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The Science Behind The “Oral-Systemic Connection”

The Inflammation Connection – The New Factor in Heart Disease, Stroke, Cancer, and other Serious Diseases
-by Marcus Gitterle MD

One of the early signs of gum disease is that your gums turn from a pretty pink to an inflamed red. Scientists are now discovering that bodily inflammation is linked with a host of diseases including heart disease, stroke, lung disease, cancers, Alzheimer’s, and others.

Gum disease is an inflammatory condition that does not go away without treatment and it is a major cause of inflammation in many people. Inflammation causes the liver to secrete a protein called C-Reactive Protein (CRP for short) to fight the problem which seems to cause a number of side effects in the body.

The best known side effect of elevated CRP levels is the connection to heart disease. CRP is more predictive of heart attacks than the bad LDL cholesterol. While CRP value of under 1 mg/liter is considered normal, a value of 2-3 triples your risk of heart attack and higher values can increase your risk up to seven and a half times!

The actual manner by which CRP causes heart attacks was only recently explained. Elevated CRP levels actually interfere with the process that prevents blood clots, thus causing a higher incidence of blockages in arteries which can result in a sudden heart attack or stroke.

By comparison, bad cholesterol slowly builds up plaque in the arteries which often allows for some advanced warning in the form of pain or weakness.

While the active process is less known, statistically people with the top 25% of CRP scores develop 2.5 times as much colon cancer as those in the bottom 25%. Also, CRP is implicated in Alzheimer’s. Seniors with the highest 1/3 of CRP levels had significantly more cognitive decline than those in the bottom third.

Clearly it pays to know your CRP number, which can be requested as a single test (a high-sensitivity CRP is the more valuable test for heart disease association) or when other blood tests are done. If your CRP is high, the causes need to be determined and corrected to reduce your number.

In addition to gum disease, bodily infections such as a urinary tract infection, high blood pressure, smoking, lymphoma, and even being overweight can contribute to elevated CRP levels. Since periodontal disease is an inflammatory disease and is capable of elevating CRP levels, we normally request this blood test for any of our patients diagnosed with periodontal disease. Centers for Dental Medicine has developed a groundbreaking protocol for the diagnosis of periodontal disease and the treatment of periodontal disease and its associated negative impact on overall health.

Centers throughout the country have found that by following our unique periodontal protocol, we are able to quickly reduce periodontal inflammation. And in so doing, we can significantly reduce the CRP level to a non-harmful range in almost all cases, unless there is another systemic factor contributing to the elevation.

If your CRP number is high to begin with and remains high after periodontal health has been established, we will collaborate with your physician to review and monitor your results and make sure that you do not have other problems as well. As a Center for Dental Medicine, we give you our exclusive commitment to help care for your total health.

A Safe, Non-Surgical, Non-Toxic Treatment:

Traditionally, physicians are trained to diagnose disease and treat with surgery or drugs. The discovery of the infection-inflammation and heart disease connection is no different.

Physicians are waiting on drug manufacturers to produce a drug that will lower the levels of CRP and thus, reduce the risk of a heart attack. An eighteen month clinical trial showed that a statin drug (Lipitor) can lower CRP levels. However, to accomplish this, 8 times the normal dosage was needed.

This approach can be expensive and unnecessarily risky. A sole drug-based approach to lowering CRP levels is not seeking and removing the underlying cause of the elevated CRP. A more ideal approach would be to find and eliminate the source of the inflammation in the first place. A commitment we make to our patients is to help to eliminate any periodontal inflammation in order to rule out this potential cause.

The Oral-Systemic Connection – More Than Just a “Gum Infection!”
- by G. Lee Ostler DDS

Periodontal disease is a local inflammatory process in gum tissues caused by the body’s response to bacterial insult. It is a chronic oral infection that is now recognized to result in the elevation of systemic inflammatory protein markers that are believed to contribute to a higher risk for cardiovascular disease and diabetes . In fact, current research shows that C-reactive protein levels are a stronger predictor of first cardiovascular events than LDL cholesterol levels.   Other systemic conditions have also been connected with chronic oral infection and/or elevations in pro-inflammatory mediator, including: metabolic syndrome , complications of pregnancy , colon cancer , kidney disease , prostate cancer , formation of blood clots , obesity , respiratory disease , damaged heart valves , endocarditis , and osteoporosis .

