Oral-Periodontal and Systemic Relationships Part II: Reproductive Issues, Osteoporosis, Cognitive Impairment, and Cancer

Alison Glascoe, DDS, MS

February 2016 Course - Expires February 28th, 2019

United Concordia

Abstract

Because the mouth is a part of the body, its health may have a crucial impact on the rest of the body. Periodontal disease is common, chronic, and inflammatory, affecting the supporting structures of the teeth. Researchers have proposed periodontal disease to be a risk factor for many common, chronic, and systemic conditions such as reproductive issues, osteoporosis, cognitive impairment, and cancer.

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The mouth is a part of the body and often provides a glimpse into overall health.1 Health is defined not only as the absence of disease but also as a state of complete physical, mental, and social well-being.2 In 1900, Hunter introduced the concept of oral sepsis to the literature in a paper entitled “Oral Sepsis as a Cause of Disease”3 and wrote about the association of oral infection and systemic disease.

A thorough examination of the oral cavity can help a clinician detect oral diseases, lesions, and abnormalities, as well as signs of systemic diseases and disorders, nutritional deficiencies, disorders of the immune system, and cancers.4 Miller, a periodontist, started the American Academy of Oral Medicine in 1945 and the American Board of Oral Medicine in 1956.5 In 1996, Offenbacher coined the term periodontal medicine,6 which is a branch of periodontology that focuses on the relationship between periodontal health and systemic disease.

Periodontal disease is perhaps the most common chronic infection7 and is caused by dental plaque. Dental plaque is the well-organized, heterogeneous structure comprised of microbial pathogens, which are the primary etiologic agents for the condition.

Gingivitis and periodontitis are the two main forms of the disease. Both are pathologic periodontal inflammatory processes that result from an accumulation of dental plaque. Gingivitis, the most common plaque-induced gingival disease, is reversible.8 As the second most common form, periodontitis is destructive, irreversible, and chronic. Periodontal disease is caused by dental plaque, which leads to atrophy or loss of bone and connective tissue support around the teeth.8

More than 500 microbial species are associated with periodontal disease.9 Despite this, just a small number are commonly linked. Socransky et al10 segregated the pathogens into red and orange complexes. The red complex includes the following Gram-negative, anaerobic pathogens: Porphyromonas gingivalis, Treponema denticola, and Tannerella forsythia. Orange includes Fusobacterium nucleatum, Prevotella intermedia, Prevotella nigrescens, Peptostreptococcus micros, Campylobacter rectus, Centruroides gracilis, Campylobacter showae, Eubacterium nodatum, and Streptococcus constellatus. Other pathogens strongly associated with periodontal disease are Aggregatibacter actinomycetemcomitans and Eikenella corrodens.

In disease, the putative periodontal pathogens colonize in the gingival tissue around the tooth. When ulceration of the periodontal pocket occurs, the pathogens gain access into the systemic circulation. The inflammatory response is activated, resulting in the production of inflammatory cytokines and mediators, such as interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-alpha (TNF-α).11 These mediators, whose effects are also systemic, may play a role in a person’s susceptibility to systemic illnesses.

Periodontal Medicine

Periodontal disease is thought to be a risk factor associated with several systemic diseases and conditions such as preterm delivery, low birth weight, preeclampsia, erectile dysfunction, osteoporosis, cognitive impairment, and cancer.

Reproductive Issues

Preterm labor occurs between Week 20 and Week 36 of gestation.12 Preterm birth is a major cause of infant mortality and morbidity. Low birth weight refers to a child weighing less than 5.5 pounds at birth.13 Low birth weight applies to premature birth or babies being too small.13

Studies have shown that the risk factors for preterm and low-birth-weight deliveries are similar to those for periodontitis, such as smoking, low socioeconomic status, lower levels of education, and ethnicity.14 Researchers have found that women who delivered prematurely had poorer oral health and worse periodontal disease compared with those without periodontal disease.15 Offenbacher et al16 found that mothers of preterm and low-birth-weight babies had significantly worse periodontal disease than mothers of normal-weight babies. Research has also indicated that mothers of preterm babies had higher levels of prostaglandin E2 (PGE2) and periodontal microbial pathogens, such as C rectus, F nucleatum, and P gingivalisin the amniotic fluid than those without periodontal disease.15,17,18 The appearance of fusobacteria may be due to types of sexual activity with a new partner.19

