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smoking cessation and the reversibility of periodontal damage
patient populations that are at greater risk for diabetes and periodontitis
a. Genetics
b. Smoking
c. Diabetes
d. Osteoporosis
d. Stress
e. Obesity
Discussion topics:
A. Can systemic factors increase the risk of developing or progression of periodontal disease?
Haffajee AD, Socransky SS, Lindhe J, et al. Clinical risk indicators for periodontal attachment loss. J Clin Periodontol 18:117-125, 1991
Grossi SG, Genco RJ, Machtei EE, et al. Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss. J Periodontol 66:23-29,1995.
Machtei E, Hausman E, Dunford R, et al. Longitudinal study of predictive factors for periodontal disease and tooth loss. J Clin Perio 26:374-380, 1999.
Page RC, Beck JD. Risk assessment for periodontal diseases. Int Dent J. 47:61-87, 1997
SALVI, H. LAWRENCE, T. OFFENBACHER & J. D. BECK: Influence of risk factors on the pathogenesis of periodontitis. Periodontology 2000, Val.14, 1997, 173-201 (from LR 22)
AAP Position Paper. Parameters on periodontitis associated with systemic conditions. J Periodontol 71 (Suppl):876-879;2000.
B. How does genetics contribute to periodontal disease? Is this true for all patient populations?
Michalowicz BS, Aeppli D, Virag JG, et al. Periodontal findings in adult twins. J Periodontol 1991;62:293-299.
HART & K. KORNMAN: Genetic factors in the pathogenesis of periodontitis: Periodontology 2000. Vol. 14. 1997,202-215 (from LR 22)
Kornman K, Crane A, Wang H-Y, et al. The interleukin-1 genotype as a severity factor in adult periodontal disease. J Clin Periodontol. 24: 72-77, 1997.
Papapanou PN, Neiderud AM, Sandros J, Dahlen G. Interleukin-1 gene poly-morphism and periodontal status: A case control study. J Clin Perio 28:389-396, 2001.
Cattabriga M, Rotundo R, Muzzi L, et al. Retrospective evaluation of the influence of the Interleukin-1 genotype on radiographic bone levels in treated periodontal patients over 10 years. J Periodontol 72:767-773, 2001.
McGuire MK, Nunn ME. Prognosis versus actual outcome. IV. The effectiveness of clinical parameters and IL-1 genotype in accurately predicting prognosis and tooth survival. J Periodontol. 70: 49-56, 1999.
C. Does smoking increase the risk of periodontal disease?
Rivera-Hidalgo, F: Smoking and periodontal disease. Periodontol 2000 32:50-58, 2003.
Bergstrom J. Tobacco smoking and risk for periodontal disease. J Clin Periodontol 2003;30:107-113.
Bergstrom, J. Influence of tobacco smoking on peridontal bone height. Long – term observations and a hypothesis. J Clin Periodontol 2004; 31:260-266.
Giovanni E et al.: Experimental gingivitis in cigarette smokers: A clinical and microbiological study. J Clin Periodontol 2005; 32: 441-447
D. How does smoking affect systemic health? Periodontal tissues?
Palmer RM, Wilson RF, Hasan AS, Scott DA. Mechanisms of action of environmental factors--tobacco smoking. J Clin Periodontol. 2005;32 Suppl 6:180-95.
Buduneli N et al. Saliva concentrations of RANKL and osteroprotegerin in smoker versus non-smoker chronic periodontits patients. J Clin Periodontol 2008; 35(10):846-52
David F, Lappin et al. Effect of smoking on serum RANKL and OPG in sex, age, and clinically matched supportive-therapy periodontitis patients. J Clin Periodonto 2007; 34:271-277
Thomson W, Broadbent J, et al. Cigarette smoking and periodontal disease among 32 year – olds: A Prospective study of a representative birth cohort. J Clin Periodontol 2007; 34: 828-834
E. Does smoking affect outcome of periodontal therapy? Wound healing?
Bain C, May P: The association between the failure of dental implants and cigareete smoking. Intl J Oral and Max Impl 8:609-615, 1993
Strietzel F eta l. Smoking interferes with the progrosis of dental implant treatment: A systematic review and meta analysis. J Clin Periodontol 2007; 34:523-544
Tonetti M, Pini-Prato G, Cortellini P: Effect of cigarette smoking on periodontal healing following GTR in infrabony defects. A preliminary retrospective study. J Clin Periodonto 22:229-234, 1995
Souza s et al. Subetpithelial connective tissue graft for root coverage in smokers and non-smokers: A clinical and histologic controlled study in humans. J Periodontol, 2008; 79(6):1014-1021
F. Can quitting smoking reverse the effects on the periodontium or are changes from smoking irreversible?
Morozumi T et al,: Smoking cessation increases gingival blood flow and gingival crevicular fuid. J Clin Periodonto, 2004, 31:267-272
Tomar SL, Asma S. Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey. J Periodontol. 2000 May;71(5):743-51.
