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Brown, R.B. Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer. Encyclopedia. Available online: https://encyclopedia.pub/entry/56165 (accessed on 15 April 2024).
Brown RB. Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer. Encyclopedia. Available at: https://encyclopedia.pub/entry/56165. Accessed April 15, 2024.
Brown, Ronald B.. "Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer" Encyclopedia, https://encyclopedia.pub/entry/56165 (accessed April 15, 2024).
Brown, R.B. (2024, March 12). Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer. In Encyclopedia. https://encyclopedia.pub/entry/56165
Brown, Ronald B.. "Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer." Encyclopedia. Web. 12 March, 2024.
Dysregulated Phosphate Metabolism, Periodontal Disease, and Cancer
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Phosphate, an essential dietary micronutrient, is dysregulated in chronic kidney disease, and both cancer and periodontal disease are associated with chronic kidney disease. Reviewed evidence includes the association between phosphate toxicity and cancer development, and the association between periodontal disease and chronic kidney disease-mineral and bone disorder includes conditions such as ectopic calcification and bone resorption, which may be indirectly related to periodontal disease. Dental calculus in periodontal disease contains calcium phosphate crystals that are deposited from excess calcium and phosphate in saliva. Alveolar bone resorption may be linked systemically to release of parathyroid hormone in response to hypocalcemia induced by hyperphosphatemia. 

phosphate toxicity periodontal disease cancer tumorigenesis chronic kidney disease-mineral and bone disorder dental calculus resorption RNA

1. Introduction

The global burden of periodontal disease, which accounts for the majority of the 442 billion USD spent on oral disease costs, share risk factors, and social determinants with other non-communicable diseases such as diabetes, heart disease, and cancer [1]. Recent studies investigating the link between periodontal disease and various cancers include meta-analyses of periodontal disease and cancer [2][3], studies of periodontal disease and cancer in postmenopausal women [4][5], in male non-smokers [6], and studies and meta-analyses of periodontal disease linked to specific cancers including breast cancer [7][8], pancreatic cancer [9][10], oral cancer [11][12], colorectal cancer [13][14], lymphoma [14][15], head and neck cancer [16], lung cancer [17][18], prostate cancer [19], and gastric cancer [20]. To the author’s knowledge, no findings from major studies published within the last five years have failed to support an association of periodontal disease with at least some type of cancer risk. Discrepancies between studies regarding specific cancers may be accounted for by the study design, population studied, and method used to measure periodontal disease [5].

2. Phosphate Toxicity as a Global Health Burden

Phosphorus, an essential dietary micronutrient, is ingested as phosphate in food and food additives. The highest amount of phosphate within the body is stored in bone as calcium phosphate. Levels of serum phosphate are regulated through a hormonal network, involving the kidneys, parathyroid glands, intestines, and the skeletal system [21]. Bioactive vitamin D, 1,25(OH)2D3, increases intestinal absorption of dietary phosphate, mainly through enhanced expression of sodium-phosphate 2b cotransporters. Fibroblast growth factor 23 (FGF23) is produced within osteocytes and osteoblasts of bone. Working in conjunction with its co-factor, Klotho, FGF23 lowers serum phosphate levels, and increases urinary phosphate excretion by suppressing reabsorption through action of sodium-phosphate cotransporters in the kidneys. Phosphorus renal reabsorption is also decreased by parathyroid hormone (PTH). If phosphate is dysregulated due to kidney burden and excessive dietary phosphate intake, serum phosphate levels may rise (hyperphosphatemia) and excessive phosphate may be sequestered in cellular tissue producing a pathological condition called phosphate toxicity.
Phosphate toxicity is emerging as a global health concern as average amounts of dietary phosphate intake increase to approximately double the Recommended Dietary Allowance of 700 mg per day for an adult [22]. An excessive amount of phosphate stored in the body tissue may not always correlate with serum levels. It is possible that phosphate toxicity may be present in the body cells even in normophosphatemia, disturbing the function of almost every system in the body, including the muscular, skeletal, and vascular systems, and increasing morbidity and mortality [23]. Genetic evidence from animal experiments shows that phosphate toxicity may also accelerate mammalian aging [24], and phosphate toxicity is associated with tumorigenesis [25].

