Quick Search Topics
a. Bacteremia
b. Cardiovascular
c. Diabetes
d. Low birth weight pre-term babies
f. Respiratory
Can periodontal disease cause systemic diseases? Is periodontal disease associated with systemic diseases?
AAP Position Paper. Periodontal disease as a potential risk factor for systemic diseases. J Periodontol 69:841-850;1998. (Review)
AAP Position Paper. Parameters on systemic conditions affected by periodontal diseases. J Periodontol 71(Suppl):880-883;2000. (Review)
Mealey BL. Influence of periodontal infections on systemic health. Periodontol 2000 21:197-209;1999. (Review)
Garcia RI, Henshaw MM, Krall EA. Relationship between periodontal disease and systemic health. Periodontol 2000 25:21-36;2000. (Review)
Loesche WJ, Lopatin DE. Interactions between periodontal disease, medical diseases and immunity in the older individual. Periodontol 2000 16:80-105, 1998. (Review)
Paquette D. The periodontal infection-systemic disease link: A review of the truth or myth. J Intern Acad Periodontol 2002; 4/3: 101-109 (Review)
Slots J. Update on general health risk of periodontal disease. Int Dent J. 53 Suppl 3:200-7, 2003. (Review).
What is a bacteremia and why is it a concern? What actions/events can cause a bacteremia? Does having periodontal disease effect this condition?
Carroll GC, Sebor RJ. Dental flossing and its relationship to transient bacteremia. J. Periodontol. 51:691-692, 1980.
Daly CG, Mitchell DH, et al. Bacteremia due to periodontal probing: A clinical and microbiological investigation. J Periodontol 72:210-214, 2001.
Forner L, Larsen T, Kilian M, Holmstrup P. Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation. J Clin Periodontol. 33:401-7, 2006
Kinane DF, Riggio MP, Walker KF, MacKenzie D, Shearer B. Bacteraemia following periodontal procedures. J Clin Periodontol. 32:708-13, 2005
Rajasuo A. Bacteremia following surgical dental extraction with an emphasis on anaerobic strains. J Dent Res 83:170-174, 2004
Brown A, Papasian C, et al. Bacteremia and intraoral suture removal: Can an antimicrobial rinse help? JADA 129:1455-1461, 1998.
What are the current guidelines for antibiotic prophylaxis?
Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al; Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group. J Am Dent Assoc. 138:739-45, 747-60. 2007
Are there any specific precautions needed for cardiac pacemakers?
Miller CS, Leonelli FM, Latham E. Selective interference with pacemaker activity by electrical dental devices. Oral Surg, Oral Med, Oral Path 85:33-36;1998
What other cardiovascular conditions can be related to periodontal disease?
Genco R, Offenbacher S, Beck J. Periodontal disease and cardiovascular disease: Epidemiology and possible mechanisms. JADA 133:14S-22S;2002
Humphrey LL, Fu R, Buckley DI, Freeman M, Helfand M. Periodontal disease and coronary heart disease incidence: A systematic review and meta-analysis. J Gen Intern Med 2008; 23:2079-2086.
Haraszthy VI, Zambon JJ, et al. Identification of periodontal pathogens in atheromatous plaques. J Periodontol 71:1554-1560;2000
Andiriankaja O, Genco R et al: The use of different measurements and definitions of periodontal disease in the study of the association between periodontal disease and risk of myocardial infarction. J Periodontol 2006; 77: 1067-1073
Joshipura K. The relationship between oral conditions and ischemic stroke and peripheral vascular disease. JADA 133:23S-30S;2002
Ridker P, Silvertown J: Inflammation, C-reactive protein, and atherothrombosis. J Periodontol 2008 Aug; 79(8suppl): 1544-51
Paraskevas S, et al: A systematic review and meta-analyses on C-reactive protein in relation to periodontitis. J Clin Periodontol 2008; 35:277-290
Does removing periodontally involved teeth affect levels of systemic inflammatory markers?
Taylor B et al: Full-mouth extraction lowers systemic inflammatory and thrombotic markers of cardiovascular risk. J Dental Res 2006; 85(1):74:78
Slade GD, Offenbacher S, Beck JD, Heiss G, Pankow JS. Acute-phase inflammatory response to periodontal disease in the US population. J Dent Res 79:49-57;2000
How does periodontal disease contribute to diabetes? Does having both diseases increase a patient’s risk for other systemic conditions?
Taylor JJ, Preshaw PM, Lalla E.A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes. J Periodontol 2013;84(4 Suppl.):S113-S134
Thorstenson H, Kuylenstierna J, Hugoson A. Medical status and complications in relation to periodontal disease experience in insulin-dependent diabetics. J Clin Periodontol 23:194-202, 1996
Does treating periodontal disease improve glycemic control?
Janket et al, Does periodontal treatment improve glycemic control in diabetic patients? A meta-analysis of intervention studies. J Dent Res. 2005 Dec;84(12):1154-9
Kiran M et al. The effect of imporoved periodontal health on metabolic control in type 2 diabetes mellitus. J Clin Periodontol 2005;32:266-272
Jones, J et al: Does periodontal care improve glycemic control? The dipartment of Veterans Affairs dental diabetes study. J Clin Periodontol 2007; 34: 46-52
Taylor. Periodontal treatment and its effect on glycemic control: review of evidence. Oral Surg, Oral Med, Oral Path 87:311-316, 1999.
Westfelt, E et al. The effect of periodontal therapy in diabetics. Results after 5 years. J Clin Periodontol 23:92-100, 1996
Can untreated periodontitis increase the risk of having a preterm birth or a baby with a low birth weight weight?
Michalowicz G, Hodges J et al: Change in periodontitis during pregnancy and the risk of pre-term birth and low birthweight. J Clin Periodontol 2009; 36: 308 – 314
Offenbacher, Jared, O’Reilly, et al. Mechanisms of periodontitis-associated pregnancy complications. Annals Periodontol 3:233-250;1998.
Does periodontal treatment during pregnancy lower the risk of having a pre-term birth or baby with low birth weight?
Lopez, J et al: Periodontal Therapy Reduces the Rate of Preterm Low Birth Weight in Women with Pregnancy –Associated Gingivitis (PAG). J Periodontol 2005; 6: 2144-2153
Jeffcoat MK, Hauth JC, Geurs NC, Reddy MS, et al. Periodontal disease and preterm birth: Results of a pilot intervention study. J Periodontol 2003;74:1214-1218.
Offenbacher S, Lin D, Strauss R, McKaig R, Irving J, Barros SP, Moss K, Barrow DA, Hefti A, Beck JD. Effects of periodontal therapy during pregnancy on periodontal status, biologic parameters, and pregnancy outcomes: a pilot study. J Periodontol. 77:2011-24. 2006
Michalowicz BS, Hodges JS, DiAngelis AJ, Lupo VR, Novak MJ, Ferguson JE, Buchanan W, Bofill J,Papapanou PN, Mitchell DA, Matseoane S, Tschida PA; OPT Study. Treatment of periodontal disease and the risk of preterm birth. N Engl J Med. 355:1885-94, 2006
Can periodontal disease affect the respiratory system? Is there a relationship between periodontal disease and COPD?
Hayes, C, Sparrow, D, Cohen, M, et al.: The association between alveolar bone loss and pulmonary function: the VA Dental Longitudinal Study. Ann Periodontol. 3, 1998, 257–261.
Scannapieco FA, Genco RJ. Association of periodontal infections with atherosclerotic and pulmonary diseases. J Perio Res 34:340-345;1999.
Hyman, JJ, Reid, BC: Cigarette smoking, periodontal disease, and chronic obstructive pulmonary disease. J Periodontol. 75, 2004, 9–15.
Abstracts
The Perio-Systemic Link: Can periodontal disease cause systemic diseases? Is periodontal disease associated with systemic diseases?
Topic: Periodontal - Systemic disease
Authors: AAP Position Paper. NO ARTICLE
Title: Periodontal disease as a potential risk factor for systemic diseases
Source: J Periodontol 69:841-850;1998. (Review)
Type: Review
Rating: Good
Keywords: Bacteremia, infective endocarditis, cardiovascular disease, prosethetic, respiratory, Pregnancy
P: Review of periodontal disease as a potential risk factor for systemic diseases.
Disc:
Bacteremia: Entry of oral microorganisms or their products into the blood stream. Can be provoked by mastication, flossing, and toothbrushing. The extent is based on amount of inflammation present. Best prevention is to maintain periodontal health.
Infective Endocarditis (IE): Bacterial infection of damaged heart valves. Bacteria gain access to bloodstream and adhere to these surfaces. Dental procedures predispose susceptible patients to IE. It has acute and subacute forms. The most common agents of SBE are oral streptococci (S.sanguis). Also gram negative bacteria such as P.g. F.n. A.a. have been detected. Thus patients having the risk factors of SBE and periodontitis are in greater risk for SBE than patients with healthy periodontal tissues. Current recommendations focus on AB prophylaxis for procedures likely to provoke bacteremia. Amoxicillin is the antibiotic of choice.
Cardiovascular disease and Atherosclerosis: Atherosclerosis is a progressive degenerative condition involving large to medium-sized arteries. Atheromatous plaques in the arteries consist of lysed cells, cholesterol ester crystals, foam cells and plasma proteins (fibrin and fibrinogen). Another mechanism proposed to explain the formation of plaques is that bacteria, mainly S.sanguis and P.g. induce aggregation of platelets through the binding of a specific surface protein. Dental infections appear to increase the risk of coronary artery disease to a degree similar to the classical risk factors for CVD including age, smoking, diabetes, hypertension, and elevated serum triglycerides. The biological basis for the hypothetical association of CVD and periodontal infections is presently unclear.
Prosthetic device infection: Prosthetic devices are vulnerable to bacterial colonization and infection, which can lead to prosthetic failure, as well as death. Most prosthetic join infections are caused by non oral bacteria such as staphylococci. Anitbiotic prophylaxis is recommended.
Respiratory disease: Bacterial pneumonia will likely assume increasing importance in the near future due to the continuing emergence of antibiotic resistant bacteria. Potential respiratory pathogens may become established in the oral flora of patients with periodontal disease. Subjects with high risk for pneumonia, such as the hospitalized patients, may be more prone to oral colonization by respiratory pathogens following mucosal modification due to prolonged exposure to plaque. COPD and chronic bronchitis may also be adversely influenced by oral conditions, however, the mechanism is not clear.
Adverse pregnancy outcomes: It is possible that subclinical infections may adversely affect pregnancy outcomes, increasing the preterm low birth weight infants. PGE2 and TNF-a levels which are normally involved in normal parturition, are increasing by the infection process which may foster premature labor. Periodontal infection may influence the pregnancy outcome by elevating the levels of LPS, PGE2 and TNF-a.
Topic: Systemic conditions
Authors: AAP Position Paper. NO ARTICLE
Title: Parameters on systemic conditions affected by periodontal diseases.
Source: J Periodontol 71(Suppl):880-883;2000.
Rating: Good
Keywords: systemic conditions, Diabetes mellitus, Pregnancy, Cardiovascular diseases.
Purpose: To describe the parameters of care on systemic conditions affected by periodontal diseases.
Discussion:
Patient evaluation:
1. A comprehensive periodontal evaluation
2. The medical history should be evaluated for existing systemic diseases or conditions, medications, and risk factors for systemic diseases.
3. Any consultation should be documented.
Therapeutic goals:
To diagnose periodontal infection which may impact health and then establish health, which will minimize periodontal infection.
Periodontal disease may have an impact on Diabetes mellitus, Pregnancy, Cardiovascular diseases.
Preliminary evidence suggests that periodontal infections may also be associated with pulmonary disease and other remote site infections.
Treatment considerations
Diabetes Mellitus:
Periodontitis may adversely affect glycemic control in diabetes.
May be associated with an increased risk of CV complications.
Periodontal treatment, especially in pts with severe periodontitis and poorly controlled diabetes, may result in improvement in glycemic control.
Tx includes dx, consult MD for diabetic status and education of the patient regarding the possible impact of periodontal infection on glycemic control.
Consideration may be given to the use of systemic antibiotics in conjunction with mechanical therapy
Pregnancy:
May have an increased risk for pre-term low birth weight delivery.
Tx includes diagnosis, consult MD, consider pregnancy status, and educate pt.on health and hygiene.
Cardiovascular Diseases:
Coronary artery disease
Individuals with periodontal disease may have sig increased risk of CHD and related events such as angina pectoris and MI.
Periodontal pathogens may contribute to atherogenic changes and thromboembolic events in the coronary arteries.
Similar processes may occur in other arteries (periodontal disease may increase the risk of cerebral ischemia and non-hemorrhagic stroke)
Infective endocarditis
Bacteremias may occur in individuals with a healthy periodontium, they may be intensified in patients with periodontitis.
Tx dx,consult,consider severity of CV dz,and educate pt
Outcomes Assessment:
Prevent adverse systemic consequences of existing periodontal infection: know pt hx status and interactions.
Reduce periodontal pathogens.
Reduction of clinical signs of gingival inflammation. Reduction of probing depths.
Stabilization or gain of clinical attachment.
Control of acute periodontal infections.
Addressing the risk factors for periodontal disease as they affect the systemic condition.
Topic: Periodontal infections and systemic health
Authors: Mealey B. ARTICLE
Title: Influence of periodontal infections on systemic health.
Source: Periodontol 2000 21:197-209;1999.