Periodontal disease is associated with elevated inflammatory markers (C-reactive protein) and increased systemic inflammation . Until now, CRP has been viewed as an ‘innocent bystander’ in the formation of heart disease. But current understandings are now viewing elevated CRP as a key culprit that causes inflammation in the arteries resulting in formation of clots and plaques which lead to cardiovascular disease . Because periodontitis is an important risk factor and predictor for atherosclerotic conditions , this information is now beginning to modify the medical standard-of-care for addressing the risk factors of heart disease such that aggressive treatment is indicated to control CRP levels even when normal cholesterol levels exist.

Pregnancy complications are also being connected with periodontal infections and elevated C-reactive protein levels. Gingivitis during pregnancy has been shown to be an independent risk factor for preterm low birth weight pregnancy complications . This is explained through the translocation of bacteria or bacterial products in the systemic circulation (prostaglandins, cytokines, C-reactive protein, etc.). Recent studies have found an increase in likelihood of preterm low birth weight babies, and that those babies who were preterm or low birth weight had mothers with significantly more periodontal disease than controls with normal babies . In fact, the Oral Conditions and Pregnancy study (OCAP) as published in Obstetrics and Gynecology found that preterm birth rates rose 255% from a level of one-in-ten (11.2% in periodontally healthy women) to almost one-in-three births (28.6%) in women with periodontal disease . Another study has documented that periodontal treatment has been shown to reduce the incidence of preterm birth - low birth weight infants between 71 and 84 percent in pregnant women with moderate to severe chronic periodontitis . To be sure, women should begin and maintain their pregnancy without gingivitis or gum disease. If oral infections are found during pregnancy, treatment should begin as soon as possible to reduce adverse pregnancy risks.
Diabetes and its related insulin resistance and metabolic syndromes are widely prevalent in our modern society. It is estimated that approximately 80% of our population has periodontal disease in one form or another . Periodontitis is known to be twice as prevalent in diabetic individuals compared to non diabetics . Studies have shown that chronic oral infections such as ‘gum disease’ affects glucose control in diabetics, and that deep gum pockets were closely related with glucose tolerance status .

Because of the increasing prevalence of diabetes in our society  and the recent research indicating the dangers of periodontal disease to diabetics , and that treatment of the periodontal disease can help patients control their blood sugar , progressive dentists performing modern tissue therapy now routinely test all their periodontal patients for glycated hemoglobin, HbA1c.

Clinically, periodontal disease usually presents with gingival inflammation, bleeding, and halitosis. Pain is not a feature until late stages. ‘Volatile sulfur compounds’ (VSCs) are more than a cosmetic problem which gives rise to the bad breath characteristic of gum disease. Hydrogen sulfide (H2S) & methyl mercaptan (CH3SH) increase permeability of intact gingival mucosal epithelium and stimulate production of cytokines associated with periodontal disease , allowing ingress of bacteria and pro-inflammatory markers into the blood stream.

Periodontitis causes a breakdown in the gum tissue and allows the periodontal bacteria, especially porphyromonas gingivalis to invade the endothelial cells . Reports are now surfacing that show the presence of invasive periodontal pathogens at sites of atherosclerotic disease, establishing an unequivocal link and supporting the idea that periodontitis is an independent risk factor for, and an exacerbating factor in cardiovascular disease . These periodontal bacteria are gram-negative anaerobes that thrive in deeper periodontal pockets in the advanced stages of periodontitis.  P. gingivalis is a potent signal for monocyte and macrophage activation, and once established in the host, complicates diabetes control and increases the occurrence and severity of microvascular and macrovascular complications.

Modern Periodontal Therapy
It’s a sad indictment that despite our best efforts to educate our patients, and in spite of following what could be now called “old-school” treatment protocols, there is still an 80% incidence of periodontal diseases amongst our population at large. To effectively deal with the oral-systemic connection today, modern treatment protocols must go beyond the “regular cleaning” and surgical mindsets dentistry has become so accustomed to. Too often, soft-tissue management is nothing more than the management of a disease state, or only slightly better, management of a static pocket with the disease process neither getting worse or better.