G. Does smokeless tobacco have the same effects on the periodontal tissues?
Bergstrom J et al. Smokeless tobacco (snuff) use and periodontal bone loss. J Clin Periodontol 2006;33:549-554
H. Is alcohol use a risk factor for periodontitis?
Tezal M et al. Alcohol consumption and periodontal disease. The NHANES III Survey. J Clin Periodonto, 2004 Jul;31(7):484-8
Amaral, C eta al. The relationship between alcohol dependence and periodontal disease. J Periodontol 2008; 79: 993-998
I. Is diabetes a risk factor for periodontitis? How does it affect the body locally? Systemically? Does it matter if it is controlled or uncontrolled?
Mealey BL, Oates TW; AAP commissioned Review: Diabetes mellitus and periodontal diseases. J Periodontol. 77:1289-303, 2006
Taylor GW, Burt BA, et al. Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years. J Periodontol 69:76-83, 1998.
Lalla E et al., Periodontal infection profiles in type 1 diabetes. J Clin Periodontol. 2006 Dec ;33(12) :855-62
J. Are there any known patient populations who are at greater risk for diabetes and periodontal disease?
Emrich LJ, Shlossman M, Genco RJ : Periodontal disease in non-insulin dependent diabetes mellitus. J Periodontol. 62:123-130, 1991
Grossi S, et al. Treatment of peridontal disease in diabetics reduces glycated hemoglobin. J Periodonto 68:713-719, 1997
K. How is osteoporosis measured? Is osteoporosis a risk factor for periodontal disease?
Wactawski-Wende, E Hausmann, K Hovey, M Trevisan, S Grossi, R Genco : The Association Between Osteoporosis and Alveolar Crestal Height in Postmenopausal Women. J Periodontol 2005, Vol. 76, No11: 2116-2124
Brennan R, Genco R, Hovey K, Trevisan M, Wactawski-Wende J. Clinical Attachment Loss, Systemic Bone Density, and Subgingival Calculus in Postmenopausal Women. J Periodontol 2007, 78; 2104 - 2111
L. Is stress a risk factor for chronic periodontal disease? Is stress a risk factor for any other periodontal diagnosis?
Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. Relationship of stress, distress, and inadequate coping behaviors to periodontal disease. J Periodontol 70: 711-723, 1999.
da Silva AMM, Newman HN, Oakley DA. Psychosocial factors in inflammatory periodontal diseases. A review. J Clin Periodontol 22:516-526, 1995.
M. Is obesity a risk factor for peridontal disease? How does obesity relate to inflammation?
Vecchia C, Susin C et al. Overweight and obesity as risk indicators for periodontitis in adults. J Periodontol 2005; 76(10) 1721-1728
Haffajee AD, Socransky SS. Relation of body mass index, periodontitis and Tannerella forsythia. J Clin Periodontol. 2009 Feb;36(2):89-99
A. Can systemic factors increase the risk of developing or progression of periodontal disease?
Topic: Risk indicators for Periodontal attachment loss
Authors: Haffajee AD, Socransky SS, Lindhe J, et al. ARTICLE
Title: Clinical risk indicators for periodontal attachment loss.
Source: J Clin Periodontol 18:117-125, 1991
Type: clinical study
Rating: Good
Keywords: risk indicators, risk factors, new attachment loss, age, sex, number of missing teeth, mean PD, CAL
Purpose: to identify risk factors for new attachment loss in patients, and to ascertain whether such risk indicators could be used to identify future attachment loss in the following year.
Methods:
271 Japanese patients were monitored for gingivitis, plaque accumulation and PPD, PAL & BOP for all teeth at baseline and 1 year without periodontal therapy, but only home care.
A patient was considered to exhibit additional attach loss if 1 or more sites increased 3 mm or more in PAL in 1 year.
Clinical variables were: age, sex, number of missing teeth, mean PD and CAL.
Results: 74/271 patients (27.3%) had additional CAL of 3 mm or more at 1 or more sites after 1 year.
Older patients had greater risk of disease progression than younger patients.
NSSD in % of patients with additional attach loss when divided on the basis of sex, number of missing teeth or % of sites with gingivitis. However, the greater the % of sites with visible plaque or BOP, the greater was the likelihood of subsequent attachment loss.
Increasing mean levels of PD or attach level or increasing % of sites exhibiting prior attachment loss were strongly related to the proportion of patients with subsequent attachment loss. Gingival recession had weaker relationships.
Conclusion: General principles observed: a small % of patients had new attachment loss when longitudinally monitored; patients with more affected sites had more new attach loss than patients with few affected sites; older patients seemed to be at more risk than younger patients.