Type: Review
Rating: Good
Keywords: Pre-term low-birth weight, diabetes, cardiovascular disease
Purpose: A review of periodontal infection and its influence on systemic health
Discussion:
Pre-term low-birth weight (PTLBW)
Low birth weight infants (< 2.5kg) are 40x more likely to die in the neonatal period than normal birth weight infants. Smoking, alcohol, drug use, inadequate prenatal care, low socioeconomic status, HTN, race, age, DM, GI infections have been shown to increase the risk of PTLBW. These are not present in ¼ of cases however. Prostaglandin increases steadily during pregnancy until sufficient levels are reached to induce labor. It has been shown that infection itself does not lead to preterm labor, however inflammatory cytokines like IL-1B, TNF-A, IL-6 have been shown to increase PG production. This premature increase has been shown to cause preterm labor. Offenbacher found a 7.5 fold increase in chance of having PTLBW for mothers with significant periodontal disease.
Diabetes Mellitus
Taylor demonstrated severe periodontitis increased the risk for poor glycemic control. All subjects had a “well controlled” HbA1c of 9% at baseline. 2 years later at follow-up appointments, more subjects had higher than 9% with severe periodontitis than did subjects without severe periodontitis.
Thostensson’s study looked at Type I DM with either severe perio or mild perio/gingivitis. The follow-up period ranged from 1-11 years later (avg of 6yrs) and found subjects with severe perio had significantly greater prevalence of proteinuria and greater number of Cardio and cerebrovascular events compared to the mild perio/gingivitis group. Williams & Mahan, Miller showed an improvement in glycemic control following periodontal therapy. Grossi compared poorly controlled type 2 DM with severe perio at 3, 6, and 12 months following non-surgical therapy combined with systemic doxycycline vs placebo. The doxycycline group showed better reduction in PD, BOP as well as significant improvements in HbA1c levels at 3 months. By 12 months, glycosylated Hb levels had returned to baseline.
Perio therapy may have no benefit in patients who are relatively well controlled prior to treatment, but may lead to improved metabolic control in patients with poorly controlled DM.
The proposed mechanism for how periodontal disease affects the glycemic status is as follows: Insulin resistance has been shown to occur following an acute bacterial or viral infection, and persists for an extended period of time following clinical resolution of the infection. It is possible that the chronic G(-) periodontal infection also causes this insulin resistance and thereby poor glycemic control.
Cardiovascular Disease (CVD)
Syrjanen’s study examined 40 pts with a Hx of stroke received a dental exam within 1 mo of the event. BOP (Male and Female), sub-g calculus (M) and suppuration (M) was found to be significantly greater in stroke patients than controls. The number of periapical and periodontal lesions was also shown to be sig greater in stroke pts. 25% of stroke pts had sig dental infections, compared to 2.5% of controls. Matilla showed a relationship of severity of periodontal and periapical infections and degree of coronary atheromatosis, accounting for confounding factors (BMI, lipid profile, HT, smoking, socioeconomic status). Another study found 130 patients with acute MI had significantly greater prevalence of periodontal disease, advanced caries and periapical lesions when compared to controls. The authors emphasize it may not be a causal relationship, rather an indicator of general health care. Periodontal and CHD are both related to lifestyle and share certain risk factors: Smoking, DM, low socioeconomic status.
DeStefano showed a 25% increased risk for CHD in patients who had periodontitis compared to those with no or minimal periodontal disease. Among younger age group males, periodontitis increased the risk by 70% for CAD. Beck demonstrated patients w/ a mean whole mouth bone loss score of 20% had a 50% increase of CHD compared to those who had less than 20% bone loss score. 40 of 1147 subjects had a stroke during the f/u period. OR of having a stroke for bn score >20% was 2.8. The authors concluded perio dz is a risk factor for CHD independent of of other classic risk factors.
Mechanism of periodontal disease and CHD: poor oral health has been shown to increase von Willebrand factor, increasing thrombus formation. Platelets actively bind Strep sanguis (commonly found in supragingival plaque), which can result in thrombus formation. Infection incudes a hypercoagulable state and increased blood viscosity. LPS has been shown to increase the amount of inflammatory cells in major blood vessels, as well as upregulation of proinflamm cytokines- TNF-A, IL-B, PDGF. The low level bacteremia may negatively affect coagulability, endothelial integrity and platelet function atherogenic changes.
Respiratory Infections
Dental plaque has been theorized as a source for bacteria associated with resp infections. Terpenning found 27% of dentate hospitalized patients developed pneumonia compared to 0% of edentulous patients. 19 % of dentate nursing home patients were found to develop pneumonia compared to 7.6% of edentulous patients. Enterobacteriaceae species, capnocytophaga, Aa have been implicated in respiratory infections- also found in subgingival plaque. It is unclear if the same pathogens from sub-g areas are causing the respiratory pathology.
Remote site infections (Brain abscess)
3 case series showed 5 of 190 cases (2.6%) were related to dental procedures or odontogenic infection. A high percentage of brain abscesses are associated with Strep mutans and Strep milleri, both commonly found in the oral cavity. F. nucleatum and Bacteriodes, E. corrodens are often found in the abscess, which are also found in the oral cavity. No study has shown definitively that the same oral bacteria are found in these abscesses.
Conclusion: Rather than being confined to the periodontium, periodontal diseases may have widespread systemic effects. These effects are likely inconsequential in most individuals but in a susceptible host w/ an underlying systemic condition/genetic predisposition, periodontal infection may adversely effect the patient’s systemic status.
Topic: Systemic Disease
Authors: Garcia RI, Henshaw MM, Krall EA ARTICLE
Title: Relationship between periodontal disease and systemic health.
Source: Periodontol 2000 25:21-36;2000
Type: Review
Rating: Good
Keywords:
Purpose: To assess the relationship between periodontal disease and systemic health.
Discussion: Effects of systemic disease on the periodontium.
Osteoporosis: Osteoporosis results in reduction in bone mass and may lead to skeletal fragility. It has been hypothetized that osteoporosis may cause decreased alveolar bone density, which may in turn be more susceptible to resorption by the effect of coexisting periodontal infection. In the larger study to date, no significant correlations were found between loss of alveolar bone height and spine bone mineral density. Additional longer-term studies are needed to determine this association.
Renal dysfunction: Renal osteodystrophy and the related skeletal bone changes are consequences of renal failure. Individuals with this disorder often experience hypocalcemia. This hypocalcemic statue results in secretion of parathyroid hormone. The body tries to maintain homeostatic balance and as a result bone resorption occurs. Clinical presentation includes bending and fracture of long bones due to a gradual softening of bones over time. It appears likely that the decreased bone mineral density in such patients would increase risk for progressive alveolar bone loss from subsequent periodontal infection.
Immune suppression: The advent of HIV infection and the improved success of organ transplantation had led to increased number of immunosuppressed patients. Oral problems that commonly occur in these patients are oral infections, hairy leukoplakia, malignant changes, drug induced gingival overgrowth and periodontal disease.
Immunodeficiency diseases: Acquired Immunodeficiency syndrome (AIDS) is characterized by a reduction in cell-mediated immune response. As a result, there is increased tendency to develop fungal, viral, and bacterial infections. Periodontal manifestations of HIV infection include linear gingival erythema, necrotizing ulcerative gingivitis and necrotizing ulcerative periodontitis. Most studies have found that the sub-g species in HIV-periodontitis patients are similar to those found in non-HIV- periodontitis patients.
Environmental immunosuppression: Most human studies have found significant associations between certain psychosocial factors and chronic inflammatory periodontal disease. Stress activates the central nervous system and the resultant release of cortisol may cause a depression in the immune response, including secretory immunoglobulin A, IgG and neutrophil functions. This may provide the periodontal bacteria an opportunity to proliferate and possibly invade the tissues, eventually causing a more extensive inflammatory response. Behavioral changes that accompany stress (smoking, poor OH, poor compliance and dental care) may be correlated to periodontal disease.
Pregnancy: Increases in gingival inflammation typically begin in the second month and reach a maximal level during eighth month of pregnancy. Increased hormone levels are associated with gingival inflammation. One of the effects of hormones is to increase capillary dilation. Also, maternal hormones are associated immunosuppression (altered T-cell response and impaired lymphocyte proliferation). Kornman & Loesche showed that the ratio of anaerobic to aerobic bacteria increase significantly during pregnancy.
Diabetes: Individuals with diabetes are found to have more periodontal attachment loss than non-diabetic subjects. Individuals with non-insulin dependent diabetes have a 3-fold increased risk for future periodontal destruction. Possible explanation is that diabetic patients have a compromised ability to respond to bacterial infections. Also, there are studies supporting that periodontal antimicrobial treatment may reduce the level of glycosylated hemoglobin in diabetic patients and affect diabetes control. More research is needed.
Periodontal disease as a risk factor for systemic disease
There is increasing evidence that individuals with periodontal disease may be at increased risk for adverse medical outcomes.
Men and women, 25-74 years old, with periodontitis had a 46% increased risk for mortality from all causes.
In another study it was found that subjects with the deepest average PD were found to be at 74% higher risk of death controlling for all relevant co-variates.
Cardiovascular disease: Studies have been shown an association between cardiovascular disease and periodontal disease. 50-100% increased risk of cardiovascular disease in patients with oral conditions. Individuals with severe types of periodontal disease have a hyper-inflammatory phenotype which secretes abnormally high levels of inflammatory cytokines, raised the possibility that this phenotype might be a risk factor for atherosclerosis and emboli formation. Research is required to determine whether there are beneficial effects of periodontal treatment
Pulmonary disease: Oral bacteria have been implicated in the pathogenesis of bacterial pneumonia and it has been hypothetized that dental plaque may be an important reservoir of these potential respiratory pathogens. A.actinomycetemcomitans, Actinomyces Israelli, Capnocytophaga species, Eikenella corrodens and others have been identified in infected sputum and lung abscesses. Patients with chronic respiratory disease had significantly worse OH index than people without respiratory disease. Possible association between periodontal disease and COPD. Both have similar pathophysiological processes. Both diseases involve recruitment of neutrophils to inflammatory sites resulting in tissue destruction. As a result, there is increased phagocytosis, connective tissue damage and complement inactivation of regulating inhibitors.
Adverse pregnancy outcomes: One important factor contributing to the continuing prevalence of infants with preterm low birth weight is the maternal burden of infection. Periodontal infection may be of importance. Gram negative periodontal anaerobic pathogens initiate a host inflammatory response that has systemic consequences. Bacterial endotoxins from periodontal infection trigger release of biologically active mediators such as PGE2 and tumor necrosis factors which may trigger premature labor.
Topic: Periodontal medicine
Author: Loesche WJ, Lopatin DE. ARTICLE
Title: Interactions between periodontal disease, medical diseases and immunity in the older individual.
Source: Periodontol 2000 16:80-105, 1998.
Type: Review
Rating: Good
Keywords: oral systemic connection, periodontal medicine, cytokine leakage
Purpose: To review interactions between periodontal disease, systemic diseases and immunity in the older individual.
DISCUSSION: Results found that:
Among dentate individuals those with periodontal disease would be more likely to develop aspiration pneumonia than individual without periodontal disease (perio pathogenic microbes are significantly elevated in saliva of pneumonia pts)
Aspiration pneumonia pts more frequently depended on others for feeding was the most dominant risk factor (fed so fast, they aspirate)
Bacteria involved were Capnocytophaga and F. nucleatum
Intervention strategy for aspiration pneumonia: feed pts slowly and improve OH
The Plaque Index and periodontal disease scores were significantly higher among the dentate members of the definite aspiration pneumonia group than among the dentate members of the no pneumonia group.
Periodontal disease would be central to the pathways involving infection and inflammation (pathway 3).
The chronic infection that is contained by the inflammatory process in the periodontium could deliver harmful levels of cytokines and other inflammatory mediators to the systemic circulation(pathway 3a). It could result in bacterial products such as lipopolysaccharide and heat shock proteins entering the circulation (pathway 3b).
Some members of the plaque flora because of poor OH or chronic infection might escape into the bloodstream, causing asymptomatic bacteremia (pathway 4) that could elevate the white blood cell count and contribute to the hypercoagulability of blood via increased levels of fibrinogen (pathway 4a). It is possible that certain invading bacteria could specifically increase the coagulability of the blood by aggregating platelets (pathway 4a). Poor OH could give rise to bacteremia without advanced forms of periodontal disease (pathway 4)
As the platelet aggregation-associated protein appears to be a heat shock protein, it is possible that autoimmune mechanisms based on pathway 3b could be involved.
All these events could occur continuously or intermittently during the progression from having diseased teeth to being edentulous. So by the time an individual arrives at the edentulous state, they may have traversed a gamut of insults ranging from bacteremia to cytokine leakage from the periodontium into the systemic circulation. Once this has ceased, there still remain the dietary changes that may put the individual at risk to cardiovasculardisease (pathway 2).
BL: Many positive associations between poor dental and oral health and adverse medical outcomes (particularly aspiration pneumonia and cardiovascular diseases). Further research is needed.
Topic: Systemic Effects of Periodontitis
Authors: Paquette D. ARTICLE
Title: The periodontal infection-systemic disease link: A review of the truth or myth.
Source: J Intern Acad Periodontol 2002; 4/3: 101-109
Type: Review
Rating: Good
Keywords: periodontal disease, pathophysiology, periodontitis, cardiovascular diseases, infant, low birth weight, risk, risk factor
P: Review of biologic plausibility for a periodontal infection-systemic disease link and the available data as related to cardiovascular disease (CVD) and preterm low birth weight in human and animal studies.
R: 5 principle lines of evidence can be used to explain a link:
1. Infection in general has been implicated in the pathogenesis of both atherosclerosis and pre-term delivery
2. Periodontal infection causes transient and low-grade bacteremias and endotoxemias in patients
3. Periodontal infections promotes systemic inflammatory and immune responses that may play roles in disease. IL6 is known to promote atheroma and thrombus formation. C reactive proteins, white blood cells, fibrinogen independently correlate with risk of cardiovascular disease.