Researchers have a theory regarding the process. The oral infection activates a cell-mediated inflammatory response that triggers the production of pro-inflammatory cytokines such as IL-1 and TNF-α. This then begins the synthesis and release of PGE2. This prostaglandin not only stimulates bone resorption, but it also can affect labor by softening the cervix, relaxing smooth muscles, and causing contractions.20

Preeclampsia, as defined by the American Congress of Obstetricians and Gynecologists, is associated with a hypertension level of ≥140 mm Hg systolic and ≥ 90 mm Hg diastolic on two occasions at least 4 hours apart after Week 20 coupled with proteinuria.21,22 Periodontal disease increases the risk for the development of preeclampsia and, thus, preterm delivery.12,23,24

Erectile Dysfunction

Erectile dysfunction (ED) is characterized by the inability to develop or maintain an erection during sexual activity.25 Common causes include medication side effects, diabetes mellitus, cardiovascular disease, atherosclerosis, hypertension, obesity, metabolic syndrome, cancer, Parkinson’s disease, inadequate blood flow to the penis, excessive alcohol consumption, smoking, physical exhaustion, and stress.26

Researchers have found a possible relationship between chronic periodontitis and ED.27,28 It is theorized that ED is associated with damage from endothelial dysfunction and systemic inflammatory changes associated with periodontal disease.27,29

Osteoporosis

Osteoporosis is a progressive, chronic, systemic skeletal disease characterized by low bone mass and density with deterioration of bone structure that increases the risk for fracture.30 Osteoporosis may also affect the jaw bones.31 The condition can occur without a known cause or can be secondary to another condition, such as hyperthyroidism, or to medications, such as steroids.32 It is strongly believed that estrogen deficiency can lead to osteoporosis.33 Postmenopausal women, women who have had their ovaries surgically removed, young women with secondary amenorrhea (exercise- or anorexia nervosa-associated), and men with testosterone deficiency are at higher risk for developing osteoporosis.33 Men require both testosterone and estrogen for bone health because they convert testosterone into estrogen.33 Risk factors for osteoporosis include older age, female gender, postmenopausal status, Caucasian or Asian race, inadequate intake of calcium, smoking, alcohol consumption, and physical inactivity.34,35

Periodontitis and osteoporosis share some common risk factors such as age, genetics, smoking, poor nutrition, alcohol consumption, and stress. Both conditions are silent, meaning that patients usually do not develop symptoms until late in the disease when destruction has already begun. They are also bone-resorptive diseases.36 Despite the fact that both osteoporosis and periodontal disease ultimately result in bone destruction and loss, research has not definitively determined that osteoporosis is a causative factor for periodontal disease but it may be a risk factor for the progression.

Hypothetical models suggest that as bone density is reduced from osteoporosis, more rapid bone resorption from periodontal disease occurs from the periodontal microbial pathogens.31 This further reduces local and systemic bone density as a result of the release of systemic inflammatory mediators such as IL-1, IL-6, and TNF-α.31 These mediators not only stimulate an inflammatory response but also bone resorption through the activation of osteoclasts, which are specialized cells that reabsorb bone.31 Researchers have found tooth loss to be greater in those with osteoporosis compared with those without.37,38 Others have observed a positive association between osteoporosis and periodontal disease.35,38 von Wowern et al surmised that osteoporosis reduces the mineral content that may be associated with less favorable levels of attachment in patients with periodontitis.38,39

Cognitive Impairment

Dementia is a broad term used for brain diseases that result in the long-term loss of the ability to think, remember, and reason such that it interferes with daily functioning.40 Alzheimer’s disease is an irreversible, progressive disease of the brain that slowly affects memories, thinking skills, and daily functioning.41 The condition is the most common form of dementia in the elderly.42

Researchers have found the inflammatory mediators associated with periodontal disease, bacteria, and their byproducts can reach the brain through systemic circulation and neural pathways.43-45 In addition, studies have shown these inflammatory changes contribute to brain amyloid accumulation and cognitive dysfunction.44,46 Others have demonstrated that infections from bacterial pathogens and spirochetes have been associated with cognitive brain decline and increases in brain amyloid deposits.46-48 Periodontal microbial pathogens have also been identified in the brains of patients with Alzheimer’s disease and from those with amyloid deposits.46,49,50