Modern periodontal tissue therapy protocols include the use of antimicrobial agents, ionized sub-gingival irrigation to break down the electro-chemical properties of the bacterial plaque and help remove the microbial biofilm, advanced nutritional support to build and repair collagen connective tissue and to inhibit pro-inflammatory cytokine/chemokine responses induced by bacterial lipo-polysaccharides, strict behavior modification, and laser-assisted periodontal therapy to remove bacterial endotoxins and polysaccharides from the gum pockets and to induce regeneration of healthy gum and bone tissues.

Modern Antimicrobial Tissue Therapy treatment regimens include:

  • thorough evaluation and medical history review
  • in-house draw or referral for appropriate blood work (CRP, HbA1c)
  • medical referral to physician for medical management
  • patient education, oral hygiene instructions, and behavior modification
  • nutritional counseling and supplementation support for improved tissue repair
  • tobacco counseling as needed
  • laser bacterial decontamination and laser-assisted periodontal tissue therapy
  • conventional scaling and root planning
  • removal of bacterial dental plaque and endotoxins impregnating the dental root surface, and other surface contaminants at the sub-gingival level
  • sub-gingival irrigation with anti-microbial agents
  • correction of dental problems contributing to their periodontal condition
  • daily sub-gingival irrigation with anti-microbial agents (such as chlorine dioxide) to control anaerobic bacteria and volatile organic compounds
  • on-going communication with patient’s physicians regarding progress of treatments

Elevation of systemic markers related to cardiovascular disease in peripheral blood of periodontitis patients. Loos BG, Craandijk, et al J Periodontology, 2000 Oct;71(10):1528-34

Periodontal infections contribute to elevated systemic C-reactive protein level. Noack et al J Periodontol. 2001 Sep;72(9):1221-7

Comparison of  C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events, abstract, New England Journal of Medicine, Nov. 14(vol.347,issue 20), Paul M. Ridker,

C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men, Konig et al, Circulation 1999;99:237-242.

C-Reactive Protein Increases Plasminogen Activator Inhibitor-1 Expression and Activity in Human Aortic Endothelial Cells, American Heart Association Journal Circulation, 2003;107:398-404.Sridevi Devaraj, PhD; University of California, Davis Medical Center, Sacramento, CA.

Inflammation Marker Predicts Colon Cancer, Feb 4,2004 The Journal of the American Medical Association, Tate P Erlinger, M.D., M.P.H., Johns Hopkins Univ.

Inflammation Linked to Cognitive Decline. . Neurology July 8, 2003. Dr. Kristen Yaffe, professor of psychiatry, neurology and epidemiology University of California San Francisco.

Periodontal therapy lowers levels of heart disease inflammation markers, S.Grossi, State University of New York at Buffalo ADA News 04/21/2004

Comparison of C-Reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of  First Cardiovascular Events, abstract, New England Journal of Medicine, Nov.14(vol.347, issue 20), Paul M. Ridker,

Woods A, Brull DJ et. al, Genetics of inflammation and risk of coronary artery disease: the central role of interleukin – 6. European Heart Journal (2000) 21, 1574-1583.

Koenig et al. C-Reactive Protein, a Sensitive Marker of Inflammation, Predicts Future Risk of Coronary Heart Disease in Initially Healthy Middle-Aged Men. Circulation. 1999;99:237-242. 

Noack B, Genco RJ, et al, Periodontal Infections Contribute to Elevated Systemic C-Reactive Protein Level. J Periodontol 2001, Vol 72, No.9, pp1221-1227.

Desvarieux M, Demmer RT, Relationship Between Periodontal Disease, Tooth Loss, and Carotid Artery Plaque, Stroke 2003;34:2120.

Wu T, Trevisan M, et al, Periodontal Disease and Risk of Cerebrovascular Disease, Arch Intern Med. 2000,160:2749-2755.

Ross R, Atherosclerosis — An Inflammatory Disease, Ross R,  NEJM Vol.340:115-126 Jan 14, 1999.

Kweider M, Lowe GD, et. al, Dental disease, fibrinogen and white cell count; links with myocardial infarction? Scott med J. 1993 Jun;38(3):73-4.

Lowe G, Dental Disease, Coronary Heart Disease and Stroke, and Inflammatory Markers.Circulation 2004;109:1076-1078.

Mattila KJ, Nieminen MS, et. al, Association between dental health and acute myocardial infarction. Brit Med Journal 189; 298:779-81.

