary pH and plasma adiponectin levels; whether increased levels of salivary adiponectin in dental decay patients reflect altered salivary pH in these patients is another issue that requires further study to be resolved. Contrary to adiponectin, the salivary vascular endothelial growth factor (VEGF) level has shown to be less in children with dental decay. As VEGF can contribute to angiogenesis and subsequent healing processes, decreased salivary levels of VEGF in dental decay patients might be reflective of the reduced or impaired healing of the pulpal tissue, thus promoting structural damages associated with dental decay.

Another important observation reported in a study conducted on 8317 children was that the intensity of dental decay was much more noticeable in children who consumed soda drinks than those who consumed fruit juice; even though both the drinks contain high levels of sugar, it is likely that soda drinks might have certain ingredients that have pro-cariogenic effects, and there are reasons to believe that phosphate is one such harmful ingredient in soda drinks.[10]

  Conclusion Top

The digestibility of animal-derived phosphate is proportionately higher than that of the plant-derived phosphate. Roughly 40%–60% of natural phosphate from food is absorbed in the intestines, while around 90% of artificial phosphate from the food and drinks is absorbed in the intestines.[27] Chemical analyses of processed meat and fish with additives found around 14.4 mg of phosphate/gram of protein, whereas unprocessed foods without additives contain 9.1 mg of phosphate/gram of protein.[28],[29]

Reported studies have shown that higher consumption of both sugar and phosphate can facilitate the occurrence of gingivitis,[9] and that, excessive intake of phosphate-rich soda drinks and foods can increase the occurrence of dental decay, even in children who take low-sugar food.[10] Further human and experimental studies, to determine how excessive dietary phosphate consumption influences oral microenvironment, to induce and influence oral diseases, are needed. More importantly, the prognostic benefit of lowering phosphate burden on disease progression is necessary. The results of such well-designed studies will lay the foundation for therapeutic manipulation of phosphate metabolism for the improved outcome in patients with various oral diseases.


Thanks to Ms. Rufsa H. Afroze, Ms. Zinnia Mosharraf, Ms. Peace Uwambaye and Dr. Sharmin Swarna for carefully reading the manuscript and providing useful suggestions. Dr. Razzaque is a Visiting Professor at the Harvard School of Dental Medicine, Boston (USA), and an Honorary Professor at the University of Rwanda College of Medicine and Health Sciences, Kigali (Rwanda).

  References Top

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Uwitonze AM, Razzaque MS. Role of magnesium in Vitamin D activation and function. J Am Osteopath Assoc 2018;118:181-9.  Back to cited text no. 2
Razzaque MS. Magnesium: Are we consuming enough? Nutrients 2018;10:pii: E1863.  Back to cited text no. 3
Cremonesi I, Nucci C, D'Alessandro G, Alkhamis N, Marchionni S, Piana G. X-linked hypophosphatemic rickets: Enamel abnormalities and oral clinical findings. Scanning 2014;36:456-61.  Back to cited text no. 4
Erem S, Atfi A, Razzaque MS. Anabolic effects of Vitamin D and magnesium in aging bone. J Steroid Biochem Mol Biol 2019;193:105400.  Back to cited text no. 5
Brown RB, Razzaque MS. Phosphate toxicity and tumorigenesis. Biochim Biophys Acta Rev Cancer 2018;1869:303-9.  Back to cited text no. 6
Razzaque MS. Phosphate toxicity: New insights into an old problem. Clin Sci (Lond) 2011;120:91-7.  Back to cited text no. 7
Ohnishi M, Razzaque MS. Dietary and genetic evidence for phosphate toxicity accelerating mammalian aging. FASEB J 2010;24:3562-71.  Back to cited text no. 8
Goodson JM, Shi P, Razzaque MS. Dietary phosphorus enhances inflammatory response: A study of human gingivitis. J Steroid Biochem Mol Biol 2019;188:166-71.  Back to cited text no. 9
Goodson JM, Shi P, Mumena CH, Haq A, Razzaque MS. Dietary phosphorus burden increases cariogenesis independent of Vitamin D uptake. J Steroid Biochem Mol Biol 2017;167:33-8.  Back to cited text no. 10
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Chapple IL, Van der Weijden F, Doerfer C, Herrera D, Shapira L, Polak D, et al. Primary prevention of periodontitis: Managing gingivitis. J Clin Periodontol 2015;42 Suppl 16:S71-6.  Back to cited text no. 12
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