Researchers are studying how Alzheimer’s disease and cognitive decline may be associated with vascular and metabolic conditions such as heart disease, stroke, diabetes, and obesity. It is suspected that one of the links is systemic inflammation.51 Various studies have suggested that systemic inflammation may be a risk factor for the progression of Alzheimer’s disease.51-53 Some systemic inflammatory mediators such as IL-6, IL-1β, TNF-α, and C-reactive protein, which are associated with periodontal disease, have been thought to increase the risk for Alzheimer’s disease and/or cognitive decline.51-53 Researchers have found an association that suggests periodontitis is a risk factor for cognitive impairment and/or Alzheimer’s disease in older adults.54-56

Cancer

Cancer refers to diseases that are associated with abnormal cell growth and the potential for these cells to spread to other parts of the body, which is known as metastasis.57 Cancer is thought to begin with a single cell in which genetic alterations occur, resulting in tumor growth (known as a malignancy), invasion, metastasis, and eventual drug resistance.58 Risk factors for cancer include smoking, obesity, alcohol consumption, poor diet, and an inactive lifestyle. Similar risk factors were noted for those at risk for atherosclerotic diseases, diabetes, osteoporosis, and rheumatoid arthritis.

Some evidence suggests that chronic infections and inflammation may be associated with an increased risk for cancer. Many patients with poor oral health have periodontal disease. Hujoel et al59 found a link between periodontitis and various cancers, with lung cancer as the strongest. Michaud et al60 conducted a study that showed an increased risk for the development of pancreatic cancer in men with periodontal disease. Treponema denticola, a red-complex periodontal pathogens, has been associated with various upper gastrointestinal tract cancers.61 Several investigators have noted a relationship between periodontal disease and oral cancers.62-64

Helicobacter pylori commonly causes gastric infections and has been associated with gastric cancers.65 H pylori, although not considered a red- or orange-complex periodontal pathogen, has been isolated from the subgingival microflora of patients with periodontal disease. Fusobacterium species are known periodontal pathogens and have been reported to be co-aggregants with H pylori in the subgingival plaque of patients with periodontal disease.66 This suggests a possible association between subgingival plaque biofilm, periodontal disease, and H pylori infection, which may be instrumental in the development of gastrointestinal cancers.65

Researchers have speculated on possible mechanisms linking poor oral health and periodontal disease with an increased risk for cancers. They believe that two pathways link inflammation with cancer. The first is an extrinsic mechanism in which a constant inflammatory state exists and contributes to the increased risk for cancer.67,68 The second is an intrinsic mechanism in which acquired genetic alterations trigger tumor development.67,68 Periodontal disease may contribute to the development of systemic inflammation and if left untreated, a chronic, smoldering inflammatory response occurs in reaction to periodontal microbial pathogens and their products such as endotoxin. The infection will ultimately stimulate the production of pro-inflammatory cytokines and mediators such as IL-1β, IL-6, TNF-α, and matrix metalloproteinases. IL-6, in particular, has tumor-inducing actions, by promoting growth and proliferation in both healthy and malignant cells in those genetically susceptible.69 IL-1 stimulates tumor growth and metastasis by inducing matrix metalloproteinase activity and other growth factors.70

Studies have also demonstrated that bacteria associated with poor oral health and periodontal disease produce nitrates, which cause genetic damage to cells. This damage decreases the cell’s ability to fight infection, thus increasing the risk for cancer.71

Conclusion

Many researchers have established an association between periodontal disease and other diseases such as reproductive issues, osteoporosis, cognitive impairment, and cancer; however, a cause-and-effect relationship has yet to be established.

Periodontal disease is a chronic infection that contributes to a chronic inflammatory response in the oral cavities of those who are susceptible. Support has been provided describing plausible biologic mechanisms by which periodontal disease may also contribute to the chronic systemic inflammatory burden. A vast amount of data demonstrates an association between periodontal disease and these systemic conditions. Further randomized, controlled studies are needed to determine causality between periodontal disease and systemic diseases such as reproductive issues, osteoporosis, cognitive impairment, and cancer. In addition, the gold standard in determining whether periodontal therapy will have a positive influence on medical outcomes is prospective, randomized, controlled, efficacy studies. Future research may demonstrate the efficacy of periodontal therapy related to positive outcomes with regard to these medical conditions. However, current data and risk-benefit ratios support the importance of periodontal therapy. 

References

1. Bansal M, Rastogi S, Vineeth NS. Influence of periodontal disease on systemic disease: inversion of a paradigm: a review. J Med Life. 2013;6(2):126-130.