Saito T, Shimazaki Y, et al, The Severity of Periodontal Disease is Associated with the Development of Glucose Intolerance in Non-diabetics: The Hisayama Study, J Dental Research. 83(6)485-490,2004.

Grossi SG, Skrepcinski FB, et al, Treatment of periodontal disease in diabetics reduces glycated hemoglobin, J Periodontol 1997Aug;68(8):713-9.

Nelson RG, Periodontal Disease Predicts Mortality in Diabetics, Diabetes Care 2005;28:27-32.

Ridker PM, Rifai N. Comparison of C-reactive Protein and Low-Density Lipoprotein Cholesterol Levels in the Prediction of First Cardiovascular Events. NEJM, Vol 347:1557-1565, Nov.14, 2002, No.20.

Devaraj S et al, C-reactive protein increases plasminogen activator inhibitor-1 expression and activity in human aortic endothelial cells. Circulation 2003;107:398.

Lopez NJ, Da Silva I, Periodontal Therapy Reduces the Rate of Preterm Low Birth Weight in Women With Pregnancy-Associated Gingivitis, J Periodontol 2005, Vol.76, No.11-s, pp 2144-2153.

Offenbacher S, Katz V, et al, Periodontal infection as a possible risk factor for preterm low birth weight. J Periodontol 1996 Oct;67(10 Suppl):1103-13.

Erlinger TP et al, C-reactive protein and the risk of incident colorectal cancer, JAMA2004;291:585-590.

Craig RG, Spittle MA, et al, Importance of periodontal disease in the kidney patient. Blood Purif. 2002;20(1):113-9.

Kshirsagar AV, Moss KL, et al, Periodontal disease is associated with renal insufficiency in the Atherosclerosis Risk In Communities (ARIC) study. Am J Kidney Dis. 2005 Apr;45(4):650-7.

Lehrer S, Diamond EJ, et al, C-reactive protein is significantly associated with prostate-specific antigen and metastatic disease in prostate cancer. BJU Int. 2005 May;95(7):961-2

UC Davis Medical School media release, Jan. 9 2003,

Hiura M, Kikuchi T, et al, Elevation of serum C-reactive protein levels is associated with obesity in boys. Hypertens Res. 2003 Jul;26(7):541-6.

Greenfield JR, Samaras K, et al, Obesity Is an Important Determinant of Baseline Serum C-Reactive Protein Concentration in Monozygotic Twins, Independent of Genetic InfluencesCirculation. 2004;109:3022-3028.

Periodontal disease, obesity associated with heart disease marker: study, ADA News, 5/27/2003, citing Slade GD, Ghezzi EM, et al, Relationship Between Periodontal Disease and C-Reactive Protein Among Adults in the Atherosclerosis Risk in Communities Study, Arch Intern Med.2003;163:1172-1179.

Otomo-Corgel et al, Periodontal disease and systemic health – what you and your patients need to know, J CA Dent Assoc, April 2002.

Okuda K et al, Involvement of periodontopathic anaerobes in aspiration pneumonia, J Periodontology 2005, Vol. 76, No. 11-s, pp2154-2160.

Kaye D, Infective endocarditis In, Isselbacker KJ, Braunwald E, et al, eds, Harrison’s Principles of Internal Medicine, 13th ed. McGraw-Hill, New York, 1994, pp 520-6.

Ibid, Otomo-Corgel

Tezal M et al, The relationship between bone mineral density and Periodontitis in postmenopausal women, J Periodontology 2000, Vol. 71, No. 9, pp 1492-1498.

Relationship Between Periodontal Disease and C-Reactive Protein Among Adults in the Atherosclerosis Risk in Communities Study, Arch Intern Med. 2003; 163:1172-1179.

Noack et al, Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol. 2001 Sep;72(9):1221-7.

Koenig et al, C-Reactive protein, a sensitive marker of inflammation, predicts future risk of coronary heart disease in initially healthy middle-aged men, Circulation. 1999;99:237-242.

Desvarieux et al, Relationship between periodontal disease, tooth loss, and carotid artery plaque.Stroke. 2003;34:2120.

Loos BG et al, Elevation of systemic markers related to cardiovascular diseases in the peripheral blood of Periodontitis patients, J Periodontology 2000 Oct; 71(10):1528-34.

Pussinen, PJ et al, Periodontal infections and atherosclerosis: mere associations? Current Opinion in Lipidology. 15(5):583-588, Oct 2004.