3. Dysregulated Phosphate Metabolism and Cancer

Evidence supporting the role of dysregulated phosphate metabolism and phosphate toxicity in tumorigenesis has been detailed elsewhere [26][27]; a very brief summary of that evidence with important relevance to periodontal disease is presented here. Cancer cells express more phosphate cotransporters within their cell membranes than normal cells [28], which allow cancer cells to absorb and retain greater amounts of phosphate from the tumor microenvironment. Solid tumors have filopodia and lamellipodia that extend cancer cell membranes throughout the tumor microenvironment [29]. Phosphorus is a limiting factor in biological growth [30] and is the least abundantly supplied element in the formation of nucleic acids DNA and RNA. The sequestration of dysregulated amounts of phosphorus in cancer cells is associated with additional biosynthesis of ribosomal RNA [31], which increases protein synthesis necessary for cancer cell growth and tumorigenesis. Of relevance, detection of the overexpression of circulating microRNA fragments associated with dysregulated RNA biogenesis has potential as a cancer biomarker [32].
While serum phosphorus levels are not always a reliable indicator of phosphate stored in the body, a study of cancer patients found that they had abnormally higher serum phosphate levels compared to control patients [33]. The Health Professionals Follow-Up Study found that high-grade prostate cancer was associated with high dietary phosphate levels [34]. High dietary phosphorus fed to experimental animals caused skin cancer [35] and lung tumors [36]. Of relevance, experimental studies showing causative effects of cancer from feeding the milk protein casein [37] may not have controlled for high levels of phosphorus within casein, which is classified as a phosphoprotein [38]. Other studies have shown that high amounts of phosphate stimulate tumor neovascularization [39] and cell signaling in cancer growth [40], and are associated with chromosome instability [41] and metastasis [42]. Phosphate toxicity also contributes to systemic inflammation and malnutrition [43], which is seen in terminally ill cancer patients with cachexia.

4. Periodontal Disease

The periodontium functions to connect teeth to bone; its structures consist of the cementum, periodontal ligament, gingiva, and alveolar bone. Periodontal disease is the most common cause of adult tooth loss [44]. Many mediators of inflammation in periodontal disease are associated with cancer risk, such as C-reactive protein (CRP), Matrix metalloprotenases (MMP), Tumor Necrosis Factor (TNF), and Interluekin (IL) [45]. Inflammation within the periodontium may begin as gingivitis and eventually progress to periodontitis, which is usually associated with the accumulation of dental plaque or calculus. Dental calculus is formed supragingvally and subgingivally when biofilms rich in bacteria are mineralized with various crystals of calcium phosphate, including octacalcium phosphate = Ca4H(PO4)3 · 2H2O, brushite = CaH(PO4) · 2H2O, hydroxyapatite = Ca5(PO4)3(OH), and whitlockite that contains a small amount of magnesium and other elements = β-Ca3(PO4)2 [46]. While growth of bacteria in the oral microbiota is associated with periodontal disease, there is currently insufficient evidence to either support or exclude a causative role of bacterial invasion in the etiology of periodontal disease [47].
As an alternative explanation for the development of periodontal disease and its association with cancer, Figure 1 in this research shows that excessive dietary phosphate and renal burden may increase the risk for dysregulated phosphate metabolism. It is hypothesized that this systemic metabolic pathology could mediate the association of tumorigenesis with periodontal disease through separate causal pathways involving phosphate toxicity and systemic chronic kidney disease-mineral and bone disorder (CKD-MBD), respectively.
Figure 1. Evidence suggests that excessive dietary phosphate and renal burden increases the risk of dysregulated phosphate metabolism. It is hypothesized that dysregulated phosphate metabolism could act as a mediator or intermediary variable linking phosphate toxicity and systemic chronic kidney disease-mineral and bone disorder (CKD-MBD). Phosphate toxicity may progress to tumorigenesis, and periodontal disease may occur as a comorbidity with systemic CKD-MBD, which forms an association between tumorigenesis and periodontal disease (dotted arrow).