4. Perio pathogens express specific virulence factors that can affect atherogenic or parturition events
5. Perio pathogens (red series) have also been isolated from non-oral tissues like atheromatous plaques
D: Experimental data derived from rodent and pig models indicate that infection or bacteremias with the perio pathogen P gingivalis can increase atheroma size or reduce litter weights as compared to controls.
While human intervention data are lacking for patients at risk from cardiovascular disease, early data indicate that perio therapy administered to pregnant mothers with periodontitis can reduce the incidence of pre-term low birth weight deliveries.
A study by Offenbacher in 1996 stated that pregnant women with perio dz were 7x more likely to have preterm low birth weight babies compared to women without perio.
Pts with untreated moderate to advanced perio may be 30% to two times more likely to exhibit CVD.
For preterm birthweight, vaginal infection with G-negative Bacteroides species (bacterial vaginosis) increases indicence rates by 40-60%. While 18-49% of placentas with inflamed chorioamnionic membranes have negative bacterial cultures, it has been postulated that infection can indirectly cause preterm low birth weight via the translocation of bacterial products like LPS to the feto-placental unit or by maternally produced inflammatory mediators.-
These data on non-oral pathogens support the basic hypothesis that infection in general can promote the pathogenesis of low preterm birthweight and atherosclerosis via common direct or indirect mechanisms.
In a study with 50 human carotid atheromas, 30% had T.f., 26% P.g., 18% A.a., and 14% P.i.
The authors hypothesize that in certain individuals there may be an underlying hyper-inflammatory trait in response to stimuli manifested by an excessive production of cytokines and arachadonic acid mediators by monocytes and other cell types. However, human experimental evidence demonstrating a reduction in the risk for systemic disease secondary to periodontal intervention is limited at present.
Topic: health risks of perio
Title: Update on general health risk of periodontal disease.
Source: Int Dent J. 53 Suppl 3:200-7, 2003.
Type: Review
Rating: good
Keywords: periodontal disease, pathogenic bacteria, focal infection, nonoral disease
Purpose: To describe the current views of the oral bacteria, yeasts and viruses in the etiology of systemic diseases, especially on the acute non-oral infections.
Discussion: Periodontal disease: Inflammatory periodontal diseases are probably the most common type of human infection in the world. In patients with periodontitis, there is a significant burden of inflammatory and immunologic mediators. Bacteremia can be detected at 60-80% of people at any given time. Can be caused by oral hygiene habits or mastication, is low-grade intensity and usually of short duration (blood becomes sterile again in 15-30min.
A.a. and P. gingivalis as well as other periodontopathic bacteria are unique to the human oral cavity and their presence to extraoral sites indicates dissemination from the mouth.
Infective endocarditis is a complication of congenital and acquired heart disease. About 8% of the cases are associated with periodontal or dental disease without a dental procedure. Streptococci and staphylococci are the most common pathogens. A.a. has also been isolated relatively frequently from cases of infective endocarditis. Although newer guidelines about antibiotic prophylaxis include fewer dental procedures and a shorter course of antibiotics, there seems to be little doubt that maintaining a healthy dentition and periodontium is an important step in preventing infective endocarditis.
Aspiration pneumonia is caused by mainly by aspiration of infected oropharyngeal content into the lung. Periodontal disease and dental caries correlate with increased risk of aspiration pneumonia.
Oral candidiasis is the most common opportunistic infection in patients with HIV infection. It is important to provide treatment to these patients in order to avoid life – threatening disseminated candidiasis. Necrotizing periodontal diseases can also occur in these patients.
Patients scheduled for cytotoxic chemotherapy should receive pretherapeutic dental care to eliminate potential sources of infection and be instructed for oral hygiene including frequent rinsing with 1% povidone – iodine or 0.12-0.2% chlorexidine and effective tooth brushing.
To avoid the risk of infected osteoradionecrosis, dentoalveolar surgery should be avoided in the region of the irradiated bone, in patients receiving radiotherapy.
Necrotizing fasciitis is a life threatening bacterial infection characterized by diffuse necrosis of fascial planes, subcutaneous tissues and blood vessels. It can have a periodontal origin and occurs mainly in individuals having poorly control diabetes or other types of compromised host defense. Mortality rates are as high as 74%. Brain abscesses, Ludwig’s angina, deep neck infection, coma and toxic shock syndrome may originate from dental infections but are very rare.
Diabetes mellitus: Current evidence incriminates chronic inflammation as one of the triggers of chronic insulin insensitivity. Improvement in insulin sensitivity may occur after treating existing infectious diseases, including periodontal disease. The antimicrobial effectiveness of periodontal therapy influences the degree of improvement in glycemic control.
Periodontal disease bacteria have been linked to coronary heart disease but further investigations are needed to reliably assess the association of these agents with CHD. The only intact infectious agents currently present in atherosclerotic plaques are C. pneumonia and herpes viruses. CRP and other inflammatory biomarkers elevated in patients with periodontal disease, have been linked to CHD.
Herpes viruses are present in the majority of advanced periodontal lesions but rarely detected in healthy periodontal sites. Productive herpes viruses in inflamed gingival tissue may seed to other body sites or shed into saliva and subsequently infect other individuals. Further studies are needed to establish the relationship between degree of periodontal disease and level of salivary herpes viruses.
Conclusion: The most effective means of preventing systemic diseases from oral microorganisms is by maintaining a healthy dentition and periodontium.
What is a bacteremia and why is it a concern? What actions/events can cause a bacteremia? Does having periodontal disease effect this condition?
Topic: Flossing
Author: Carroll GC. ARTICLE
Title: Dental flossing and its relationship to transient bacteremia
Source: J. Periodontol. 51:691-692, 1980
Type: Clinical trial
Rating: Good
Keywords: Flossing; bacteremia
Purpose: to determine the role of dental flossing in producing transient bacteremias.
Methods: Four healthy patients (1m, 3f) were included, only one of these subject (subject A) flossed regularly before the study. 2 patients didn't have periodontal disease; the other 2 had marginal gingivitis. Blood samples were taken before the study. Subjects began flossing immediately after phlebotomy and continued for 3 min. Blood cultures were then taken again after completion of flossing. The different subjects underwent different flossing protocols and had cultures drawn at different intervals. A total of 32 blood cultures were taken. The occurrence of gingival bleeding was also recorded.
Results:
-No positive blood cultures were obtained when the subjects flossed daily (on-floss blood culture)
-6/7 flossings performed after an interval of 2 or more days without flossing resulted in detectable bacteremia.
-Gingival bleeding was observed in 2/7 of the daily flossing subjects, but no bacteremia was found. The presence of gingival bleeding was not a requirement of bacteremia.
-Routine daily flossing eliminated flossing related bacteremia
-Less than daily flossing resulted in an 86% risk of bacteremia.
Discussion: When flossing is done alone every second day, or less frequently, it is highly likely to induce a bacteremia. When flossing is done daily, no bacteremia was found. There is a high risk of bacteremia during initiation of an oral hygiene program. This indicates the need for antibiotic prophylaxis in a patient for whom bacteremia poses a hazard.
Topic: Bacteremia with probing
Authors: Daly CG, Mitchell DH, et al ARTICLE
Title: Bacteremia due to periodontal probing: A clinical and microbiological investigation
Source: J Periodontol 72:210-214, 2001
Type: Clinical study
Rating: Good
Keywords: Bacteremia/prevention and control; gingivitis/microbiology; periodontitis/microbiology; periodontal probes; endocarditis; bacterial/prevention and control
Purpose: (1) To investigate the occurrence of bacteremia with full mouth probing in patients with adult periodontitis and chronic gingivitis, (2) identify microbes present within positive blood cultures, (3) asses factors such as age, smoking status, PI, number of teeth probed, BOP, and PD for any association with bacteremia.
Methods: 40 patients, 20 with periodontitis (10 male, 10 female) and 20 with chronic gingivitis (11 male, 9 female) were used in this study. Prior to and immediately after probing, 20 mL of venous blood were obtained from each patient and inoculated into aerobic/anaerobic blood culture bottles and incubated. Negative bottles were monitored continuously for 3 weeks before being discarded. Positive bottles were subcultured and isolates identified. Probing was done at 6 points around each tooth. BOP, number of teeth, and PI were also recorded.
Results: The periodontitis group showed significantly higher PD, BOP, and PI. No bacterial growth was detected in any of the blood samples taken prior to probing. Probing caused bacteremia of oral origin in 8 (40%) of the periodontitis patients and 2 (10%) of the gingivitis patients. Gram positive Streptococcus species were the most common isolates in both groups (which accounts for the majority of IE). BOP and mean PD were significantly associated with bacteremia. No significant correlation was found between bacteremia and age, number of teeth probed, smoking status, PI, or total PD.
Discussion: Patients with untreated adult periodontitis are at greater risk of bacteremia due to probing than patients with chronic gingivitis. For people at risk of infective endocarditis, radiographic assessment prior to probing would be advisable to identify those w/ periodontitis so that appropriate antibiotic prophylaxis can be provided.
Topic: Bacteremia scaling
Authors: Forner L, Larsen T, Kilian M, Holmstrup P. ARTICLE
Title: Incidence of bacteremia after chewing, tooth brushing and scaling in individuals with periodontal inflammation.
Source: J Clin Periodontol. 33:401-7, 2006
Type: Clinical study
Rating: Good
Keywords: bacteremia, chewing, tooth brushing, scaling
P: To determine the incidence, magnitude, duration, and nature of bacteremia in individuals with peridontitis, gingivitis, and clinically healthy periodontium after chewing, toothbrushing, and scaling.
M&M: 60 systemically healthy individuals were chosen. 20 participants in each group:
periodontitis (10 sites with PD > 5 mm). 11 were diagnosed with aggressive and 9 with chronic periodontitis.
gingivitis (distance from CEJ-alveolar bone < 2 mm on radiograph , PPD < 4 mm, GI > 1.5
healthy periodontium (same as gingivitis, but GI < 0.5)
A clinical exam was performed that included PD, GI, PI, BOP, and CAL, and radiographs (pa and bitewings) were taken.
3 experimental procedures were performed: 1. Chewing on gum for 10 minutes, 2. Supervised toothbrushing for 2 minutes (thorough instructions were given to ensure standardization among the participants and 3. Full mouth scaling using hand instruments and an air scaler. All participants were exposed to the 3 experimental procedures in the following order: chewing, toothbrushing and scaling on separate days with at least 6 days in between. Blood was collected on each participant at baseline and at 0.5, 10, and 30 minutes following each experimental procedure.
R: None of the 60 subjects showed bactermia prior to starting any of the experiments.
Following chewing gum, 20% (4) of the periodontitis patients were bacteremic whereas none of the healthy or gingivitis patients were bacteremic.
Following toothbrushing, none of the healthy or gingivitis patients were bacteremic. Immediately after toothbrushing, one (5%) of the periodontitis patients was bacteremic. After 30 min., bacteremia was found in another patient from whom no bacteria were recovered in the blood samples collected at 0.5 or 10 min. after tooth brushing.
Following scaling, 10% (2) of the healthy participants had bacteremia, 20% (4) of the gingivitis patients, and 75% (15) of the periodontitis patients.
Of the 29 patients that had a bacteremic episode, only 4 remained after 30 minutes (among these 4 episodes, one occurred after chewing, one after toothbrushing and two after scaling.
A total of 163 isolates were collected from 29 bacteremic episodes. The isolates were from two healthy individuals, four gingivitis patients and 17 periodontitis patients after chewing, toothbrushing and scaling.
The bacterial isolates included a range of Streptococcus, Enterococcus, Actinomyces, Lactobacillus, Corynebacterium, Porphyromonas, Prevotella and Fusobacterium species in addition to one isolate of Candida. The most predominant Streptococcus species were S. mitis, S. oralis, and S. sanguis. Among the anaerobic Gram- negative rods Prevotella intermedia and Fusobacterium nucleatum were most frequently isolated.
There were NSSD between any of the groups regarding the incidences or magnitudes of bacteremia after chewing or tooth brushing at any time following the experimental procedures.
After scaling, the incidences and magnitudes of bacteremia were significantly higher in the periodontitis group than in the gingivitis group and healthy periodontium group. There was no significant difference in the incidences of bacteremia between the gingivitis group and the healthy individuals at 0.5 min. or between any of the groups at 10 or 30min. after scaling.
The magnitude of bacteremia (CFU/ml) immediately after scaling was moderately positively correlated with GI, PI and number of sites with BOP. No statistical association was detected between bacteremia and number of sites with PPD>5.
The magnitude of bacteremia was independent on age, gender, smoking, periodontal diagnosis (chronic or aggressive periodontitis), and time used for scaling.
C: This study demonstrates that patients with periodontitis, as compared to healthy individuals and gingivitis patients, are at increased risk of experiencing bacteremia in association with scaling.
Topic: Bacteremia
Authors Kinane DF, Riggio MP, Walker KF, MacKenzie D, Shearer B. ARTICLE
Title Bacteremia following periodontal procedures.
Source: J Clin Periodontol. 32:708-13, 2005
Type: Prospective study
Rating: Good
Keywords: Bacteremia
Purpose: To assess patient and practitioner-induced bacteremia within periodontitis patients following routine periodontal procedures, namely periodontal probing, toothbrushing and ultrasonic scaling.