Topic: Risks
Authors: Grossi SG, Genco RJ, Machtei EE ARTICLE
Title: Assessment of risk for periodontal disease. II. Risk indicators for alveolar bone loss.
Source: J Periodontol 66:23-29,1995.
Type: Clinical study
Rating: Good
Keywords: Risks, systemic conditions
Purpose: To examine the risk indications for alveolar bone loss associated with periodontal disease.
Method: 1,361 pts (25-74 yrs) were evaluated for interproximal alveolar bone loss using 10 intraoral radiographs, 4 posterior vertical bitewings and 6 anterior periapicals. The clinical examination included assessment of soft tissue, dental caries, supragingival plaque, gingival
bleeding, subgingival calculus, probing depth (PD), and clinical attachment level (CAL) for all teeth present in the dentition. Samples were analyzed using immunofluorescence microscopy for the presence of the following microorganisms: Actinobacillus actinomycetemcomitans, T forsythus, Campylobacter rectus, Capnocytophaga species, Eubacterium saburreum, Fusobacterium nucleatum, Porphyromonas gingivalis, and Prevotella intermedia. Interproximal alveolar bone loss was measured from the alveolar crest to the CEJ and a mean computed for each subject. The mean bone loss per subject ranged from 0.4-8.8 mm.
Results:
Factors which were positively associated with more severe bone loss included subg colonizations with B. Forsythus (O.R. 2.52) or P Gingivalis (O.R. 1.73), race (native Americans, asian, or pacific islanders) with an O.R. 2.4, and gender with males having higher odds ratio than females. Smokers had greater odds for more severe bone loss compared to non-smokers ranging from 3.25 to 7.28 for light and heavy smokers. Individuals at older ages also showed more severe levels of bone loss. History of kidney disease (O.R. 0.55) and history of allergies (O.R. 0.76) were inversely associated with severity of bone loss.
Conclusion: The risk indicators identified with the present study utilizing BL as the outcome variable, in addition, to those from our previous analysis utilizing AL as the outcome variable, serve as a basis for their further evaluation of potential risk factors from longitudinal analyses.
Topic: Periodontal disease and tooth loss
Authors: Machtei E, Hausman E, Dunford R ARTICLE
Title: Longitudinal study of predictive factors for periodontal disease and tooth loss
Source: J Clin Perio 26:374-380, 1999
Type: Longitudinal study
Rating: Good
Keywords: clinical attachment level, alveolar bone height, risk factors, smoking, systemic condition, tooth loss
Purpose: To explore longitudinally a variety of markers (clinical, systemic and microbiological markers) as possible periodontal risk factors in subjects with mild periodontal dz.
Methods: 1426 subjects were examined at baseline. Of these, 415 subjects with mild or little periodontal disease were included from a follow up exam 2-4 yrs later: medical and dental history; socioeconomic profile, clinical measurements, microbial samples (paper points from MB of 12 index teeth) and radiographic assessment of bone height were performed at baseline. Excluded if any one site had PD>5 or CAL>6. Florida probe to measure PD, PI, GI, CAL. Intraoral radiographs taken and examined for change between the 2 time points.
Results:
Mean PD at baseline were 1.99+/-0.37 mm while mean overall change was 0.1 mm which amounts to an annual rate of 0.04 mm. M
ean CAL (1.75+/-0.6 mm) at baseline resulted in mean attachment change of 0.28 mm (0.12 mm annually); however, this varied widely from 2.11 mm loss to 1.60 mm gain.
Alveolar crestal height (ACH) at baseline (mean 2.05+/-0.85 mm) resulting in a mean net loss of 0.1 mm. Approximately 10% of all sites presented for the second visit with attachment loss exceeding the threshold (4.4% annually), while only 2.2% of all sites exhibited attachment gain (0.88% annually).
Patients exhibiting CALoss had great variance in individual site loss, from 0-74%.
Age is factor that affected change: pts >60 yrs old exhibited 50% greater mean annual bone loss than those <40 yrs old, and had a sig greater percentage of losing sites, but less overall CALoss. Age does not correlated sig with tooth loss.
Current smokers exhibited greater disease progression compared to non-smokers, especially for changes in soft tissue (sig greater mean CALoss).
Baseline disease level seems to be related to future tooth loss, for both crest height and CAL.
Systemic factors related to tooth loss (most NSD) included systemic gout, history of cancer, thyroid disorder and gallbladder disease, as well as high blood pressure (lost 2x as many teeth and normal blood pressure). Having B. forsythus at baseline showed greater loss of ACH and higher chance of tooth extraction.
Conclusion: Baseline clinical parameters correlated strongly with the outcome, i.e., subjects with deeper mean PD at baseline exhibited greater increase in PD over time; subjects with greater CALoss at baseline exhibited greater attachment loss between the 1st and 2nd visits. Having more severe form of dz at baseline is associated with greater tooth mortality.