5. Chronic Kidney Disease-Mineral and Bone Disorder

Phosphate metabolism is often dysregulated in chronic kidney disease (CKD), and hyperphosphatemia contributes to patient morbidity and mortality [48]. CKD is often comorbid with cancer [49], and an association of periodontal disease with CKD has been confirmed in observational studies [50][51][52]. As in cancer, it is plausible that the association of periodontal disease with CKD also involves dysregulated phosphate and calcium metabolism, seen in systemic CKD-MBD [53]. In addition to endocrine disturbances in the metabolism of ions and hormones associated with bone, characterization of chronic kidney disease-mineral and bone disorder (CKD-MBD) includes abnormalities in bone mineralization, bone growth, and bone turnover. Jaw bones affected with CKD-MBD increase the risk of bone loss in periodontitis [54].
While severity of periodontal disease was found to increase with stages of CKD, serum albumin levels declined as periodontal disease severity increased [55]. Of relevance, increasing hyperphosphatemia in CKD is also associated with declining serum albumin levels [56], implying that hyperphosphatemia may also be positively associated with periodontal disease severity. It has been observed that dental calculus formation appears to be similar to ectopic calcification such as that which occurs in kidney stone formation [57], and an association has been found between calculus formation and renal calculi [58]. Of relevance, ectopic calcification, including calcification of the vascular system, is associated with dysregulated phosphate metabolism and hyperphosphatemia [27].
Hyperphosphatemia is a common condition in dialysis patients [59], and dialysis patients were found to have a higher rate of dental calculus formation compared to healthy controls [60], further implying a role for high serum phosphate levels in calculus formation. Calculus that formed in closer proximity to salivary gland ducts was also found to contain more calcium and phosphate than calculus in other oral locations [46]. Increased phosphate and calcium in saliva has been associated with higher risk for inflammation of the periodontium [61], and high levels of phosphorus have been linked to systemic inflammation [43], which is often present in periodontal disease and cancer. Of relevance, detection of ribose nucleic acids in saliva is used in oral cancer diagnosis [62], and as previously mentioned, phosphorus is a key element in the formation of nucleic acids detected in circulating microRNA [32]. Furthermore, increased periodontal risk has been associated with carotid artery calcifications [63] and increased aortic arch plaque thickness [64], which may be related to vascular ectopic calcification caused by elevated serum phosphate associated with periodontal disease.