Method: Single blind parallel trial, 30 patients with untreated periodontal disease. Blood sample sequencing as follows:
1st visit: SAMPLE 1 blood sample for baseline----charting----blood sample (SAMPLE 2)
2nd visit two weeks later: SAMPLE 3 blood sample for baseline---supervised toothbrushing for 2 minutes---blood sample (SAMPLE 4)—full mouth ultrasonic scaling ---- final blood sample (SAMPLE 5).
Used two methods to detect bacteria in blood: first was culture, the second was PCR
Results:
|
Method of detection |
Incidence of bacteremia from ultrasonic scaling |
Incidence of bacteremia from probing |
Incidence of bacteremia from brushing |
|
Culture |
13% |
20% |
3% |
|
PCR |
23% |
16% |
13% |
Group I: elevated whole mouth scores for B-glucuronidase
Group II: could not be identified by whole mouth scores for any of the enzymes, but individual site of B-glucuronidase
B-glucuronidase was found to be a predictable indicator of attachment loss. It is associated with PMN granule releaseà clinical attachment loss can be related to exuberant PMN response. B-glucuronidase is a common marker for attachment loss.
Arylsulfatase and lactate dehydrogenase had NSSD in measurement of localized clinical attachment loss in patients with at least 2.5 mm attachment loss in two sites before samples were taken.
Conclusion: Although this study showed lower numbers than previously reported, bacteremia is evident and detectable following oral manipulation
Topic: Bacteremia extraction
Authors: Rajasuo A. ARTICLE
Title: Bacteremia following surgical dental extraction with an emphasis on anaerobic strains
Source: J Dent Res 83:170-174, 2004
Type: Clinical
Rating: Good
Keywords: bacteremia, tooth extraction, molar, third
Purpose: To investigate bacteremia caused by surgical extraction of partially erupted mandibular 3rd molars.
Methods: Sixteen healthy individuals without diagnosed periodontal disease had partially erupted 3rd molars. Although plaque free at the time of exam, 25% had calculus deposits at the lingual of the mand incisors. Pts were diagnosed with pericoronitis, and treatment planned for extraction of single mand 3rd molar. Mean PD at the 3rd molars was 8.1±2.5mm w/ visible pus detected at 38% of them. Gingival tissue was cleaned with ethanol around the 3rd molars and bacterial samples were obtained utilizing endo paper-points in the pocket for 30 seconds before ext and in socket after ext. Blood samples were taken 1 minute after the initial incision, 1 minute after extraction and 5, 10, 15, and 30 minutes after surgery. Bacterial and blood cultures were initiated.
Results: Bacteremia was detected in 88% of subjects (14/16). 50% showed bacteremia after the initial incision, and 44% were culture-positive 1 and 10 minutes after extraction. By 30mins after surgery, only 12.5% showed a positive culture. Anaerobic species were found in every case. A mean of 3.9±2.6 bacterial species were detected per blood sample. 93% had at least one common species in the blood and the pericoronal pocket samples. 43% of the cases showed the same species in the serum and extraction socket at the time of extraction.
Discussion: In these cases, the majority of bacteria detected in serum samples were anaerobic. Other studies show the majority of endocarditis cases are caused by aerobic gram + staph or strep. The emphasis for preventing bacterial endocarditis should be on preventing periodontal disease, including gingival inflammation, as any manipulation of oral tissue can result in a bacteremia, since there is evidence that prophylactic administration of antibiotics does not significantly lower the incidence or magnitude of bacteremia after tooth extraction (Hall 1993, Kaneko 1995).
Conclusion: The frequency of post ext bacteremia is higher than previously thought, and the duration can be at least 30mins, indicating that the 10 min follow-up reported in earlier studies was insufficient for the duration of transient bacteremia to be visualized. The majority of bacterial species detected were anaerobic in nature.
Topic: Bacteremia after suture removal
Authors: Brown A, Papasian C, et al ARTICLE
Title: Bacteremia and intraoral suture removal: Can an antimicrobial rinse help?
Source: JADA 129:1455-1461, 1998
Type: Review
Rating: Good
Keywords:
Purpose: To determine whether a relationship exists between the incidence of bacteremia and suture removal.
Method: 71 patients requiring the removal of 3rd molars were included in the study. 10 patients failed to return for follow-up, leaving 61 participants (37F/24M) aged 15-35 years. Exclusion criteria: patients with systemic diseases, patients taking steroids or had used systemic antibiotics or oral rinses within the preceding 4 weeks, had moderate to severe periodontitis or residual pericoronitis, or required antibiotic prophylaxis. 3rd molars were removed using similar flap designs and 3-0 silk sutures were placed. Surgeons used no medications in the sockets, no pre-op irrigations or rinses were used. Post-op only warm salt water rinses were allowed. Patients returned for suture removal at 7 days and were divided into two groups: Group 1(test) used 0.12% CHX preprocedural rinse and Group 2(control) received no preprocedural rinse. Blood samples (10 mL) were taken pre and post suture removal and sent to lab for culturing. Bleeding following suture removal was also noted.
Results: Data analyzed for 55 subjects (31 for test group and 24 for control group). 6/55 blood cultures were positive .10.9% of all subjects developed procedure-related bacteremias. Of the 6 patients with bacteremia 4/6 were from the test group (12.9%) and 2/6 were from the control group (8.3%). Only 1 of the 6 subjects with bacteremia was labeled as having less than good OH. Preprocedural use of an antimicrobial oral rinse (0.12% CHx) did not significantly reduce the incidence of bacteremia when compared with no rinse at all. No SS relationship between the presence of bleeding after suture removal and the incidence of bacteremia was found. In all but one patient, colony counts of positive bacteremia were quite low.
Discussion: Forceful rinsing of inflamed tissues along with a very short period for antibacterial action of CHx provides explanations for the higher incidence of bacteremia found in test group. Should be included a control group that used a saline rinse.
Conclusion: The results support the rationale for the American Heart Association's 1997 recommendations for use of antibiotic prophylaxis to prevent bacteremia.
What are the current guidelines for antibiotic prophylaxis?
Topic: Infective Endocarditis
Author: Wilson W, Taubert KA, et al ARTICLE
Title: Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group.
Source: J Am Dent Assoc. 138:739-45, 747-60. 2007
Type: Discussion/ Guidline
Rating: Good
Keywords: infective endocarditis, oral systemic connection, antibiotic prophylaxis
Purpose: This is the 2007 update the recommendations by the American Heart Association (AHA) for the prevention of infective endocarditis (IE), which were last published in 1997.
Materials and methods:
A writing group appointed by the AHA for their expertise in the prevention and treatment of infective endocarditis were selected. The group performed a MEDLINE search from 1950 – 2006, and formed a new set of recommendations.
Results:
An extremely small number of cases of IE might be prevented by antibiotic prophylaxis for dental procedures even if such prophylactic therapy were 100% effective.
IE prophylaxis for dental procedures should be recommended only for patients with underlying cardiac conditions associated with high risk of adverse outcome from IE:
Prosthetic cardiac valve
Previous history of IE
Congenital heart disease (unrepaired cyanotic CHD including shunts and conduits), completely repaired congenital heart defects, repaired congenital heart defects with residual defects)
Cardiac transplant patients with valvulopathy
For patients with these underlying cardiac conditions, prophylaxis is recommended for all dental procedures that involve manipulation of gingival tissue or the periapical region of teeth or perforation of the oral mucosa.
Prophylaxis is not recommended based solely on an increased lifetime risk of acquisition of IE.
Are there any specific precautions needed for cardiac pacemakers?
Topic: Systemic Effects of Periodontitis
Authors: Miller CS, Leonelli FM, Latham E.
Title: Selective interference with pacemaker activity by electrical dental devices.
Source: Oral Surg, Oral Med, Oral Path 85:33-36;1998
Type: In vitro study
Rating: Good
Keywords: electromagnetic interference, cardiac, pacemaker, ultrasonic instruments
P: To determine whether electromagnetic interference with cardiac pacemakers occurs during the operation of contemporary electrical dental equipment in vitro.
M&M: Fourteen electrical dental devices were tested in vitro for their ability to interfere with the function of two Medtronics cardiac pacemakers (one a dual-chamber, bipolar Thera 7942 pacemaker, the other a single-chamber, unipolar Minix 8340 pacemaker). The pacemakers were programed to maximum sensitivity. Atrial and ventricular pacemaker output and electrocardiographic activity were monitored by means of telemetry with the use of a Medtronics 9760/90 programmer. Dental devices were turned on and off, operated at all power levels directly against the pacemaker, and moved from the pacemaker until no interference was recorded. Trials were performed in triplicate.
R: Atrial and ventricular pacing were inhibited by electromagnetic interference produced by the electrosurgical unit up to a distance of 10 cm, by the ultrasonic bath cleaner up to 30 cm, and by the magnetostrictive ultrasonic scalers up to 37.5 cm. In contrast, operation of the amalgamator, electric pulp tester, composite curing light, dental handpieces, electric toothbrush, microwave oven, dental chair and light, ENAC endodontic ultrasonic instrument, radiography unit, and sonic scalar did not alter pacing rate or rhythm. There was no significant difference between the proportion of interference with the unipolar and bipolar pacemakers, although the unipolar model was more sensitive.
BL: Certain electrosurgical and ultrasonic instruments may produce deleterious effects in medically fragile patients with cardiac pacemakers.
What other cardiovascular conditions can be related to periodontal disease?
Topic: perio and cardiovascular disease
Authors: Genco R, Offenbacher S, Beck J. ARTICLE
Title: Periodontal disease and cardiovascular disease: Epidemiology and possible mechanisms.
Source: JADA 133:14S-22S;2002
Type: review
Rating: good
Keywords: periodontal disease, cardiovascular disease, specific bacteria,
Purpose: To summarize the current findings regarding the association between periodontal disease and cardiovascular disease.
Discussion:
Epidemiologic studies of oral and systemic disease connection:
A series of case-control and cross-sectional studies has shown a significant association between various indices of poor periodontal health and coronary heart disease, or CHD. Direct relationship between heart disease and increasing levels of periodontal disease was confirmed by these studies. Specific periopathogenic bacteria (B. forsythus, P. gingivalis) may also be associated with myocardial infraction (or MI).
There are eight longitudinal published studies. 6 of them suggested that indicators of poor periodontal health precede cardiovascular events while 3 found no such relationship (study by Joshipura and colleagues in both categories).
There is not enough evidence to conclude that the associations between periodontal disease and heart disease are causal, they appear to be moderate in nature.
Concerns about the current evidence:
Strength of associations. In any epidemiologic study, there is concern that the reported associations could be confounded by other factors, especially when the adjusted associations are in moderate range and since the mechanisms involved are not fully understood. Therefore, these studies have to be large enough.
Inconsistent findings serve as a warning that we should be conservative in making conclusions about causality. Difference in the way studies were conducted can bias the findings.
The outcome of the studies may be different because of the inclusion criteria or because different measurements are used e.g. in some studies evidence of a “silent” or nonsymptomatic MI or a stroke are used while most use new fatal and non-fatal MIs and hospitalization for cardiovascular procedures. Studies that focused on stroke appear to demonstrate stronger relationships with periodontal disease than do studies that used CHD as an outcome.
Not all studies used the same measures to describe periodontal disease. Different dental indexes were used while one study did not specify the measure used. In addition to these some investigators believe that non – clinical signs of periodontal disease should also be measured (some measure of the infection).
Disease mechanisms:
It has been proposed that bacteria found in dental plaque enter the bloodstream during bacteremic episodes. S. sanguis and P. ginigvalis have been shown to induce platelet activation and aggregation through the expression of collagenlike platelet aggregation – associated proteins. The aggregated platelets may then play a role in atheroma formation and thrombosis.
Periodontal pathogens. B. forsythus (30%), P. gingivalis (26%), A.a. (18%), P. intermedia (14%) were found in human carotid atheromas. In addition C. pneumonia was found in 18% of these atheroms.
Cytokines (TNF-α, IL-1, IL-6, IL-8) produced because of periodontal infection can play a role in atherosclerotic heart disease, either through a direct action on the vessel wall or by inducing the liver to produce acute-phase proteins.
Recent studies provide evidence that periodontal disease is associated with cardiovascular risk factors, including acute-phase proteins, CRP, and plasma fibrinogen (these proteins are increased in people with periodontitis).
Animal studies suggest that infection with P. gingivalis activates the acute-phase response, increases lipemia and enhances atheroma lesion formation.
Conclusion: Evidence so far support but not prove a causal association between periodontal infection and atherosclerotic cardiovascular disease or its results.
latelets may then play a role in atheroma formation and thrombosis.
Periodontal pathogens. B. forsythus (30%), P. gingivalis (26%), A.a. (18%), P. intermedia (14%) were found in human carotid atheromas. In addition C. pneumonia was found in 18% of these atheroms.
Cytokines (TNF-α, IL-1, IL-6, IL-8) produced because of periodontal infection can paly a role in atherosclerotic heart disease, either through a direct action on the vessel wall or by inducing the liver to produce acute – phase proteins.
Recent studies provide evidence that periodontal disease is associated with cardiovascular risk factors, including acute – phase proteins, CRP and plasma fibrinogen (thee proteins are increased in people with periodontitis).
Animal studies suggest that infection with P. gingivalis activates the acute – phase response, increases lipemia and enhances atheroma lesion formation.