Cr: 95.6% of pts sampled were Caucasian
Topic: Risk Assessment
Authors: Page RC, Beck JD ARTICLE
Title: Risk assessment for periodontal diseases.
Source: Int Dent J. 47:61-87, 1997
Type: Review
Rating: Good
Keywords:
Purpose: To summarize existing information about risks for periodontitis.
Discussion:
Risk factor is used as a general term meaning those characteristics that strongly associate groups of individuals who have the disease in question in contrast to those who do not. Factor is found to be associated with outcome of interest in longitudinal studies and the association is consistent with current understanding of disease process. Risk indicator is a putative risk factor that is identified through cross-sectional study designs. There are characteristics that can predict individuals at high risk for disease and are called risk markers or risk predictors. “Significantly elevated levels of PGE2 in GCF may be marker/predictor for active periodontal disease. There is also another group of predictors, such as gender, race and age that are associated with higher probability of disease but currently cannot be changed are called background characteristics.
Risk for periodontitis
Smoking (most possible risk factor)
Heavy smokers may be up to 5-7 times more likely to manifest severe periodontitis than individuals who have never smoked.
Smoking is strongly related to severity of disease and to recurrent of refractory disease.
Bergstrom: Smokers had significantly more mean alveolar bone loss than those who never smoked. Those who smoked more than 10 cig/day manifested 2.06mm alveolar bone loss whereas those who smoked <10 cig/day had 1.6mm bone loss.
Haber: Prevalence and severity of periodontitis was significantly higher in current smokers than in those who had never smoked.
Grossi et al: The odds ratio for association between smoking and adult periodontitis was even stronger than the association between the disease and the gram-negative bacteria that cause it.
Clinical features: gingival tissue tends to be fibrotic and hyperkeratotic and to manifest minimal erythema and edema relative to disease of equal severity in non-smokers. Attachment loss is more severe in the anterior regions, especially on the palatal aspects of the maxillary anterior teeth.
Both surgical and non-surgical therapies are less effective in smokers than in non-smokers.
No prospective longitudinal studies of the effects of smoking cessation have yet been reported.
Smoking tends to mask gingival inflammation by causing constriction of the blood vessels.
Functional activities of both salivary and tissue neutrophils are reported to be suppressed.
Negative significant association has been found between smoking and serum antibody levels to certain periodontal bacteria.
T-cell subset ratios appear to be altered in smokers.
Aging (Background factor)
Widely claimed that increasing age is a risk for periodontitis and that elderly people are more susceptible than younger persons to periodontal deterioration. Whether the increased prevalence in older people results from a lifetime accumulation of periodontal lesions or a truly enhanced susceptibility to periodontal deterioration remains unresolved.
Prevalence and severity of CAL and PD has been directly related to increasing age in numerous cross-sectional studies.
Longitudinal data are inconclusive.
Abdellatif and Burt: Effects of age on disease progression is negligible when good OH is maintained.
Diabetes (probable risk factor)
The prevalence of advanced periodontal disease is substantially higher in both type I and type II diabetes than in non-diabetics.
Individuals with uncontrolled or poorly controlled diabetes are at greater risk for periodontitis than are those with controlled diabetes and non-diabetic individuals.
Periodontal therapy may improve metabolic control of diabetes.
Fundamental lesion is thickening of the basement membranes of small vessels with non-enzymatic glycosylation of proteins and accumulation of deposits within the vessel wall and on the luminal surfaces. These changes may narrow the vessel lumen and interfere with transport across the vessel wall.
Abnormalities in PMN chemotaxis, adherence and phagocytosis have been reported.
Collagen production by PDL and gingival fibroblasts may be decreased and production of gingival collagenase increased.
Osteoporosis (Risk indicator)
Groen et al: 36/38 osteoporotic women were either edentulous or manifested severe periodontitis.
Von Wowern et al: Osteoporotic women had significantly more clinical attachment loss than healthy women.
Smoking is a risk factor for severe periodontitis and osteoporosis.
HIV infection (Risk indicator)
HIV infection appears to elevate risk for severe periodontitis.
Most reports indicate that periodontitis is more prevalent in these individuals, including infected children than in other persons of comparable age and levels of OH.
Prevalence of periodontitis in HIV infected individuals ranges 4-6%.
These cases many not respond to treatment and attachment loss may be extremely rapid.
Pathogenic bacteria (most likely risk factor)
Specific species of predominantly gram negative, anaerobic, motile bacteria have been implicated in the etiology of periodontitis.
P. gingivalis and T. forsythia have been especially implicated in adults with severe disease and A.a in younger individuals with aggressive periodontitis.
Whether the presence of putative pathogenic species can be used as strong indicator for future CAL loss remains controversial.