References

  1. Tonetti, M.S.; Jepsen, S.; Jin, L.; Otomo-Corgel, J. Impact of the global burden of periodontal diseases on health, nutrition and wellbeing of mankind: A call for global action. J. Clin. Periodontol. 2017, 44, 456–462.
  2. Corbella, S.; Veronesi, P.; Galimberti, V.; Weinstein, R.; Del Fabbro, M.; Francetti, L. Is periodontitis a risk indicator for cancer? A meta-analysis. PLoS ONE 2018, 13, e0195683.
  3. Michaud, D.S.; Fu, Z.; Shi, J.; Chung, M. Periodontal disease, tooth loss, and cancer risk. Epidemiol. Rev. 2017, 39, 49–58.
  4. Mai, X.; LaMonte, M.J.; Hovey, K.M.; Freudenheim, J.L.; Andrews, C.A.; Genco, R.J.; Wactawski-Wende, J. Periodontal disease severity and cancer risk in postmenopausal women: The Buffalo OsteoPerio Study. Cancer Causes Control 2016, 27, 217–228.
  5. Nwizu, N.N.; Marshall, J.R.; Moysich, K.; Genco, R.J.; Hovey, K.M.; Mai, X.; LaMonte, M.J.; Freudenheim, J.L.; Wactawski-Wende, J. Periodontal Disease and Incident Cancer Risk among Postmenopausal Women: Results from the Women’s Health Initiative Observational Cohort. Cancer Epidemiol. Prev. Biomark. 2017, 26, 1255–1265.
  6. Michaud, D.; Kelsey, K.; Papathanasiou, E.; Genco, C.; Giovannucci, E. Periodontal disease and risk of all cancers among male never smokers: An updated analysis of the Health Professionals Follow-up Study. Ann. Oncol. 2016, 27, 941–947.
  7. Freudenheim, J.L.; Genco, R.J.; LaMonte, M.J.; Millen, A.E.; Hovey, K.M.; Mai, X.; Nwizu, N.; Andrews, C.A.; Wactawski-Wende, J. Periodontal disease and breast cancer: Prospective cohort study of postmenopausal women. Cancer Epidemiol. Prev. Biomark. 2016, 25, 43–50.
  8. Shi, T.; Min, M.; Sun, C.; Zhang, Y.; Liang, M.; Sun, Y. Periodontal disease and susceptibility to breast cancer: A meta-analysis of observational studies. J. Clin. Periodontol. 2018, 45, 1025–1033.
  9. Michaud, D.S.; Izard, J. Microbiota, oral microbiome, and pancreatic cancer. Cancer J. 2014, 20, 203.
  10. Maisonneuve, P.; Amar, S.; Lowenfels, A.B. Periodontal disease, edentulism, and pancreatic cancer: A meta-analysis. Ann. Oncol. 2017, 28, 985–995.
  11. Javed, F.; Warnakulasuriya, S. Is there a relationship between periodontal disease and oral cancer? A systematic review of currently available evidence. Crit. Rev. Oncol./Hematol. 2016, 97, 197–205.
  12. Yao, Q.-W.; Zhou, D.-S.; Peng, H.-J.; Ji, P.; Liu, D.-S. Association of periodontal disease with oral cancer: A meta-analysis. Tumor Biol. 2014, 35, 7073–7077.
  13. Momen-Heravi, F.; Babic, A.; Tworoger, S.S.; Zhang, L.; Wu, K.; Smith-Warner, S.A.; Ogino, S.; Chan, A.T.; Meyerhardt, J.; Giovannucci, E. Periodontal disease, tooth loss and colorectal cancer risk: Results from the Nurses’ Health Study. Int. J. Cancer 2017, 140, 646–652.
  14. Barton, M.K. Evidence accumulates indicating periodontal disease as a risk factor for colorectal cancer or lymphoma. CA: Cancer J. Clin. 2017, 67, 173–174.
  15. Bertrand, K.A.; Shingala, J.; Evens, A.; Birmann, B.M.; Giovannucci, E.; Michaud, D.S. Periodontal disease and risk of non-Hodgkin lymphoma in the Health Professionals Follow-Up Study. Int. J. Cancer 2017, 140, 1020–1026.