Topic: Coronary heart disease
Author: Humphrey LL NO ARTICLE
Title: Periodontal disease and coronary heart disease incidence: A systematic review and meta-analysis
Source: J Gen Intern Med 2008; 23:2079-2086
Type: Systematic review
Rating: Good
Keywords: Coronary heart disease; periodontal disease; risk factor
Purpose: to aid the United States Preventive Services Task Force in evaluating whether periodontal disease is an independent novel risk factor for incident CHD
Background: Coronary heart disease is the leading cause of death and morbidity in the US and many developed countries. Periodontal disease is associated with elevation of several markers of chronic inflammation. Recently, several lines of evidence have implicated a chronic inflammation etiologically in CHD and cardiovascular disease (CVD)
Methods: MEDLINE database search was complete for studies completed between 1966 and 2008. Two investigators reviewed all the articles and selected the ones rated as fair or good quality for the meta-analysis
Results:
-143 abstracts were reviewed and identified. 68 full papers from which 7 studies of fair or good quality conducted in 7 cohorts were identified.
-These 7 cohort studies were conducted in North America and Finland and represent cohorts of 175-170.000 men and women with follow up ranging from 5-21 years.
-Baseline periodontal disease was significantly associated with an increased risk of CHD in three cohorts, and three showed no significant association.
-Tooth loss was considered a consequence and another form of periodontal disease; in one study the baseline number of missing teeth was directly related to CHD events/death.
-Gingivitis as a measure of periodontal disease was evaluated in two cohorts, and both showed or suggested elevated rates of CHD death among individuals with baseline gingivitis.
Discussion:
- This review shows that periodontal disease is a independent, though relatively weak, risk factor for CHD
-These analysis suggest that various measures of periodontal disease confer approximately a 24-35% increase in risk of CHD
- There are several limitations of the review. First, it relied on each study’s definition and diagnosis of CHD
- Although the authors did not systematically review literature evaluating this relationship among individuals with prevalent CHD, studies among those cohorts have also shown an association between periodontal disease and CHD
Topic: Coronary vascular disease
Authors: Haraszthy VI, Zambon JJ, et al ARTICLE
Title: Identification of periodontal pathogens in atheromatous plaques
Source: J Periodontol 71:1554-1560. 2000
Type: Clinical study
Rating: Good
Keywords: Coronary disease/etiology, cerebrovascular disorders/etiology, periodontal diseases/pathology, atherosclerosis/etiology, bacteremia/complications
Purpose: To determine if chronic oral infection associated with periodontitis may be involved in the development and progression of atherosclerosis through the examination of atheromas obtained from patients during carotid endarterectomy.
Methods: 50 human specimens were obtained during carotid endarterectomy to examine for the presence of Chlamydia pneumoniae, human cytomegalovirus (HCMV), and periodontal pathogens A.actinomycetemcomitans, B.forsythus, P.gingivalis, and P.intermedia using PCR assays.
Results: 80% of the specimens were positive in the PCR assays for the presence of bacteria, as well as either C. pneumonia or HCMV. 72% were positive for bacterial ribosomal DNA; 83% of these samples were positive for one or more of the targeted bacterial species, meaning that 44% of the 50 atheromas were positive for at least one of the periodontal pathogens. B. forsythus was most frequently detected, followed by P.gingivalis, A.a., and P. intermedia. 59% of these samples were positive for 2 species of periodontal pathogens.
Discussion: Periodontal pathogens are present in atherosclerotic plaques. Like other infectious microbes such as C. pneumoniae, These pathogens may play a role in the developmental and progression of atherosclerosis leading to coronary vascular disease and other clinical sequelae.
Topic: Periodontal disease and incident MI
Authors: Andiriankaja O, Genco R et al: ARTICLE
Title: The use of different measurements and definitions of periodontal disease in the study of the association between periodontal disease and risk of myocardial infarction.
Source: J Periodontol 2006; 77: 1067-1073
Type: prospective study
Rating: Fair
Keywords: periodontal disease, myocardial infarction
BG: Periodontitis as an independent risk factor for myocardial infarction (MI) has been under debate, part of that is due to the inconsistency in definition of periodontitis and its measurement.
P: To assess whether the observed association between periodontal disease and incident MI depends on the choice of measurements or criteria used to define periodontal disease.
M&M: 537 patients with a recent non-fatal MI and 800 controls, medical history, PD, attachment level, alveolar crestal height, and number of missing teeth. Four case definitions of periodontal disease used. 1) mean CAL ≥3 mm, 2) ≥35.79% of tooth sites with ≥3 mm, 3) ≥7.14% tooth sites with 3 mm CAL and PD ≥ 4 mm at the same site 4) at least one tooth site with PD ≥4 mm.
R: After adjusting for age, gender, hypertension, cholesterol, diabetes, and smoking, OR for with the first definition were 2.08, 2.77 for the second definition, 2.4 for the third, and 1.65 for the fourth. OR for mean attachment loss was 1.46, mean PD OR of 2.19, alveolar crest height OR of 1.3 and missing teeth was 1.04.
BL: Regardless of the definition of periodontal disease there was always an association with higher incidence of a non-fatal MI. The association seems most significant when measuring probing depths, and least significant when measuring missing teeth.
Topic: Stroke
Authors Joshipura K. ARTICLE
Title: The relationship between oral conditions and ischemic stroke and peripheral vascular disease.
Source: JADA 133:23S-30S;2002
Type: Clinical study
Rating: Good
Keywords: CVD, PVD, Diabetes
Purpose: Review of epidemiologic studies linking or disassociating oral conditions with stroke (cardiovascular dz: CVD) and/or peripheral vascular disease (PVD)
Discussion:
Stroke:
Damage to brain from reduced blood supply (hemorrhagic: blood vessel bursts and ischemic: obstruction).
Risk factors for stroke: smoking, HTN, diabetes, CVD (including CAD, PVD).
7 studies evaluating tooth loss and/or periodontal disease and association w/stroke Not a clear association found in every study, and most studies do not control for the same conditions (risk factors for stroke and/or perio dz).
One case control study that controlled for age, sex, social status, diabetes, current smoking and pre-existing vascular disease found a SS association between ischemic stroke and periodontal disease and PA lesions, but did not control for past smoking, # of cigarettes, obesity and physical activity.
Other studies show association between periodontal diasease and stroke that were SS, found no association between periodontal disease and hemorrhagic stroke, and no association between periodontal disease and total fatal stroke.
Another comparison is between tooth loss and stroke, found similar association as between periodontal disease and stroke. Even though there is a SS association in many of these studies, no information on cause and effect can be ascertained.
Possibly, the link between oral conditions and CVD may be explained as common risk factors such as: age, smoking/alcohol/health behavior/habits, genetics, socioeconomic status, stress, obesity, diet, physical activity, access to care, DM.
Peripheral Vascular Disease (PVD):
Caused by diminished blood flow to the extremities; including symptoms of: intermittent claudication; extreme cases could lead to disability and amputation.
Only two studies have reported on the relationship between oral conditions and PVD.
Men with periodontal disease (defined as mean bone loss > 20 percent of the root surface) had a 2.3 times higher risk of incidence of PVD vs. men without periodontal disease.
Among 45,167 male health professionals, those who lost one or more teeth during the follow-up period had a relative risk of 1.33 of experiencing PVD compared with men who did not lose any teeth during the follow-up period.
Conclusion: Possible that both associations (tooth loss and stroke vs periodontal disease and stroke) may be explained by common risk factors; tooth loss is as likely as periodontal disease to be an independent risk factor; dentist should not extract teeth only on the basis of preventing CVD. Several longitudinal
studies corroborating these results are needed before interpreting a causal relationship b/w PVD and oral conditions.
Topic: C-reactive protein
Authors: Ridker P, Silvertown J: ARTICLE
Title: Inflammation, C-reactive protein, and atherothrombosis
Source: J Periodontol 2008 Aug; 79(8suppl): 1544-51
Type: Review
Rating: Good
Keywords: cardiovascular disease, cholesterol, myocardial infarction, periodontal disease, Reynolds risk score, statin
Purpose: To focus on the epidemiological data linking inflammation to atherothrombosis, highlighting recent advances in establishing new biomarkers and understanding the role of genetics in the inflammatory process, and suggest new pathways for treatment.
Discussion: Atherothrombus pathogenesis is a combination of disorders of inflammation, innate immunity, and lipid accumulation. Cellular adhesion, monocyte and macrophage attachment, and transmigration of immune cells across the endothelium are crucial steps in early atherogenesis and in the later stages of mature plaque rupture, particularly the transition of unstable plaque at the time of acute thrombosis. Much evidence exists demonstrating that many biomarkers of inflammation are elevated years before cardio or cerebrovascular event. These same biomarkers are highly predictive of recurrent MI, recurrent stroke, diabetes, and cardiovascular death. The inflammatory biomarker in widest use is high-sensitivity C-reactive protein (hsCRP); Accounting for confounding factors, levels of hsCRP <1, 1 to 3, and >3 mg/l denote low, average, and high relative risk for future vascular events. For cerebral vessels, increased biomarkers of inflammation, including hsCRP, have been associated with increased stroke risk and an increased rate of atherosclerosis progression in the carotid vessels. Although the proportion of variation in hsCRP explained by genetic factors may be as large as 20% - 40%, diet, exercise, and smoking cessation have been show to decrease risk of an event and CRP levels. There is data supporting a role for inflammation in cardiovascular disease and offers the possibility that other disorders characterized by inflammation (periodontal disease), may have an indirect role by influencing the risk, manifestation, and progression of vascular events. Reducing the levels of periodontal disease would decrease inflammatory markers common to both periodontal and cardiovascular disease (IL-6, TNF, and hsCRP) which may directly or indirectly change the risk and progression of CVD. Carefully designed randomized trials are needed to test this possible connection.
Conclusion: By reducing the progression of periodontal disease, levels of inflammatory markers common to both diseases (IL-6, TNF, and hsCRP) would likely be decreased. More studies are needed to confirm this theory.
Topic: Cardiovascular Disease
Authors: Paraskevas S, et al ARTICLE
Title: A systematic review and meta-analyses on C-reactive protein in relation to periodontitis.
Source: J Clin Periodontol 2008; 35:277-290
Type: Review
Rating: Good
Keywords: cardiovascular diseases; C-reactive protein (CRP); meta-analysis; periodontitis; systematic review
Background: Periodontal disease is a destructive inflammatory disease caused by a chronic bacterial infection. The host responds to the periodontal infections with an array of events involving both innate and adaptive immunity. Acute phase reactants, such as C-reactive protein (CRP), have pro-inflammatory factors and are part of the innate immunity in periodontitis. CRP is a key marker of atherosclerosis. Elevated levels of CRP>2.1mg/l are associated with higher incidence of acute thrombotic events (stroke and myocardial infarction) .
Purpose: To investigate the observations that plasma/serum levels of CRP are elevated in patients with destructive periodontal disease in comparison with subjects without periodontitis.
Methods: Two internet databases (MEDLINE, Cochrane Central Register of Controlled trials) were searched. Screening of the initially 448 identified studies and reference checking resulted in 18 suitable papers (cross sectional, longitudinal studies). Meta-analysis was performed.
Results: Most studies showed significantly higher CRP in periodontal patients over healthy control. All studies reported mean CRP >2.1 mg/l for periodontitis patients and 8/10 papers reported values 2.1mg/l for controls. A meta-analysis of 10 cross sectional studies showed that the mean difference of CRP between periodontitis patients and controls was 1.56mg/l. Periodontal treatment, especially if it included systemic or local antibiotics, resulted in decrease in CRP plasma levels, but not statistically significant in every study.
Conclusion: This systematic review provides evidence that periodontitis elicits a mild acute-phase response with elevation of CRP levels compared with healthy controls. It is possible that chronically elevated CRP levels in periodontal patients exacerbate ongoing inflammatory processes in atherosclerotic lesions, thereby increasing the risk for cardiovascular events. CRP levels > 2.1 mg/l are associated with a higher incidence of acute thrombotic events.
Does removing periodontally involved teeth affect levels of systemic inflammatory markers?
Topic: Oral systemic connection
Author: Taylor B et al ARTICLE
Title:: Full-mouth extraction lowers systemic inflammatory and thrombotic markers of cardiovascular risk.
Source: J Dental Res 2006; 85(1):74:78
Type: RCT
Rating: Good
Keywords: thrombotic markers, inflammatory markers, oral systemic connection
Background: Inflammatory cells have been shown to play an important role in the thinning and weakening of the cap overlying atherosclerotic plaques. Whether thrombosis occurs following plaque disruption depends on a complex balance of factors, including PAI-1, TPA, and fibrinogen. PAI-1, the major antifibrinolytic, and TPA are mainly produced in endothelium and platelets. TPA forms inactive complexes with PAI-1 in the blood and tissues. Higher levels of TPA antigen therefore reflect impaired fibrinolytic potential. Increased levels of fibrinogen result in its binding to platelets, causing platelet aggregation and promotion of fibrin formation, thus contributing to plasma viscosity. Epidemiological studies have shown that increased levels of CRP, fibrinogen, and PAI-1 are strong predictors of CVD.
Purpose: To investigate whether elimination of periodontal disease by full mouth extraction (FME) reduces levels of known hemostatic indicators of risk.
Materials and methods:
76 subjects were enrolled in study, 67 completed the study.
Patients were recruited only when FME was indicated by hospital clinicians independent from this study.
Medical history focused on hypertension, diabetes mellitus, hyperlipidemia, smoking and any history of cardiac, cerebral or peripheral vascular disease.
FME was completed within 1-4 weeks for 42 patients, 4-8 weeks for 15, and >8 weeks for 10 patients. Approximately 3 months after FME, health history was repeated. ECG was done and blood samples were collected at 3 time points, T1 at the initial visit, T2 after relief of acute symptoms, and T3 12 weeks after FME.
C-reactive protein (CRP), fibrinogen, plasminogen activator inhibitor antigen (PAI-1) and tissue plasminogen activator antigen (TPA) were measured. Statistical analysis was done.