Assessment of the sub-g flora for the presence or absence of periodontal pathogens is a worthwhile assessment of risk.
Microbial deposits (most likely a Risk factor)
Meticulous professional and daily plaque control prevents clinical attachment loss in most individuals.
Supra-g plaque control following treatment delays recolonization of the sub-g area following treatment.
In individuals receiving regular dental care and with good OH, the presence of calculus does not result is significant attachment loss.
Bleeding on probing (Risk marker with negative predictive value)
BOP alone is not a predictor for elevated risk for future clinical attachment loss.
Lack of BOP is an excellent indicator of periodontal health with a predictive value of 0.972.
History of periodontitis (Risk predictor)
Risk for future periodontal deterioration is strongly associated with presence and severity of disease at baseline. Individuals who have the most severe disease at the initial examination are at the greatest risk for future disease.
Familial history and genetic factors (Background factor)
Genetic factors are strongly associated with the early onset forms and to a lesser extent with the adult form.
Functional defects in leukocytes, especially in the phagocytic cells comprise the largest group of genetically transmitted traits with associated enhanced susceptibility to periodontitis.
Patients with IL-I genotype positive are more susceptible to periodontal disease.
Topic: Periodontal medicine
Author: SALVI, H. LAWRENCE, T. OFFENBACHER & J. D. BECK. NO ARTICLE
Title: : Influence of risk factors on the pathogenesis of periodontitis
Source: Periodontology 2000, Val.14,1997, 173-201
Type: Review
Rating: Good
Keywords: oral systemic connection, periodontal medicine, cytokine leakage
Background: Risk factor is an aspect of personal behavior or lifestyle, an environmental exposure, or an inborn or inherited characteristic, which on the basis of epidemiological evidence is known to be associated with a health related condition. Presence of a risk factor implies a direct increase in the probability of a disease occurring. Risk predictor or marker, are the consequence of disease and vary over time, marking the natural history of disease progression and not thought to be part of the causal chain of a disease. Intervention should not be aimed at predictor but at the risk factor.
Purpose: To examine seven systemic modifiers of periodontal disease: diabetes, tobacco, psychosocial stress, allergy, HIV, osteoporosis and anemia.
Factors not reviewed: Age, Medication, Nutiriton, Oral hygiene status and microorganisms, low socioeconomic and educational status, detal services, existing disease, diabetes.
Conclusion: The categories listed in the boxes correspond to the stages of pathogenesis cycle presented.
Topic: Systemic Effects of Periodontitis
Authors: AAP Position Paper. ARTICLE
Title: Parameters on periodontitis associated with systemic conditions.
Source: J Periodontol 71 (Suppl):876-879;2000.
Type: Position paper
Rating: Good
Keywords: Periodontitis/diagnosis; periodontitis/complications; periodontitis/therapy; risk factors; systemic
diseases; disease progression
Purpose: Describe parameters of care on systemic conditions affected by perio dz.
Discussion:
Pts must be informed about the significance of systemic conditions with respect to the periodontal disease process so they may make an informed decision regarding their health.
Diabetes Mellitus - Periodontitis may adversely affect glycemic control in diabetes. Treatment should include: Identification of signs and symptoms of undiagnosed DM, medical consult, consider adjunctive antibiotic therapy if diabetes is poorly controlled, and attempt to reduce stress anxiety.
Pregnancy- Hormonal fluctuations may alter periodontal health. Changes may also be associated with puberty, menstrual cycle, pregnancy (the most pronounced changes), or oral contraceptives. Treatment considerations: medical consultation, consider postponing treatment until after first trimester, emergency treatment can be done anytime during pregnancy, consider postponing any surgery until after delivery, maintenance as needed, administer drugs with caution, local anesthesia should always be done instead of general or conscious. May have an increased risk for pre-term low birth weight delivery.
Hematological disorders/leukemia- Gingival enlargement with or without necrosis is a common manifestation of acute leukemia and somewhat common and less pronounced in chronic. Chemotherapy associated with bone marrow transplantation may also adversely affect the gingiva. Tx considerations: consultation and coordination of treatment with physician, minimize periodontal infection prior to undergoing chemo, avoid elective therapy during treatment, consider antimicrobial therapy for emergency perio tx when granulocyte counts are low, monitor for evidence of host vs graft disease and drug induced gingival overgrowth following bone marrow transplant. Periodontal sx may be performed on pts with stable, chronic leukemia.
Immune system disorders – HIV/AIDS, pts undergoing organ transplants and other immunocompromised pts: tx considerations- medical consultation, control acute periodontal disease, administer systemic or local medications in a manner that avoids opportunistic infections.
B. How does genetics contribute to periodontal disease? Is this true for all patient populations?
Topic: perio risk factors
Authors: Michalowicz BS, Aeppli D, Virag JG, et al NO ARTICLE
Title: Periodontal findings in adult twins.