  16. Zeng, X.-T.; Deng, A.-P.; Li, C.; Xia, L.-Y.; Niu, Y.-M.; Leng, W.-D. Periodontal disease and risk of head and neck cancer: A meta-analysis of observational studies. PLoS ONE 2013, 8, e79017.
  17. Zeng, X.T.; Xia, L.Y.; Zhang, Y.G.; Li, S.; Leng, W.D.; Kwong, J.S. Periodontal Disease and Incident Lung Cancer Risk: A Meta-Analysis of Cohort Studies. J. Periodontol. 2016, 87, 1158–1164.
  18. Chrysanthakopoulos, N. Correlation between periodontal disease indices and lung cancer in Greek adults: A case—control study. Exp. Oncol. 2016, 38, 49–53.
  19. Lee, J.-H.; Kweon, H.H.-I.; Choi, J.-K.; Kim, Y.-T.; Choi, S.-H. Association between periodontal disease and prostate cancer: Results of a 12-year longitudinal cohort study in South Korea. J. Cancer 2017, 8, 2959.
  20. Chrysanthakopoulos, N.A.; Oikonomou, A.A. A case-control study of the periodontal condition in gastric cancer patients. Stomatol. Dis. Sci. 2017, 1, 55–61.
  21. Brown, R.B.; Razzaque, M.S. Phosphate toxicity: A stealth biochemical stress factor? Med. Mol. Morphol. 2016, 49, 1–4.
  22. Erem, S.; Razzaque, M.S. Dietary phosphate toxicity: An emerging global health concern. Histochem. Cell Biol. 2018, 150, 711–719.
  23. Osuka, S.; Razzaque, M.S. Can features of phosphate toxicity appear in normophosphatemia? J. Bone Miner. Metab. 2012, 30, 10–18.
  24. Ohnishi, M.; Razzaque, M.S. Dietary and genetic evidence for phosphate toxicity accelerating mammalian aging. FASEB J. 2010, 24, 3562–3571.
  25. Razzaque, M.S. Phosphate toxicity: New insights into an old problem. Clin. Sci. 2011, 120, 91–97.
  26. Brown, R.B.; Razzaque, M.S. Phosphate toxicity and tumorigenesis. Biochimica et Biophysica Acta (BBA)-Rev. Cancer 2018, 1869, 303–309.
  27. Brown, R.B.; Razzaque, M.S. Dysregulation of phosphate metabolism and conditions associated with phosphate toxicity. Bonekey Rep. 2015, 4, 705.
  28. D’Arcangelo, M.; Brustugun, O.; Xiao, Y.; Choi, Y.; Behrens, C.; Solis, L.; Wang, Y.; Firestein, R.; Boyle, T.; Lund-Iversen, M. 194 Prevalence and prognostic significance of sodium-dependent phosphate transporter 2B (NaPi2B) protein expression in non-small cell lung cancer (NSCLC). Ann. Oncol. 2014, 25, iv66–iv67.
  29. Jacquemet, G.; Hamidi, H.; Ivaska, J. Filopodia in cell adhesion, 3D migration and cancer cell invasion. Curr. Opin. Cell Biol. 2015, 36, 23–31.
  30. Kuang, Y.; Nagy, J.D.; Elser, J.J. Biological stoichiometry of tumor dynamics: Mathematical models and analysis. Discret. Contin. Dyn. Syst. Ser. B 2004, 4, 221–240.
  31. Ward, D.; Griffin, A. Phosphorus incorporation into nucleic acids and proteins of liver nuclei of normal and azo dye-fed rats. Cancer Res. 1955, 15, 456–461.
  32. Wang, H.; Peng, R.; Wang, J.; Qin, Z.; Xue, L. Circulating microRNAs as potential cancer biomarkers: The advantage and disadvantage. Clin. Epigenetics 2018, 10, 59.
  33. Papaloucas, C.D.; Papaloucas, M.D.; Kouloulias, V.; Neanidis, K.; Pistevou-Gompaki, K.; Kouvaris, J.; Zygogianni, A.; Mystakidou, K.; Papaloucas, A.C. Measurement of blood phosphorus: A quick and inexpensive method for detection of the existence of cancer in the body. Too good to be true, or forgotten knowledge of the past? Med. Hypotheses 2014, 82, 24–25.