Results:
There were NSSD in weight, BP, smoking, ECG and the patients’ medical condition between baseline and 3 months.
NSSD for all markers from T1 to T2.
CRP levels fell significantly from T1 to T3 and from T2 to T3. PAI-1 levels fell significantly from T1 to T3. Values for TPA and fibrinogen also showed a downward trend from T1 to T3, although this was NSSD.
Fibrinogen values decreased significantly from T2 to T3.
Total white blood cell count, PMNs, lymphocytes and platelets displayed a significant reduction after tooth extraction.
The magnitudes of change were greater for non-smokers than smokers, with significant reductions in CRP, WBC, lymphocytes, PMNs and platelets.
NSS correlations were found between clinical parameters and lab values, besides the mean PPD which was found to be inversely associated with hematocrit values.
BL: Blood levels of CRP, PAI-1, and fibrinogen, established indicators of risk for CVD, are reduced in patients with severe periodontitis after extraction of all teeth. The results from this study suggest that eradication of periodontitis may reduce the risk of cardiovascular disease, however, FME is a severe treatment and not suitable for most patients.
Topic: Systemic Effects of Periodontitis
Authors: Slade GD, Offenbacher S, Beck JD, Heiss G, Pankow JS. ARTICLE
Title: Acute-phase inflammatory response to periodontal disease in the US population.
Source: J Dent Res79:49-57;2000
Type: Retrospective study
Rating: Good
Keywords: electromagnetic interference, cardiac, pacemaker, ultrasonic instruments
Background: C-reactive protein (CRP) is an acute-phase reactant produced by the liver in response to diverse inflammatory stimuli, including heat, trauma, infection, and hypoxia. It is a useful marker for tracking the course of the infection. Established risk factors for "high-normal" values of CRP within the general population include older age, cigarette smoking, chronic bacterial infections, and chronic bronchial inflammation (Palosuo et al., 1986; Saikku et al., 1992; Patel et al., 1995; Mendall et al., 1996; Ridker et al., 1997). Individuals with moderate-high CRP vales have increased risks for chronic diseases that have an inflammatory basis, including CVD. However, raised CRP levels have been observed among people with no apparent established risk factors for elevated CRP, suggesting that other pathological conditions may constitute an additional stimulus for a systemic inflammatory response among some individuals.
P: To evaluate associations among periodontal disease, established risk factors for elevated CRP, and CRP levels, and to determine whether total tooth loss is associated with reduced CRP.
M&M: Data obtained from NHANES III (1988-1994). A random sample of the US population was interviewed in their homes and examined at mobile centers. CRP was quantified from peripheral blood samples and analyzed for the prevalence of elevated CRP. 12,949 dentate people (≥18 yr) and 1,817 edentulous people included in the analysis.
R: Dentate people with extensive perio disease (> 10% of sites w/ PD ≥4mm) had a 33% increase in mean CRP & 2 fold increase in odds of elevated CRP compared with perio healthy people. Raised CRP levels among people with extensive perio disease persisted with established risk factors for elevated CRP (males, diabetes HbA1c> 5.7, arthritis, bronchitis, smoking, and anti-inflammatory meds), but the strongest periodontal-CRP association occurred with subgroups that had no other risk factors. However, CRP levels for some groups of the population were not related to perio disease (Blacks had a higher mean CRP level in people with no perio pockets). CRP levels were similarly raised in edentulous people (the authors hypothesized that it would be lower in edentulous people). Analysis shows that most edentulous people had at least one established risk factor for elevated CRP, which could confound this association.
Oral conditions had their strongest association with CRP levels in population subroups that did not have systemic diseases.
BL: Periodontitis and edentulism were associated with elevated CRP levels in the US population, with active periodontal disease representing a similar risk as the five established risk factors for elevated CRP.
How does periodontal disease contribute to diabetes? Does having both diseases increase a patient’s risk for other systemic conditions?
Topic: perio and diabetes
Authors: Taylor JJ, Preshaw PM, Lalla E NO ARTICLE
Title: A review of the evidence for pathogenic mechanisms that may link periodontitis and diabetes.
Source: J Periodontol 2013;84(4 Suppl.):S113-S134
Type: review
Rating: good
Keywords: adipokines; AGE; cytokines; diabetes; hyperglycaemia; inflammation; periodontal disease; plaque bacteria; RAGE.
Purpose: To provide a review of the molecular and cellular processes which might underpin the relationship between periodontal disease and diabetes.
Discussion: The impact of diabetes on periodontal pathogenesis
Microbial factors: Presence of diabetes has no significant effect on the composition of microflora, and the level of glycemic control in people with diabetes does not influence the composition of the subgingival biofilm.
Cytokines and adipokines:
The most consistent findings have been associations between elevated levels of IL-1β and IL-6 and T2DM in patients with chronic periodontitis. Several animal studies have shown elevated pro-inflammatory cytokines and chemokines. They have also highlighted the importance of TNF-a in possibly prolonging the immune response to plaque bacteria in both types of diabetes and therefore promote periodontitis. Evidence for any association between levels of TNF-α in oral fluid or gingival tissues and T2DM in chronic periodontitis is inconsistent.
GCF IL-1β, salivary IL-6 were found to be correlated with HbA1c, and GCF OPG and RANKL associated with poor glycemic control in T2DM in patients with chronic periodontitis.
There is good evidence for elevated IL-1β, IL-6 and RANKL/OPG ratios in patients with T2DM and periodontitis as compared with periodontitis alone as well as a quantitiative relationship between these cytokines and glycemic control.
Immune cell function: Evidence for a role of altered monocyte and T-cell function in diabetic patients with periodontitis is limited. Although there is some evidence for abnormal neutrophil function in diabetes and periodontitis, the complexity of neutrophil functions and the diversity of the experimental approaches make this relation difficult to identify.
Hyperglycemia and cellular stress:
Have positive correlation between severity of periodontitis due to:
Impairment of neutrophil adherence, chemotaxis and phagocytosis may facilitate bacterial persistence
Neutrophil priming caused by increased levels of protein kinase C
Oxydative stress cause by hyperglycemia
Priming effect on monocytes, key cells in the hyper-inflammatory cytokine response.
Hyperglycemia, advanced glycation end-products (AGEs), and their receptor RAGE: hyperglycaemia in diabetes drives the irreversible formation of AGEs that can have direct pro-inflammatory and pro-oxidant effects on cells. Importantly, when AGEs bind to their signaling receptor RAGE (which is increased in diabetes and its activation has an established role in the development and progression of other diabetic complication), cellular phenotype and function are critically impacted, and enhanced inflammation, oxidative stress and impaired tissue repair.
Hyperglycemia and alveolar bone homeostasis: There are studies supporting that in poorly controlled diabetic patients with periodontitis compared to well-controlled or non-diabetic subjects with similar periodontal status increased RANKL and RANKL/OPG ratios are found in the GCF. This at least plays a role in the enhanced alveolar bone destruction in diabetes. Studies made in humans and animals too suggest that altered alveolar bone homeostasis (which occurs through the action of several molecules e.g. RANKL/OPG, TNF-α) is an important pathway in the pathogenesis of periodontitis in both T1DM and T2DM.
The impact of periodontal disease in diabetes: Although literature is limited, there are clinical investigations that show an impact of periodontal inflammation on the diabetic state and/or diabetic complications (increased HbA1c in people without diabetes, poorer glycemic control in diabetic patients, increased risk of diabetic complications). Treatment of periodontitis is associated with improved glycemic control and 0.4% reduction of HbA1c. At the moment there in no strong evidence that periodontal microbiota has any direct impact on the diabetic state or glycemic control.
Topic: Type I Diabetes
Author: Thorstenson H ARTICLE
Title: Medical status and complications in relation to periodontal disease experience in insulin-dependent diabetics
Source: J Clin Periodontol 23:194-202, 1996
Type: Case-control study
Reviewer: Phillip Crum
Rating: Good
Keywords: diabetes mellitus; insulin-dependent diabetes; long-duration diabetes; medical complications; periodontal disease
Purpose: to define a population of diabetics exhibiting an increased risk of developing severe periodontitis by comparing the medical history status of two groups of diabetics, 1 with no/minor periodontal disease and 1 with severe periodontal disease.
Methods:
-There were two parts to this study, a baseline and follow up study.
-39 case control studies were selected. Case: patients diagnosed with severe periodontal disease. Control: patients that exhibited gingivitis or only minor alveolar bone loss.
-The mean proximal alveolar bone level was 47% for case group and 60% for the control.
-The median follow up time was 6 years
-A full mouth clinical and radiological dental examination was carried out the same year
Results:
-There were no differences between the case and the control in each pair regarding weight, insulin dose, systolic and diastolic blood pressure, vibration perception, HbA1, triglycerides, total-cholesterol, HDL-cholesterol, or creatinine, proteinuria, ECG, retinopathy, stroke, and smoking habit.
-In the Baseline study; Biochemical analyses and clinical variables used as a routine in monitoring of diabetics failed to differentiate between diabetics with severe and minor periodontal disease.
Discussion:
-The method for the analysis of HbA1c changed during the course of the study.
-In this study, there were no significant differences between the case and control in each pair in the baseline study concerning metabolic control evaluated as HbA1c and known cardiovascular risk factors.
-In the follow up study: there was a significant increased prevalence of proteinuria and cardiovascular complications such as stroke, TIA, angina, myocardial infarct and intermittent claudication in the case group.
-There might be an association between renal disease, cardiovascular complications, and severe periodontitis.
Does treating periodontal disease improve glycemic control?
Topic: Diebetes
Authors: Janket et al. NO ARTICLE
Title: Does periodontal treatment improve glycemic control in diabetic patients? A meta-analysis of intervention studies
Source: J Dent Res. 2005 Dec;84(12):1154-9
Type: Meta-analysis
Rating: Good
Keywords: meta-analysis, inflammatory mediators, hemoglobin A1c, non-surgical periodontal treatment, antibiotics treatment
Purpose: To review all published evidence systematically and to quantify the impact of periodontal treatment on HbA1c.
Methods: A Medline search on all published articles using search terms diabetes, periodontal disease, HbA1c and glycemic control was conducted. Inclusion criteria included: original investigation where causal inferences may be made, duration of study at least 2 months, primary or secondary outcome was a measure of glycemic control (HbA1c level) with the predictor being periodontal treatment, and reports published between 1980 and January 2005. Most studies included non-surgical treatment, while some included surgical therapy and antibiotic treatment.
Results: 10 studies were identified that met all inclusion criteria. Publication bias, heterogeneity, and validity assessment were acceptable for all 10 studies. 456 type 1 and 2 patients were included in these studies. The result of meta-regression analysis showed a non-significant decrease of 0.38% reduction in HbA1c among the 10 studies. Periodontal therapy with antibiotics showed a non-significant decrease of 0.71% in HbA1c in type 2 DM patients in 6 of the studies.
Discussion: Although this percent improvement in glycemic value may be of value in some patients, the evidence was not strong enough to reject the study’s null hypothesis: “periodontal treatment does not affect glycemic control in patients with diabetes”. Further studies are needed to discern whether there is a significant clinical benefit of periodontal therapy on blood sugar control in DM2 patients.
Topic: periodontal health and type 2 diabetes
Authors: Kiran M et al. NO ARTICLE
Title: The effect of imporoved periodontal health on metabolic control in type 2 diabetes mellitus.
Source: J Clin Periodontol 2005;32:266-272
Type: Clinical study
Rating: Good
Keywords: Periodontal disease, Type 2 diabetes mellitus, periodontal health
P: to investigate the effect of improved periodontal health on metabolic control in type 2 DM.
M&M: 44 (26F/18M) patients (mean age 54.39 years) with type 2 DM HbA1C values 6%-8%. No major diabetic complications, no systemic antibiotics within the last three months, no periodontal treatment 6 months prior to the study.
Subjects were randomly assigned into treatment and control groups. 5 patients in the treatment group and 2 patients in the control group were smokers. Periodontal examination was performed by single examiner. PI, GI, PD, CAL, recession, BOP were recorded at baseline at 1 and 3 months after periodontal treatment. PDs were recorded using customized acrylic stents. Treatment group received OHI, and full mouth scaling and root planing. Control group received no treatment during the study. Fasting plasma glucose (FPG), 2-h post-prandial glucose (PPG), HbA1c, total cholesterol (TC), triglyceride (TG), HDL and LDL-cholesterol were analyzed at baseline and 3 months in the treatment group and at baseline, 1 month and 3 months in the control group.
R: At baseline treatment and control groups had similar mean values for age, sex medications, duration of diabetes, toothbrushing frequency, smoking habits, denture usage and number of missing teeth.
PI and GI dropped significantly in the treatment group. PDs at baseline in both groups the examined sites were 3-4mm. After SRP a significant improvement was noticed in the treatment group and minor changes in the control group.
0.39mm CAL gain in the treatment group and 0.05mm in the control at the end of 3 months. NSSD between the two groups.
Non- surgical periodontal therapy caused a significant decrease in BOP in the treatment group and slight increase in the control group.
No significant difference in metabolic data between the two groups at baseline.
FPG : there was tendency towards decrease in the treatment group ( from 132.82 to 128.86). In the control group, no change was seen. Differences between the two groups were not statistically significant.
HbA1C: mean values were 7.3 for the treatment and 7 for the control group. The treatment group showed a reduction in HbA1C to 6.5 ( -0.8). This reduction equates to a level of approximately 10.94% of the baseline HbA1C level. The control group showed 4.42% increase in level of HbA1C compared to baseline. TC, TG, LDL levels decreased in our study group whereas these values increased slightly in the control group.