Source: J Periodontol 1991;62:293-299.
Type: clinical
Rating: good
Keywords: periodontitis/etiology; gingivitis/etiology; twins; genetics.
Purpose: To examine the relative contribution of environmental and host genetic factors to clinical measures of periodontal disease through the study of both reared-together twins and monozygous twins reared-apart.
Materials and methods: 110 pairs of adult twins. Mean age of 40.4 years old, 63 MZ reared-together, 33 like-sexed dizygous pairs reared together, and 14 monozygous reared-apart. Average age at separation date was 187 days.
AL, PD, GI and PI were assessed from the mesiobuccal or mesiolingual surface of the six Ramfjord teeth by two examiners. If an index tooth was missing it was replaced by nearest distal tooth. AL was adjusted for age and PI for age and gender. Environmental variances between groups were tested.
Results: Mean unadjusted values of the clinical parameters in the twin population were: AL 0.9mm, PD 2.9mm, GI 1.2 and PI 1.3. There was not a significant difference in these values for reared-together twins after they were adjusted for gender and age. Data did not contradict the assumptions that the twins had similar environments and were samples of the same gene pool.
Data from these 110 pairs of adult twins suggest there is a genetic component to levels of supragingival plaque and clinical measures of the periodontium.
Conclusion:
1. Based on the ratio of within-pair variances of raised-together twins a significant genetic component was identified for probing depth, gingivitis, and plaque.
2. Based on heritably estimates from reared-together and reared-apart twins, a significant genetic component was identified for PD, AL, and plaque.
3. 38-82% of the population variance for these measures may be attributed to genetic factors.
4. While there is general agreement that bacteria are important in the pathogenesis of periodontal disease, future studies should consider the influence of host genetic influences on disease.
Topic: Genetics
Author: Hart T., Kornman K. NO ARTICLE
Title: Genetic factors in the pathogenesis of periodontitis
Source: Periodontology 2000. Vol. 14. 1997,202-215
Type: Review
Rating: Good
Keywords: Genetics; periodontitis; risk factors; pathogenesis
Discussion:
- Periodontal disease may be regarded as a range of different diseases for which certain individuals are at relatively high risk. This risk may be partly under genetic control.
- In multifactorial diseases the genetics are not by themselves sufficient for the disease to present itself, and the clinical signs and symptoms are not usually evident until adulthood
- Considerable evidence suggests that there is some genetic basis for early-onset forms of periodontal disease consistent with single-gene inheritance. The results of twin studies clearly indicate that a significant part of the variance in clinical and radiographic measures of adult periodontitis may be explained by genetic factors.
- Although microbial factors are required for disease, they alone do not predict the presence or severity of periodontitis.
-The levels of specific microbes can explain less than 20% of variability in periodontal disease expression. Bacteria are essential for the initiation and progression of periodontitis, but other factors, such as smoking and genetics, appear to strongly influence severity of the disease that results
- Perhaps the most significant aspect of this paradigm shift has been the realization of the centrality of host susceptibility as a modifier of the clinical outcomes of the bacterial challenge
-Evidence for a genetic influence on periodontitis comes from multiple sources including familial aggregation and formal genetic studies of early-onset forms of periodontitis
Genetic susceptibility to microbial infections
- Studies showing that stable immune phenotypic characteristics such as antibody titer, monocyte function and cytokine production may result from specific genetic polymorphisms have begun to fuel the search for genes important in susceptibility and resistance to various microbial infections, including periodontitis.
Candidate genes important in periodontitis
- The key will be to identify the genetic factors that are important enough to impart significant clinical risk
- The association of decreased serum immunoglobulin levels, particularly of the IgG2 subclass, with poorer outcome for a number of different microbial challenges, is consistent with the hypothesis that these responses contribute to protection
- IgG2 antibodies, the primary immunoglobulin subclass that reacts with bacterial carbohydrates and lipopolysaccharides, have been reported to be the dominant immunoglobulin in both early-onset periodontitis and adult periodontitis
- Serum IgG2 levels in localized juvenile periodontitis cases are higher than serum levels of generalized juvenile periodontitis cases and age- matched controls with no disease, which supports the concept that a robust serum antibody response is associated with protection in juvenile periodontitis cases
-The FcyRIIa (CD32) receptor recognizes the Fc region of IgG2, and therefore neutrophils expressing this receptor are capable of recognizing bacteria that have been opsonized
The genetic polymorphism that defines the FcyRII receptor, therefore, appears to be a promising marker for susceptibility to localized juvenile periodontitis.
-Prostaglandin E2: Prostaglandins are potent biological mediators with diverse physiological effects that have also been implicated in a variety of pathological conditions including periodontitis
-The prostaglandin endoperoxide synthase 2 enzyme appears to be the predominant effector of prostaglandin activity in inflammation
-Interleukin 1:The association of severe periodontitis with smoking and the IL-1 genotype suggest that they play an important role in the pathogenesis and clinical course of adult periodontitis.