  34. Wilson, K.M.; Shui, I.M.; Mucci, L.A.; Giovannucci, E. Calcium and phosphorus intake and prostate cancer risk: A 24-y follow-up study. Am. J. Clin. Nutr. 2015, 101, 173–183.
  35. Camalier, C.E.; Young, M.R.; Bobe, G.; Perella, C.M.; Colburn, N.H.; Beck, G.R. Elevated phosphate activates N-ras and promotes cell transformation and skin tumorigenesis. Cancer Prev. Res. 2010, 3, 359–370.
  36. Jin, H.; Xu, C.-X.; Lim, H.-T.; Park, S.-J.; Shin, J.-Y.; Chung, Y.-S.; Park, S.-C.; Chang, S.-H.; Youn, H.-J.; Lee, K.-H. High dietary inorganic phosphate increases lung tumorigenesis and alters Akt signaling. Am. J. Respir. Crit. Care Med. 2009, 179, 59–68.
  37. Cheng, Z.; Hu, J.; King, J.; Jay, G.; Campbell, T. Inhibition of hepatocellular carcinoma development in hepatitis B virus transfected mice by low dietary casein. Hepatology 1997, 26, 1351–1354.
  38. Reeves, P.G.; Nielsen, F.H.; Fahey, G.C., Jr. AIN-93 purified diets for laboratory rodents: Final report of the American Institute of Nutrition ad hoc writing committee on the reformulation of the AIN-76A rodent diet. J. Nutr. 1993, 123, 1939–1951.
  39. Lin, Y.; McKinnon, K.E.; Ha, S.W.; Beck, G.R. Inorganic phosphate induces cancer cell mediated angiogenesis dependent on forkhead box protein C2 (FOXC2) regulated osteopontin expression. Mol. Carcinog. 2015, 54, 926–934.
  40. Liu, P.; Cheng, H.; Roberts, T.M.; Zhao, J.J. Targeting the phosphoinositide 3-kinase (PI3K) pathway in cancer, Nature reviews. Drug Discov. 2009, 8, 627.
  41. Chudek, J.; Nagy, A.; Kokot, F.; Podwinski, A.; Wiecek, A.; Ritz, E.; Kovacs, G. Phosphatemia is related to chromosomal aberrations of parathyroid glands in patients with hyperparathyroidism. J. Nephrol. 2007, 20, 164–172.
  42. Bobko, A.A.; Eubank, T.D.; Driesschaert, B.; Dhimitruka, I.; Evans, J.; Mohammad, R.; Tchekneva, E.E.; Dikov, M.M.; Khramtsov, V.V. Interstitial Inorganic Phosphate as a Tumor Microenvironment Marker for Tumor Progression. Sci. Rep. 2017, 7, 41233.
  43. Yamada, S.; Tokumoto, M.; Tatsumoto, N.; Taniguchi, M.; Noguchi, H.; Nakano, T.; Masutani, K.; Ooboshi, H.; Tsuruya, K.; Kitazono, T. Phosphate overload directly induces systemic inflammation and malnutrition as well as vascular calcification in uremia. Am. J. Physiol.-Renal Physiol. 2014, 306, F1418–F1428.
  44. NIDCR. Periodontal (Gum) Disease. 2018. Available online: https://www.nidcr.nih.gov/research/data-statistics/periodontal-disease (accessed on 28 December 2018).
  45. Pendyala, G.; Joshi, S.; Chaudhari, S.; Gandhage, D. Links demystified: Periodontitis and cancer. Dent. Res. J. 2013, 10, 704.
  46. Akcalı, A.; Lang, N.P. Dental calculus: The calcified biofilm and its role in disease development. Periodontology 2000 2018, 76, 109–115.
  47. Mendes, L.; Azevedo, N.F.; Felino, A.; Pinto, M.G. Relationship between invasion of the periodontium by periodontal pathogens and periodontal disease: A systematic review. Virulence 2015, 6, 208–215.
  48. Askar, A.M. Hyperphosphatemia: The hidden killer in chronic kidney disease. Saudi Med. J. 2015, 36, 13.
  49. Iff, S.; Craig, J.C.; Turner, R.; Chapman, J.R.; Wang, J.J.; Mitchell, P.; Wong, G. Reduced Estimated GFR and Cancer Mortality. Am. J. Kidney Dis. 2014, 63, 23–30.