2. World Health Organization. Definition of Health. 1948. http://who.int/about/definition/en/print.html. Accessed October 19, 2015.

3. Hunter W. Oral sepsis as a cause of disease. Br Med J. 1900;2(2065):215-216.

4. Dreizen S. Oral indications of the deficiency states. Postgrad Med. 1971;49(1):97-102.

5. Terezhalmy GT. Proceedings of the American Academy of Oral Medicine. The medical history. Special Committee for Clinical Investigation—report no. 1. J Oral Med. 1982;37(4):141-143.

6. Williams RC, Offenbacher S. Periodontal medicine: the emergence of a new branch of periodontology. Periodontol 2000. 2000;23:9-12.

7. Loesche WJ, Grossman NS. Periodontal disease as a specific, albeit chronic, infection: diagnosis and treatment. Clin Microbiol Rev. 2001;14(4):727-752.

8. Laurence B, Glascoe A, McIntosh C, Brown A. Periodontal Disease and Systemic Health for Medical Students. 2013. https://www.mededportal.org/publication/9468. Accessed October 21, 2015.

9. Guthmiller JM, Novak KF. Chapter 8. Periodontal Diseases. Polymicrobial Diseases. Brogden KA, Guthmiller JM, eds. Washington, DC: ASM Press; 2002.

10. Socransky SS, Haffajee AD, Cugini MA, et al. Microbial complexes in subgingival plaque. J Clin Periodontol. 1998;25(2):134-144.

11. Kim J, Amar S. Periodontal disease and systemic conditions: a bidirectional relationship. Odontology. 2006;94(1):10-21.

12. Pattanashetti JI, Nagathan VM, Rao SM. Evaluation of periodontitis as a risk for preterm birth among preeclamptic and non-preeclamptic pregnant women—a case control study. J Clin Diagn Res. 2013;7(8):1776-1778.

13. US National Library of Medicine Website. Medline Plus. Birth Weight. 2014. https://www.nlm.nih.gov/medlineplus/birthweight.html. Accessed October 21, 2015.

14. Huck O, Tenenbaum H, Davideau JL. Relationship between periodontal diseases and preterm birth: recent epidemiological and biological data. J Pregnancy. 2011;2011:164654.

15. Offenbacher S, Jared HL, O’Reilly PG, et al. Potential pathogenic mechanisms of periodontitis associated pregnancy complications. Ann Periodontol. 1998;3(1):233-250.

16. Offenbacher S, Katz V, Fertik G, et al. Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol. 1996;67(10 Suppl):1103-1113.

17. Offenbacher S, Madianos PN, Suttle M. Elevated human IgM suggests in utero exposure to periodontal pathogens. J Dent Res. 1999;78:2191.

18. Engebretson SP, Lalla E, Lamster IB. Periodontitis and systemic disease. N Y State Dent J. 1999;65(8):30-32.

19. Hill GB. Preterm birth: associations with genital and possibly oral microflora. Ann Periodontol. 1998;3(1):222-232.

20. Ueland K, Conrad JT. Characteristics of oral prostaglandin E2-induced labor. Clin Obstet Gynecol. 1983;26(1):87-94.

21. Papapanou PN. Periodontal diseases: epidemiology. Ann Periodontol. 1996;1(1):1-36.

22. Yaghini J, Mostajeran F, Afshari E, Naghsh N. Is periodontal disease related to preeclampsia? Dent Res J (Isfahan). 2012;9(6):770-773.

23. Nabet C, Lelong N, Colombier ML, et al. Maternal periodontitis and the causes of preterm birth: the case-control Epipap study. J Clin Periodontol. 2010;37(1):37-45.

24. Boggess KA, Lieff S, Murtha AP, et al. Maternal periodontal disease is associated with an increased risk for preeclampsia. Obstet Gynecol. 2003;101(2):227-231.

25. National Institute of Diabetes and Digestive and Kidney Diseases Web site. Erectile Dysfunction. http://www.niddk.nih.gov/health-information/health-topics/urologic-disease/erectile-dysfunction/Pages/facts.aspx. Accessed October 27, 2015.

26. Mayo Foundation for Medical Education and Research Website. Erectile Dysfunction. http://www.mayoclinic.org/diseases-conditions/erectile-dysfunction/care-at-mayo-clinic/research/CON-20034244. Accessed October 21, 2015.

27. Matsumoto S, Matsuda M, Takekawa M, et al. Association of ED with chronic periodontal disease. Int J Impot Res. 2014;26(1):13-15.