-Polymorphonuclear neutrophils represent a major cellular component of the innate cellular defense system in humans, particularly against bacterial infections.
Conclusion:
A multitude of host factors are involved in responses to microbial challenge and in the sub- sequent immune responses. Genetic polymorphisms probably exist in many if not most of the inflammatory and immune mediators. However, it is likely that: 1) not all polymorphisms impart differential susceptibility to destructive aspects of the disease; 2) a number of genes will be identified as important in this regard; and 3) knowledge of these may permit determination of individual risk for many individuals
Topic: Interleukin-1 genotype
Authors: Kornman K, Crane A, Wang H-Y, et al ARTICLE
Title: The interleukin-1 genotype as a severity factor in adult periodontal disease
Source: J Clin Periodontol. 24: 72-77, 1997
Type:
Rating: Good
Keywords: Genetics, severe periodontitis, periodontal disease, IL-1, TNF, periodontitis
Purpose: To investigate the association of specific cytokine genotypes (IL-1) with the clinical severity of periodontitis.
Methods: Subjects over 35 years of age in good general health were used in this study. PD, CAL, plaque, and BOP were evaluated as well as full mouth radiographic series. Patients were placed in 3 disease categories: (1) mild to no periodontal disease (no PD > 3 mm, no bone loss > 15%), (2) moderate periodontal disease (< 4 interproximal sites with > 50% bone loss, and total mean bone loss of 17-28%), (3) generalized severe periodontal disease (> 7 interproximal sites with ≥ 50% bone loss, and total mean bone loss of > 34%). Smoking status was also taken into account. Genetic polymorphisms were evaluated with blood collected from a finger prick test. Polymorphisms for IL-1A gene, IL-1B gene, IL-1RN gene, and the TNFA gene were detected using PCR analysis.
Results: A strong association was observed between severity of periodontitis and the composite genotype comprising allele 2 of IL-1A polymorphism plus allele 2 of the IL-1B gene. In non-smokers in the 40-60 year age range, the composite genotype was present in 78% of severe cases, 26% of moderate cases, and 16% of mild cases. For single alleles, no associations were found. The genetic association with periodontitis was only evident when smokers were excluded, confirming the importance of this risk factor. Smoking or the specific composite genotype accounted for 86% of the severe cases in this study.
Discussion: The association of severe periodontitis with smoking and the IL-1 genotype reported in this study suggests a role for these factors in the pathogenesis and clinical course of adult periodontitis.
Topic: IL-1 gene polymorphism
Authors: Papapanou PN, Neiderud AM, Sandros J, Dahlen G. ARTICLE
Title: Interleukin-1 gene polymorphism and periodontal status: A case control study.
Source: J Clin Perio 28:389-396, 2001.
Type: a case control study
Rating: Good
Keywords: IL-1, Genotype positive, periodontitis, bacteria
Purpose: To examine polymorphisms at the interleukin-1 (IL-1) gene level in relation to periodontal status, subgingival bacteria and systemic antibodies to periodontal microbiota.
Methods: Case control study.
132 periodontitis patients were age and gender matched with 73 periodontally intact controls (PD < 5 mm, CAL < 1 mm, in ages < 45 y.o., no interproximal or lingual sites with CAL > 3 mm, in ages > 45 y.o. no more than 4 interproximal sites with CAL maximally 5 mm.).
All participants were interviewed with respect to systemic health history and current medication, and smoking habits.
Two calibrated examiners performed all clinical assessments.
Subgingival plaque samples (min of 14 sites/pt) were analyzed by genomic DNA probes, and serum IgG antibodies to periodontal microbiota were assessed by an immunoassay. Polymorphisms in the IL-1A gene were studied by PCR.
Results: No difference in the distribution of the positive composite IL-1 genotype was observed between a group of periodontitis patients and a control group of age and gender matched periodontally ‘‘intact’’ subjects. In cases, both the composite genotype and the number of #2 alleles were positively correlated with the severity of attachment loss. No relationship between genotype and subgingival microbial profiles was observed. Genotype positive patients revealed both overall lower serum antibody levels and specific titers against selected bacteria.
Conclusion: IL-1 polymorphism is related to the severity of periodontitis in patients with confirmed disease.
Topic: Genetics
Authors Cattabriga M, Rotundo R, Muzzi L, et al. ARTICLE
Title: Retrospective evaluation of the influence of the Interleukin-1 genotype on radiographic bone levels in treated periodontal patients over 10 years.
Source: J Periodontol 72:767-773, 2001.