BL: Non-surgical periodontal treatment is associated with improved glycemic control in type 2 patients and should be considered as part of the standard of care for the diabetic patient.
Topic: Systemic Conditions
Authors Jones, J et al: NO ARTICLE
Title: Does periodontal care improve glycemic control? The department of Veterans Affairs dental diabetes study.
Source: J Clin Periodontol 2007; 34: 46-52
Rating: Good
Keywords: Diabetes
Purpose: To report 4-month results of a clinical trial of the efficacy of periodontal care in the improvement of glycemic control in veterans with poorly controlled diabetes.
Method: Multi-site, single-blind, randomized, controlled clinical trial examined the efficacy of periodontal care in the improvement of glycemic control in veterans (Dec 2000-Nov 2004). HbA1c values >8.5% within the last 6 months. Veterans indicated interest (yes/no) using a pre-addressed, postage-paid postcard. Outcomes were change in HbA1cin the Early Treatment group versus untreated (Usual Care) groups and percent of participants with decreases in HbA1c.
Randomized into 4 groups:
Early Treatment/4 months therapy: SRP + doxy 100mg/14 days+ CHX rinse bid for 4 months
Early Treatment/12 months: SRP + doxy 100mg/14 days+ CHX rinse bid for 12 months, participants seen every 4 months for SRP
Usual Care/ 4months: Usual Care (participants used did not alter their medical and dental care routine), then 4 months of treatment, then Usual Care.
Usual Care/12 months: Usual Care, then 12 months of treatment.
Analyses included simple/multiple variable linear/logistic regressions, adjusted for baseline HbA1c, age, and duration of diabetes.
Results:
193 participants from the VA with HbA1c >8.5%. No differences between groups.
After adjustment for baseline HbA1c, age, and diabetes duration, the mean absolute HbA1c change in the Early Treatment group was −0.65% vs. −0.51% in the Usual Care group (p=0.47) NSSD
Adjusted OR for improvement by both 0.5% and 1% in the Early Treatment group were 1.67
Usual Care subjects were twice as likely to increase insulin from baseline to 4 months (20% vs. 11%) and less likely to decrease insulin (1% vs. 6%) than Early Treatment subjects.
Among insulin users at baseline, more increased insulin in the Usual Care group (40% vs. 21%).
Conclusion: The addition of periodontal therapy to current medical therapy may have promise in regard to improvement of glycemic control. Large-scale, multi-site, randomized clinical trials, including
measurements of inflammatory mediators, are needed to definitively test the hypotheses.
Topic: Glycemic control
Authors: Taylor G. ARTICLE
Title: Periodontal treatment and its effect on glycemic control: review of evidence.
Source: Oral Surg, Oral Med, Oral Path 87:311-316, 1999
Type: Review
Rating: Good
Keywords: glycemic control, diabetes mellitus
Purpose: A review of literature containing reports of clinical research that has considered the relationship between tx of perio dz and improvement in glycemic control in humans.
Discussion: Williams and Mahan 1960 showed reduction in insulin requirements in 7 of 9 patients who had “gross evidence” of perio dz after treatment (extractions, SRP, perio sx, systemic atb). Wolf compared 23 subjects with improvement in oral infection after treatment to 23 subjects with no improvement and showed a significant difference in decrease in glycosuria, blood glucose and insulin dose after 8 and 12 mo follow-up. Miller showed and improvement in BOP and improved glucose levels after SRP, CHX rinse and systemic doxy in patients with poorly controlled Type 1 DM. Aldridge found, in 2 single blinded clinical studies, SRP, extractions and OHI led to improvement in metabolic control in controlled type I DM at baseline. Westfeldt compared type I and type II diabetics to non-diabetics with moderate to advanced periodontal disease. Significant differences were seen in both groups from baseline in periodontal parameters. No significant difference in HbA1c levels was found in the diabetic patients at the 24 and 60 mo intervals. Grossi found systemic doxy and topical antimicrobial irrigation with ultrasonic scaling produced a reduction of 0.5-1% in HbA1c levels. Taylor’s longitudinal study found that subjects with severe periodontal disease were 6x more likely to have poor glycemic control 2 years into follow-up.
It is difficult to compare many of the studies due to lack of homogeneity of study design with regards to defining diabetes (fasting glucose, HbA1c…), criteria for periodontal disease, type of diabetes studied, etc.
Conclusion: Although there is supportive clinical and epidemiologic evidence, equivocal and contrary evidence also exists. It is concluded from this review that the quantity, breadth, and strength of evidence-based knowledge are currently insufficient to establish perio tx as influential in improving glycemic control in either type 1 or type 2 diabetes. Further rigorous, systematic study of the effects of treating periodontal infection on glycemic control is needed.
Topic: Diabetes
Authors: Westfelt, E et al NO ARTICLE
Title: The effect of periodontal therapy in diabetics. Results after 5 years
Source: J Clin Periodontol 23:92-100, 1996
Type: Clinical
Rating: Good
Keywords: diabetes meliitus: control of diabetes; periodontal therapy; periodontal maintenance therapy
Purpose: To study during a 5-year period whether the frequency of recurrence of periodontitis was higher in diabetics than in non-diabetic controls.
Methods: 20 patients with diabetes and 20 non-diabetic controls, 46-65 years of age, with moderate to severe periodontitis, with at least 10 remaining teeth in each jaw were included in the study. Diabetic subjects: duration of diabetes>10years, s-creatinine<150. Non-diabetic controls: HbA1c<5.4%. The subjects in 2 groups were matched regarding sex, age and severity of periodontal disease. After screening examination, all patients were subjected to basic periodontal treatment including OHI, sc/rp. 3months after the completion of basic treatment a baseline examination was performed (# of teeth, plaque, BOP, PD, AL). After baseline examination, all subjects received additional professional plaque removal. The plaque control program was repeated once every 3 months for the duration of the trial. 6 months after the baseline examination all 40 subjects were recalled for a second exam. All clinical parameters were assessed. Sites exhibiting BOP and PD >5 were scheduled for surgical therapy (MWF). Clinical parameters were evaluated 12, 24 and 60 months after the baseline examination. Statistical analysis was performed.
Results: At the screening examination, the mean number of teeth in the diabetic group was 23.7 and in the control 24.6. During the 5 years of maintenance 4 molars in the diabetic group and 3 molars in the control group were extracted. At 60 months, there was a significant improvement of OH in both groups and reduction in gingivitis. At baseline examination 21.3% of all sites in diabetic patients and 23.4% of all sites in controls had a PD 4mm. At 60-month re-examination, only 11.1% (diabetics) and 13.5% (controls) of sites had a PD 4mm. Marked reduction was noticed in both groups, no SSD was noticed between the two groups. No SSD was found in AL between the two groups. A total of 26 sites in the diabetic group and 28 sites in the control group were treated surgically. During the maintenance phase, 3 surgically treated sites in the diabetic group and 1 site in the control group were lost due to tooth extraction.
Conclusion: Diabetic patients, who following treatment of periodontal disease are enrolled in a careful plaque control program, exhibit similar low frequency of recurrent periodontitis as non-diabetic controls.
Can untreated periodontitis increase the risk of having a preterm birth or a baby with a low birth weight weight?
Topic: Pregancy
Author: Michalowicz G, Hodges J et al ARTICLE
Title: Change in periodontitis during pregnancy and the risk of pre-term birth and low birth weight.
Source: J Clin Periodontol 2009; 36: 308 – 314
Type: RCT
Rating: Good
Keywords: low birth weight babies, pregnancy, oral systemic connection, reproductive system
Purpose: To determine if periodontitis progression during pregnancy is associated with adverse birth outcomes
Materials and methods:
Data used from the Obstetric and Periodontal Therapy Study, a randomized, single-blind controlled trial.
Randomly selected women with periodontitis (≥4 teeth with PD ≥4mm, CAL ≥2mm, BOP ≥35%) received periodontal treatment before 21 weeks of gestation (413 subjects) or after delivery (410 subjects).
Periodontal disease progression was defined as ≥ 3mm loss of clinical attachment. Comprehensive periodontal examinations done at baseline, 21-24 and 29-32 weeks gestation.
Birth outcomes were compared between progressing and non-progressing using log rank and t test, separately in all women an in untreated controls.
Results:
The distribution of gestational age at the end of pregnancy and mean birth weight were NSSD between women with and without disease progression.
Gestational age and mean birth weight were not associated with change from baseline in percentage of tooth sites with BOP.
BL: Disease progression was not associated with an increased risk for delivering a pre-term or a low birth weight infant.
Topic: Systemic Effects of Periodontitis
Authors: Offenbacher, Jared, O’Reilly, et al. ARTICLE
Title: Mechanisms of periodontitis-associated pregnancy complications.
Source: Annals Periodontol 3:233-250;1998.
Type: Clinical study
Rating: Good
Keywords: Infant, low birth weight, periodontal diseases/complications, pregnancy, risk factors, periodontal diseases/pathogenesis, gingival crevicular fluid/analysis.
WHO Definitions:
Low birth weight: less than 5 lbs 8 oz (2.5 kg)
Very low birth weight: less than 3 lbs 5 oz (1.5 kg)
Extremely low birth weight: less than 2 lbs 3 oz (1 kg)
Prematurity: less than 37 weeks of gestation
Very premature: less than 32 weeks of gestation
Preterm Low Birth Weight (PLBW)
BG: Prematurity is mainly due to inflammatory response in the mother. Most common neurological abnormality of preterm children is cerebral palsy, blindness occurs commonly, and preterm children are more likely to have mild learning disability, attention disorders, developmental impairments, and asthma. Intraoral manipulation, like toothbrushing, can cause bacteremia, inflammatory mediatory PGE2 increases in periodontitis and can cause pathologic prematurity. LPS has also been associated with pregnancy complications in animal studies. Although periodontitis in the oral cavity represents a distant site of infections, it can affect pregnancy.
P: To relate PGE2, IL-1b, and sub-g plaque levels of T.f., A.a., P.g., and T.d. to preterm low birth weight.
M&M: 44 in-patient female volunteers, either immediately before delivery or within 3 days post-partum divided into 2 groups: PLBW or history of PLBW, and controls. Medical and social histories, full periodontal exam, GCF samples using strips, and four plaque samples from the distal of each second molar before probing. Used ELISA to quantify PGE2 and IL-1b, and checkerboard hybridization to quantitate and identify T.f., P.g., A.a., and T.d.
R: NSSD in attachment level between the two groups although a trend towards more attachment loss in the PLBW group. GCF-PGE2 level was twice as high in the PLBW group (SS). Point estimates of OR indicated that mothers with elevated GCF-PGE2 were 9x more likely to be in the PLBW group. A trend to higher IL-1b in GCF of PLBW group but NSSD. SS higher levels of all 4 pathogens especially for T.f. (P=0.0001).
D: Bacterial vaginosis is reported to be a major risk factor for preterm delivery. Women with urinary tract infection were more likely to give PLBW babies.
BL: PLBW is associated w/a 2-fold increase of GCF-PGE2 and increased colonization of T.f., P.g., A.a., & T.d.
Does periodontal treatment during pregnancy lower the risk of having a pre-term birth or baby with low birth weight?
Topic: perio and preterm babies
Authors: Lopez, J et al ARTICLE
Title: Periodontal Therapy Reduces the Rate of Preterm Low Birth Weight in Women with Pregnancy –Associated Gingivitis (PAG).
Source: J Periodontol 2005; 6: 2144-2153
Type: RCT
Rating: good
Keywords: clinical trials; controlled clinical trials; randomized; gingivitis; infant; low birth weight; infant; premature; risk factor
Background: The relation between periodontal disease and preterm/low birth weight (PT/LBW) is that periodontal infection is a source of bacteria and bacterial products in the systemic circulation, which may reach the placental tissues providing the inflammatory effect for labor induction.
Purpose: To investigate if pregnancy associated gingivitis is related to PT/LBW and if periodontal therapy reduces the PT/LBW rate in pregnant women with gingivitis.
Methods: 870 pregnant women (aged 18-42). were enrolled while receiving prenatal care
Women were randomly assigned in a 2:1 fashion to either a treatment group (N = 580), receiving periodontal treatment before 28 weeks of gestation or to a control group (N = 290), receiving periodontal treatment after delivery. Oral hygiene status, gingival inflammations were recorded, as well as PD, CAL, BOP in six sites/tooth.
Periodontal therapy consisted of plaque control, scaling, and daily rinsing with 0.12% chlorhexidine. Maintenance therapy was provided q 2 to 3 wks until delivery, and consisted of oral hygiene instruction and supragingival plaque removal by instrumentation as needed.
The control group were monitored 2-3 times during pregnancy.
The primary outcomes assessed were delivery at less than 37 weeks of gestation or an infant weighing less than 2,500 g.
Results:
27 women were excluded from the analysis. 553 in the treatment group and 81 in the control. There were 24 PT and 7 LBW infants.
Women in the control group had a significantly higher incidence of PT/LBW compared to women in the treatment group, 6.71% vs 2.14%. The incidence of PT/LBW was more than three times higher in control group.
In addition, women with gingivitis were at a higher risk of PT/LBW than women who received periodontal treatment.
Conclusion: Women with gingivitis who received periodontal therapy before 28 weeks of gestation had a significantly lower incidence of PT/LBW than women who did not receive periodontal therapy. Pregnancy associated gingivitis appeared to be an independent risk factor for PT/LBW and affords more than a two-fold increase in the risk for PT/LBW.
Discussion: If a periodontal infection is diagnosed at any time during pregnancy, the treatment should be administered as soon as possible in order to reduce the risk of PT/LBW.