Wu T et al, Periodontal disease and risk of cerebrovascular disease, Arch Intern Med. 2000; 160:2749-2755.

Ridker PM et al, Comparison of C-reactive protein and low-density lipoprotein cholesterol levels in the prediction of first cardiovascular events, New England Journal of Medicine, Nov 14, 2002 Vol. 347:1557-1565 No 20.

Effect of treating Periodontitis on C-reactive protein levels: a pilot study, BMC Infectious Diseases2002, 2:30.

Loos BG, Craandijk, et al, Elevation of systemic markers related to cardiovascular disease in peripheral blood of periodontitis patients. J Periodontology, 2000 Oct;71(10): 1528-34

Schillinger et al, Joint Effects of C-Reactive Protein and Glycated Hemoglobin in Predicting Future Cardiovascular Events of Patients With Advanced Atherosclerosis, Circulation. 2003;108:2323.

Lopez NJ, Periodontal therapy reduces the rate of preterm low birth weight in women with pregnancy-associated gingivitis. J of Periodontology 2005, Vol. 76, No.11-s, pp 2144-2153.

Offenbacher S et al, Periodontal infection as a risk factor for preterm low birth weight, J Periodontol 67:1103-13, 1996.

Lopez NJ et al, Periodontal therapy reduces the rate of preterm low birth weight in women with pregnancy-associated gingivitis, J Periodontology 2005 Nov; 76(11 Suppl):2144-53.

Periodontal therapy may reduce incidence of preterm births, American Academy of Periodontology media release, Nov 21, 2005.

Research presented today provides further evidence on the importance of good oral health in pregnant women. American Academy of Periodontology media release, May 7, 2000.

Gibbs RS, Romero R, et al, A review of premature birth and subclinical infections. Am J Obstet Gynecol 166:1515-28, 1992.

Offenbacher S, Boggess KA, et. al. Progressive Periodontal Disease and Risk of Very Preterm Delivery. Obstetrics & Gynecology 2006;107:29-36.

American Academy of Periodontology, November 21, 2005 Media release.

American Dental Association, American Academy of Periodontology

Detection and prevention of periodontal disease in diabetes – The Diabetes Monitor

Grossi SG, Treatment of periodontal disease and control of diabetes: An assessment of the evidence and need for future research, Annals of Periodontology 2001, Vol. 6, No. 1, Pages 138-145.

The Severity of Periodontal Disease is Associated with the Development of Glucose Intolerance in Non-diabetics: The Hisayama Study. J Dent Res 83(6): 485-490, 2004.

Periodontal Disease Predicts Mortality in Diabetics, Diabetes In Diabetes Care2005;28:27-32 Dr. Robert G. Nelson, of the National Institute of Diabetes and Digestive and Kidney Disease, Phoenix, AZ.

Sara Grossi, Treatment of Periodontal Disease in Diabetics Reduces Glycated Hemoglobin, J Periodontol 1997;68:713-719., SUNY Buffalo.

Saremi et al,Periodontal Disease Predicts Mortality in Diabetics, Diabetes Care, Vol. 28, No , Jan 2005

Ibid. Hisayama Study

Grossi et al, Treatment of Periodontal Disease in Diabetics Reduces Glycated Hemoglobin, J of Periodontology Aug 1997 (Vol. 68, No 8).

Ratcliff et al, The relationship between oral malodor, gingivitis, and Periodontitis. A review. J Periodontol. 1999 May;70(5)”485-9.

Grossi, SG, Treatment of Periodontal Disease and control of diabetics : an assessment of evidence and need for future research. Ann Periodontol. 2001 Dec 6 (1):138-45

Meyer DH et al, Evidence for invasion of a human ral cell line by Actinobacillus actinomycetemcomitans, Infect Immuno 59:2719-26, 1991.

Riviere GR et al, Pathogen-related oral spirochetes from dental plaque are invasive. Infect Immuno 59:3377-80, 1991.

Invasion of aortic and heart endothelial cells by porphyromonas gingivalis, Infect Immuno66:5337-43, 1998.

Haraszthy VI et al, Identification of pathogens in atheromatous plaques, J Dent Res 77:273, 1998.

Kozarov et al, Human atherosclerotic plaque contains viable invasive actinobacillus actinomycetemcomitans and porphyromonas gingivalisArteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:e17.