  50. Linden, G.J.; Lyons, A.; Scannapieco, F.A. Periodontal systemic associations: Review of the evidence. J. Periodontol. 2013, 84, S8–S19.
  51. Grubbs, V.; Vittinghoff, E.; Taylor, G.; Kritz-Silverstein, D.; Powe, N.; Bibbins-Domingo, K.; Ishani, A.; Cummings, S.R. The association of periodontal disease with kidney function decline: A longitudinal retrospective analysis of the MrOS dental study. Nephrol. Dial. Transpl. 2015, 31, 466–472.
  52. Cholewa, M.; Madziarska, K.; Radwan-Oczko, M. The association between periodontal conditions, inflammation, nutritional status and calcium-phosphate metabolism disorders in hemodialysis patients. J. Appl. Oral Sci. 2018, 26, e20170495.
  53. Hou, Y.C.; Lu, C.L.; Lu, K.C. Mineral bone disorders in chronic kidney disease. Nephrology 2018, 23, 88–94.
  54. Kanjevac, T.; Bijelic, B.; Brajkovic, D.; Vasovic, M.; Stolic, R. Impact of Chronic Kidney Disease Mineral and Bone Disorder on Jaw and Alveolar Bone Metabolism: A Narrative Review. Oral Health Prev. Dent. 2018, 16, 79–85.
  55. Ausavarungnirun, R.; Wisetsin, S.; Rongkiettechakorn, N.; Chaichalermsak, S.; Udompol, U.; Rattanasompattikul, M. Association of dental and periodontal disease with chronic kidney disease in patients of a single, tertiary care centre in Thailand. BMJ Open 2016, 6, e011836.
  56. Zitt, E.; Lamina, C.; Sturm, G.; Knoll, F.; Lins, F.; Freistätter, O.; Kronenberg, F.; Lhotta, K.; Neyer, U. Interaction of time-varying albumin and phosphorus on mortality in incident dialysis patients. Clin. J. Am. Soc. Nephrol. 2011, 6, 2650–2656.
  57. Lieverse, A.R. Diet and the aetiology of dental calculus. Int. J. Osteoarchaeol. 1999, 9, 219–232.
  58. Tawfig, A. Dental Calculus Formation among Recurrent Renal Calculi Formers. Int. J. Dent. Oral Heal 2017, 3, 1–7.
  59. Lim, E.; Hyun, S.; Lee, J.M.; Kim, S.; Lee, M.-J.; Lee, S.-M.; Oh, Y.-S.; Park, I.; Shin, G.-T.; Kim, H. Effects of education on low-phosphate diet and phosphate binder intake to control serum phosphate among maintenance hemodialysis patients: A randomized controlled trial. Kidney Res. Clin. Pract. 2018, 37, 69.
  60. Martins, C.; Siqueira, W.L.; Oliveira, E.; Nicolau, J.; Primo, L.G. Dental calculus formation in children and adolescents undergoing hemodialysis. Pediatr. Nephrol. 2012, 27, 1961–1966.
  61. Fiyaz, M.; Ramesh, A.; Ramalingam, K.; Thomas, B.; Shetty, S.; Prakash, P. Association of salivary calcium, phosphate, pH and flow rate on oral health: A study on 90 subjects. J. Indian Soc. Periodontol. 2013, 17, 454.
  62. Panta, P.; Venna, V.R. Salivary RNA signatures in oral cancer detection. Anal. Cell. Pathol. 2014, 2014, 450629.
  63. Kamak, G.; Yildirim, E.; Rencber, E. Evaluation of the relationship between periodontal risk and carotid artery calcifications on panoramic radiographs. Eur. J. Dent. 2015, 9, 483.
  64. Sen, S.; Chung, M.; Duda, V.; Giamberardino, L.; Hinderliter, A.; Offenbacher, S. Periodontal disease associated with aortic arch atheroma in patients with stroke or transient ischemic attack. J. Stroke Cerebrovasc. Dis. 2017, 26, 2137–2144.
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