28. Keller JJ, Chung SD, Lin HC. A nationwide population-based study on the association between chronic periodontitis and erectile dysfunction. J Clin Periodontol. 2012;39(6):507-512.

29. Zadik Y, Bechor R, Galor S, et al. Erectile dysfunction might be associated with chronic periodontal disease: two ends of the cardiovascular spectrum. J Sex Med. 2009;6(4):1111-1116.

30. Alldredge BK, Koda-Kimble MA, Lloyd Y, et al, eds. Applied Therapeutics: The Clinical Use of Drugs. Philadelphia, PA: Wolters Kluwer Health; 2009.

31. Guiglia R, Di Fede O, Lo Russo L, et al. Osteoporosis, jawbones and periodontal disease. Med Oral Patol Oral Cir Bucal. 2013;18(1):e93-e99.

32. American Academy of Orthopaedic Surgeons Website. Osteoporosis and bone health.  http://www.aaos.org/news/aaosnow/may09/clinical8.asp. Accessed October 21, 2015.

33. National Osteoporosis Foundation Website. http://nof.org/learn. Accessed October 27, 2015.

34. Lane NE. Epidemiology, etiology, and diagnosis of osteoporosis. Am J Obstet Gynecol. 2006;194(2 Suppl):S3-S11.

35. Koduganti RR, Gorthi C, Reddy PV, Sandeep N. Osteoporosis: “a risk factor for periodontitis.” J Indian Soc Periodontol. 2009;13(2):90-96.

36. Sultan N, Rao J. Association between periodontal disease and bone mineral density in postmenopausal women: a cross sectional study. Med Oral Patol Oral Cir Bucal. 2011;16(3):e440-e447.

37. Kribbs PJ. Comparison of mandibular bone in normal and osteoporotic women. J Prosthet Dent. 1990;63(2):218-222.

38. Aspalli SS, Shetty VS, Parab PG, et al. Osteoporosis and periodontitis: is there a possible link? Indian J Dent Res. 2014;25(3):316-320.

39. von Wowern N, Klausen B, Kollerup G. Osteoporosis: a risk factor in periodontal disease. J Periodontol. 1994;65(12):1134-1138.

40. Budson AE, Solomon PR. Memory Loss: A Practical Guide for Clinicians. Philadelphia, PA: Elsevier Saunders; 2011.

41. National Institute on Aging Website. Alzheimer’s Disease Fact Sheet. https://www.nia.nih.gov/alzheimers/publication/alzheimers-disease-fact-sheet. Accessed October 21, 2015.

42. Berchtold NC, Cotman CW. Evolution in the conceptualization of dementia and Alzheimer’s disease: Greco-Roman period to the 1960s. Neurobiol Aging. 1998;19(3):173-189.

43. Holmes C, Cotterell D. Role of infection in the pathogenesis of Alzheimer’s disease: implications for treatment. CNS Drugs. 2009;23(12):993-1002.

44. Kamer AR, Dasanayake AP, Craig RG, et al. Alzheimer’s disease and peripheral infections: the possible contribution from periodontal infections, model and hypothesis. J Alzheimers Dis. 2008;13(4):437-449.

45. Rivest S. Molecular insights on the cerebral innate immune system. Brain Behav Immun. 2003;17(1):13-19.

46. Kamer AR, Pirraglia E, Tsui W, et al. Periodontal disease associates with higher brain amyloid load in normal elderly. Neurobiol Aging. 2015;36(2):627-633.

47. Miklossy J. Alzheimer’s disease—a neurospirochetosis. Analysis of the evidence following Koch’s and Hill’s criteria. J Neuroinflammation. 2011;8:90.

48. Miklossy J. Chronic inflammation and amyloidogenesis in Alzheimer’s disease—role of Spirochetes. J Alzheimers Dis. 2008;13(4):381-391.

49. Riviere GR, Riviere KH, Smith KS. Molecular and immunological evidence of oral Treponema in the human brain and their association with Alzheimer’s disease. Oral Microbiol Immunol. 2002;17(2):113-118.

50. Poole S, Singhrao SK, Kesavalu L, et al. Determining the presence of periodontopathic virulence factors in short-term postmortem Alzheimer’s disease brain tissue. J Alzheimers Dis. 2013;36(4):665-677.