Topic: Preterm birth
Author: Jeffcoat MK ARTICLE
Title: Periodontal disease and preterm birth: Results of a pilot intervention study
Source: J Periodontol 2003;74:1214-1218
Type: Pilot study
Rating: Good
Keywords: preterm birth; periodontal disease; intervention
Background: Preterm birth (PTB) is the major cause of perinatal morbidity and mortality as well as long-term neurologic disability.
-Nearly 12% of all infants are now born preterm
-Studies have shown a 3-8 fold increase in the odds of PTB to mothers with periodontal disease.
-The more severe the periodontitis, the more likely a baby is to be born at earlier gestational ages
Purpose: to determine the feasibility of an interventional trial during gestation, and to determine whether there was a trend for SRP with or without systemic metronidazole, to decrease the rate of PTB as compared to a minimal treatment control (Prophylaxis)
Methods:
-Patients criteria: > 3 sites wit CAL >= 3mm
-366 pregnant women participated
-Body mass index, presence of bacterial vaginosis and history of SPTB prior to 35 weeks gestation
-All participants had vaginal fetal fibronectin testing.
-3 treatment groups: 1) Dental prophylaxis, 2) SRP+ placebo 3) SRP + 250mg Metronidazole tid.
-An additional 723 pregnant women with periodontitis were identified.
Results:
-The population studied was 85% African American, 13.4% married, and a mean age of 22.5 +4.6 years.
-The rate of PTB at <35 weeks for the groups receiving 1) prophylaxis plus placebo was 4.9%, 2) SRP plus placebo was 0.8% and 3)SRP plus metronidazole was 3.3% respectively. The rate of PTB at <35 weeks was 6.3% in the reference group.
-Women who were assigned metronidazole had a higher rate of PTB than those assigned to a systemic placebo.
Discussion:
-Results show that as much as 84 % reductions in SPTB at <35 weeks in subjects receiving SRP in comparison to the prophylaxis plus placebo group.
-No trend was found indicating that the addition of metronidazole to SRP was beneficial
-Larger trial will be needed to achieve statistical significance.
Topic: Pregnancy
Authors: Offenbacher S, NO ARTICLE
Title: Effects of periodontal therapy during pregnancy on periodontal status, biologic parameters, and pregnancy outcomes: a pilot study
Source: J Periodontol. 77:2011-24. 2006
Type: Pilot study (randomized clinical trial)
Rating: Good
Keywords: periodontitis; pregnancy; prematurity; therapy
Purpose: To investigate is maternal periodontal therapy during pregnancy would be safe to the mother and fetus and would decrease the level of oral infection and chronic inflammation, resulting in reduction of preterm birth rates.
Methods: A randomized, blind clinical trial was conducted using patients recruited from a high risk prenatal clinic (35 in treatment group, 32 in no treatment group). Some inclusion criteria included 1) pregnant and <22 weeks gestation at time of SRP or supragingival polish; 2) two or more sites measuring ≥5 mm probing depths (PDs) plus periodontal attachment loss of 1 to 2 mm at one or more of these sites; 3) ≥20 teeth; 4) prior preterm/low birth weight delivery. Treatment group subjects received SRP and polishing and were given a power toothbrush with OHI. 4 and 6 week follow up visits were carried out to ensure treatment did not result in harm. No treatment group (delayed treatment) received a manual tooth brush with no OHI.
GI, PI, PD, recession and BOP were assessed at baseline and postpartum. GCF and subgingival plaque samples were also collected, as well as a maternal serum sample (first OBGYN visit and at birth). GCF samples were measured to determine concentrations of prostaglandin E2 (PGE2), total (also known as ‘‘direct’’) PGF2a (d-8-isoprostane[iso] PGF2a), interleukin-1b (IL-1b), and IL-6 by ELISA. Serum C-reactive protein was also measured. The bacterial concentration of plaque was tested for the presence of 8 periodontal pathogens: Porphyromonas gingivalis, Prevotella intermedia, Prevotella nigrescens, Tannerella forsythensis, Treponema denticola, Campylobacter rectus, Fusobacterium nucleatum, and Actinobacilus actinomycetemcomitans.
Results: Periodontal intervention resulted in a significantly decreased incidence odds ratio (OR) for preterm delivery (OR = 0.26, 95% CI). Pregnancy without periodontal treatment was associated with significant increases in probing depths, plaque scores, GCF IL-1b (38% increase), and GCF IL-6 (2.1-fold increase) levels. Intervention resulted in significant improvements in clinical status (attachment level, probing depth, plaque, gingivitis, and bleeding on probing scores) and significant decreases in levels of P. nigrescens and P. intermedia, serum IL-6sr, and GCF IL-1b. Subjects in the delayed treatment group had a significantly increased risk for preterm delivery with an OR of 3.8.
Discussion: Intervention of SRP with a power toothbrush and OHI can be deemed safe for mother and fetus based on the results of this study. The intervention, presumably via the improvement in periodontal status and prevention of progression, resulted in a statistically significant reduction in preterm birth for the intervention group with an OR of 0.26, indicating that these mothers had ~70% lower odds of preterm birth. The findings of this pilot study need to be confirmed by larger studies to make any generalizations regarding the potential benefits of therapy.
Topic: Periodontal disease and preterm birth
Authors: Michalowicz BS, et Al. ARTICLE
Title: Treatment of periodontal disease and the risk of preterm birth.
Source: N Engl J Med. 355:1885-94, 2006
Type: Retrospective study
Rating: Good
Keywords:
P: To study the effect of nonsurgical periodontal treatment on preterm birth
M&M: Women between 13 and 17 weeks of gestation were randomly assigned to undergo scaling and root planing either before 21 weeks (413 patients in the treatment group) or after delivery (410 patients in the control group). All women had at least 20 teeth with 4 or more teeth with PD ≥ 4mm and BOP of at least 35%. Patients in the treatment group also underwent monthly tooth polishing and received instruction in oral hygiene.
The gestational age at the end of pregnancy was the prespecified primary outcome.
Secondary outcomes were birth weight and the proportion of infants who were small for gestational age.
R: Scaling and root planing before 21 weeks of gestation plus monthly tooth polishing thereafter did not significantly alter the risk of preterm delivery before 37 weeks, increase birth weight or reduce either the rate of admission to a neonatal intensive care unit or the proportion of infants who were small for gestational age. Treatment improved clinical measures of periodontal disease and was not associated with adverse medical events.
BL: Treatment of periodontitis in pregnant women improves periodontal condition and is safe but does not significantly alter rates of preterm birth, low birth weight, or fetal growth restriction.
Can periodontal disease affect the respiratory system? Is there a relationship between periodontal disease and COPD?
Topic: pulmonary function
Authors: Hayes, C, Sparrow, D, Cohen, M ARTICLE
Title: The association between alveolar bone loss and pulmonary function: the VA Dental Longitudinal Study.
Source: Ann Periodontol. 3, 1998, 257–261.
Type: Clinical study
Rating: Good
Keywords: Lungs, COPD
Purpose: To examine whether the risk of chronic obstructive pulmonary disease (COPD) is increased among individuals with moderate to severe radiographic alveolar bone loss (ABL) as compared to individuals with less severe or no ABL.
Method: The diagnosis of COPD was based on pulmonary function testing. Forced expiratory volume in a second (FEV1) was measured by standard spirometric techniques. Subjects with an FEV1 < 65% of predicted volume were categorized as having COPD. Subjects who were considered free of COPD were selected from the VA Dental Longitudinal Study, a long-term study of aging and health in male veterans.
ABL was assessed by using full-mouth series periapical films measured by a 5 point Schei ruler. Bone loss at each mesial and distal interproximal was separately assessed in 20% increments, and the mean whole-mouth bone loss score was calculated (as %ABL per site per person). Logistic regression analysis was used to determine the independent contribution of bone loss measurement at baseline to the subsequent risk of developing COPD over a 25-year follow-up period. Covariates included measures of smoking, height, age, education, and alcohol consumption.
Results:
1,118 medically healthy at baseline, 261 subsequently developed COPD.
ABL at baseline was an independent risk factor for COPD, with subjects in the worst population quintile of bone loss (mean ABL > 20% per site) found to be at significantly higher risk (OR = 1.8).
Conclusion: The results of this analysis indicate that increased ABL is associated with an increased risk for COPD.
Critique: Used PA radiographs to measure ABL. Information on cigarette smoking habits, and alcohol consumption was self-reported.
Topic: Periodontal infections and atherosclerotic and pulmonary diseases
Authors: Scannapieco FA, Genco RJ. ARTICLE
Title: Association of periodontal infections with atherosclerotic and pulmonary diseases
Source: J Perio Res 34:340-345;1999.
Type: Discussion
Rating: Good
Keywords: cardiovascular disease, coronary artery disease, pneumonia, chronic obstructive pulmonary disease
Purpose: Discussion on association of periodontal infections with atherosclerotic and pulmonary diseases.
Discussion:
Periodontal disease and atherosclerosis
Atherosclerosis is an inflammatory disease. The initial lesion results from injury to the endothelium resulting in a chronic inflammatory process in the artery. Accumulation of lipids is a key feature of this process and in later stages, the atheromatous plaque can be covered with a fibrous cap over the focal necrotic area.
Longitudinal, case study, cross sectional & prospective studies have associated periodontal disease & coronary artery disease (CAD), specially in men < 60 years old, but the relationship is weak for men after 65 yr. Wu et al. found that periodontitis at baseline was associated with non-hemorrhagic (ischemia) stroke (due to atherosclerosis). No association with hemorrhagic stroke.
Possible mechanism by which infection may contribute to atherosclerosis: 1) direct effect of infectious agent in atheroma formation; 2) host mediated effects triggered by infection; 3) common genetic predisposition for periodontal disease & atherosclerosis; 4) common risk factors such as lifestyle.
Three lines of evidence suggesting oral bacteria may have direct effects on atheroma formation: 1) P.g has been found in carotid & coronary atheromas; 2) P.g invades & may proliferate in aortic & heart endothelial cells in vitro; 3) S. sanguis & P.g induce platelet aggregation. It is reasonable to expect that bacteria, which infect atheromatous plaques, may contribute to their formation.
Periodontitis induces an inflammation rate that elevates acute phase proteins (CRP, fibrinogen) in circulation; both are independent risk factors for CAD. Periodontal bacteria produce proteins, which cross-react with human heat shock proteins and may provide excess LPS & host-response inflammatory cytokines (IL-1, PGE2 & TNF).
Periodontal disease and respiratory diseases
It appears that teeth may serve as reservoir for respiratory infection. Anaerobic lung infection can occur after aspiration of salivary secretions, especially from periodontal patients.
Potential mechanism in pathogenesis of respiratory infection: a) aspiration of oral pathogens into lungs; b) periodontal disease-associated enzyme in saliva promoting adhesion & colonization by respiratory pathogens; c) those enzymes may destruct protective salivary pellicles; d) cytokines from periodontal tissue may alter respiratory epithelium to promote infection by respiratory pathogens.
It’s possible that periodontal patients are at higher risk for aspiration pneumonia-common risk factors (smoking) affect defense factors (cilia). Elevated hydrolytic enzyme in subjects with poor OH may destroy protective salivary mucins to clear respiratory pathogens. Oral bacteria in secretions may bind & stimulate respiratory epithelial cells to produce cytokines, which then recruit inflammatory cells, which in turn release hydrolytic enzymes resulting in increasing susceptible of epithelium to respiratory pathogens.
Conclusion: Periodontal disease may have significant impact on systemic health. Further research is needed to definitively establish the role of oral disease in the initiation and progression of pathological processes like atherosclerosis and respiratory infection.
Topic: COPD
Authors: Hyman, JJ, Reid, BC NO ARTICLE
Title: Cigarette smoking, periodontal disease, and chronic obstructive pulmonary disease
Source: J Periodontol. 75, 2004, 9–15
Type: Clinical
Rating: Good
Keywords: National Health and Nutrition Examination Survey III; periodontal disease/ etiology; pulmonary diseases, chronic obstructive/ etiology; risk factors; smoking; adverse effects.
Purpose: To investigate the role of smoking in the association between periodontal disease and chronic obstructive pulmonary disease (COPD).
Methods: The study population consisted of 7,625 participants in the Third National Health and Nutrition Examination Survey (NHANES III) during 1988-1994. Inclusion criteria: age >30 years, successful completion of 3 or more spirometric examinations, periodontal examination. Examination: Periodontal probing was conducted at the mesio-buccal and mid-buccal sites of all teeth in two randomly selected quadrants-one mandibular and one maxillary. At each site PD, REC, AL were assessed. Interexaminer reliability was measured repeatedly. Lung function was evaluated on NHANES III using spirometry. To address the interaction between smoking, periodontal disease and COPD, the logistic regression analyses were stratified by smoking status: never, former and current.
Results: 13% of the population had COPD and 3.8% had moderate or severe obstructive disease. Overall those with COPD were older, were more likely to have 2mm or more of mean attachment loss, to be non-Hispanic white and female, and to have a history of cigarette smoking, heart attack and hypertension. Approximately 16.2% of those with COPD also had a severe level of periodontal disease and 74.7% had a history of current of former smoking. The only significant increase in risk for COPD occurred among current smokers with very severe periodontal disease ( ≥4mm mean attachment loss). No SS association was found between periodontal disease and COPD among former or non-smokers. Current smokers with ≥4mm mean attachment loss had an odds ratio of 3.71. When mean PD was used as measure of periodontal disease, no relationship between periodontal disease and COPD at any level of smoking was found.
Conclusion: Smoking may be a cofactor in the relationship between periodontal disease and chronic obstructive pulmonary disease
Designed By Steven J. Spindler, DDS LLC