51. Holmes C, Cunningham C, Zotova E, et al. Systemic inflammation and disease progression in Alzheimer disease. Neurology. 2009;73(10):768-774.

52. Engelhart MJ, Geerlings MI, Meijer J, et al. Inflammatory proteins in plasma and the risk of dementia: the rotterdam study. Arch Neurol. 2004;61(5):668-672.

53. Holmes C, El-Okl M, Williams AL, et al. Systemic infection, interleukin 1beta, and cognitive decline in Alzheimer’s disease. J Neurol Neurosurg Psychiatry. 2003;74(6):788-789.

54. Noble JM, Borrell LN, Papapanou PN, et al. Periodontitis is associated with cognitive impairment among older adults: analysis of NHANES-III. J Neurol Neurosurg Psychiatry. 2009;80(11):1206-1211.

55. Sparks Stein P, Steffen MJ, Smith C, et al. Serum antibodies to periodontal pathogens are a risk factor for Alzheimer’s disease. Alzheimers Dement. 2012;8(3):196-203.

56. Kamer AR, Craig RG, Dasanayake AP, et al. Inflammation and Alzheimer’s disease: possible role of periodontal diseases. Alzheimers Dement. 2008;4(4):242-250.

57. World Health Organization. Cancer. http://www.who.int/mediacentre/factsheets/fs297/en/. Updated February 2015. Accessed October 21, 2015.

58. Pendyala G, Joshi S, Chaudhari S, Gandhage D. Links demystified: periodontitis and cancer. Dent Res J (Isfahan). 2013;10(6):704-712.

59. Hujoel PP, Drangsholt M, Spiekerman C, Weiss NS. An exploration of the periodontitis-cancer association. Ann Epidemiol. 2003;13(5):312-316.

60. Michaud DS, Joshipura K, Giovannucci E, Fuchs CS. A prospective study of periodontal disease and pancreatic cancer in US male health professionals. J Natl Cancer Inst. 2007;99(2):171-175.

61. Narikiyo M, Tanabe C, Yamada Y, et al. Frequent and preferential infection of Treponema denticola, Streptococcus mitis, and Streptococcus anginosus in esophageal cancers. Cancer Sci. 2004;95(7):569-574.

62. Tezal M, Sullivan MA, Reid ME, et al. Chronic periodontitis and the risk of tongue cancer. Arch Otolaryngol Head Neck Surg. 2007;133(5):450-454.

63. Tezal M, Sullivan MA, Hyland A, et al. Chronic periodontitis and the incidence of head and neck squamous cell carcinoma. Cancer Epidemiol Biomarkers Prev. 2009;18(9):2406-2412.

64. Tezal M, Sullivan Nasca M, Stoler DL, et al. Chronic periodontitis-human papillomavirus synergy in base of tongue cancers. Arch Otolaryngol Head Neck Surg. 2009;135(4):391-396.

65. Farinati F, Cardin R, Cassaro M, et al. Helicobacter pylori, inflammation, oxidative damage and gastric cancer: a morphological, biological and molecular pathway. Eur J Cancer Prev. 2008;17(3):195-200.

66. Andersen RN, Ganeshkumar N, Kolenbrander PE. Helicobacter pylori adheres selectively to Fusobacterium spp. Oral Microbiol Immunol. 1998;13(1):51-54.

67. Slattery ML, Wolff RK, Herrick J, et al. Tumor markers and rectal cancer: support for an inflammation-related pathway. Int J Cancer. 2009;125(7):1698-1704.

68. Del Prete A, Allavena P, Santoro G, et al. Molecular pathways in cancer-related inflammation. Biochem Med (Zagreb). 2011;21(3):264-275.

69. Naugler WE, Karin M. The wolf in sheep’s clothing: the role of interleukin-6 in immunity, inflammation and cancer. Trends Mol Med. 2008;14(3):109-119.

70. Dinarello CA. The paradox of pro-inflammatory cytokines in cancer. Cancer Metastasis Rev. 2006;25(3):307-313.

71. Maeda H, Akaike T. Nitric oxide and oxygen radicals in infection, inflammation, and cancer. Biochemistry (Mosc). 1998;63(7):854-865.

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SOURCE: United Concordia | February 2016

Learning Objectives:

  • Understand the concept of periodontal medicine.
  • Explain the current literature regarding the association between periodontal medicine and reproductive issues.
  • Discuss the association between periodontal medicine and other systemic conditions such as osteoporosis, cognitive impairment, and cancer.