Type: Clinical study
Rating: Good
Keywords: interleukin-1 (IL-1)
Purpose: To evaluate if interleukin-1 (IL-1) genotype impact on the rate of bone and tooth loss in non-smoking periodontally treated patients during maintenance.
Methods: 60 non-smoking patients with moderate to severe periodontitis were treated and maintained for over a 10-year period. At the baseline examination, radiographic evaluation (CEJ-root apex, CEJ-bottom of defect mesial and distal, CEJ-bone crest mesial and distal, crown-root ratio) was performed using the long-cone technique. Radiographs were placed on a diaphanoscope without any magnification. All patients received SRP. 36 patients then underwent surgery. Subsequently, all patients were enrolled in a periodontal maintenance program with recall visits every 3-4 months for at least 10 years. At the latest recall visit the same radiographic measurements evaluated at baseline were taken and a DNA sample for IL-1 genetic susceptibility testing was collected on a DNAase-free blotting paper and sent for blinded analysis to the genetic testing laboratory.
Results:
IL-1 genotype: 23 pts (38.3%) were positive and 37 pts (61.7%) negative.
Tooth loss: 52 (3.3%) out of 1,566 tth were lost due to periodontitis between baseline and latest recall visit; 28 of 957 (2.9%) in the IL-1 genotype negative group, and 24 of 609 (3.9%) in IL-1 genotype positive group. These differences were not SS.
The mean variation in bone defect level averaged -0.04 mm in IL-1 genotype negative patients and 0.01 mm in IL-1 genotype positive patients. The mean variation in bone crest level averaged 0.24 mm in IL-1 genotype negative patients and 0.28 mm in IL-1 genotype positive patients.
Conclusion: NSSD related to IL-1 genotype in tooth loss after 10 yrs in a non-smoking, well-maintained periodontal population as a group.
On an individual patient basis, the IL-1 genotype, in combination with the initial bone level, may be useful at the beginning of therapy for predicting bone level variation.
Topic: IL-1 genotype
Authors: McGuire MK, Nunn ME. ARTICLE
Title: Prognosis versus actual outcome. IV. The effectiveness of clinical parameters and IL-1 genotype in accurately predicting prognosis and tooth survival.
Source: J Periodontol. 70: 49-56, 1999.
Type: Clinical study
Rating: Fair
Keywords: periodontal diseases/diagnosis; prognosis; genotype, IL-1; forecasting; risk factors; smoking/adverse effects; tooth loss/etiology; tooth loss/prevention and control; outcome assessment
Purpose: To determine if the patient's IL-1 genotype would improve accuracy in assignment of prognoses and prediction of tooth loss.
Methods: 42 patients (1,044 teeth) in maintenance for 14 years; 16 pts tested IL-1 genotype-positive (IL-1GP). 9 were current smokers, and 30 had a Hx of smoking, w/ an average of 29.44 pack years.
Results: Both IL-1GP and heavy smoking were sig related to tooth loss. Positive IL-1 genotype increased the risk of tooth loss by 2.7 times, and heavy smoking (defined as >/= 40 pack years) by 2.9 times. The combined effect of IL-1GP and heavy smoking increased the risk of tooth loss by 7.7 times. The value of clinical parameters traditionally used to assign prognosis was found to be dependent on IL-genotype and smoking status. In the model that included IL-1 genotype and heavy smoking, none of the clinical parameters added significantly to the model for tooth loss while mobility, probing depth, crown-to-root ratio, and percent bone loss added significantly to the model, which included IL-1 genotype in non-smokers.
Conclusion: Knowledge of IL-1 genotype status would be important in developing a treatment plan and predicting tooth survival, especially for smokers. It would also help maintenance patient's therapy for non-responding areas; one would be less likely to take a "wait and see approach" with IL-1GP patients. IL-1 positive non-smokers can be successfully treated and maintained over long periods of time.
C. Does smoking increase the risk of periodontal disease?
Topic: Smoking
Authors: Rivera-Hidalgo, F ARTICLE
Title: Smoking and periodontal disease
Source: Periodontol 2000 32:50-58, 2003
Type: Review
Rating: Good
Keywords:
Purpose: To review recent publications about smoking and periodontal disease and draw opinions based on reported findings.
Discussion: Summary of findings on smoking and periodontal disease
Fewer gingival bleeding in smokers than in non-smokers. Gingival inflammatory symptoms appear to be suppressed in smokers. Smokers had a higher proportion of small blood vessels and a lower proportion of large blood vessels.
Greater alveolar bone loss in smokers.
Hafajee & Socransky: Smokers had more attachment loss, deeper PDs, more missing teeth, fewer sites with BOP and similar dental plaque levels to those who had never smoked.
IL-1 genotype-positive increased the risk of tooth loss by 2.7 times compared to 2.9 times for heavy smoking. When both were present, the risk increased to 7.7 times.
More than one-half of the cases of periodontitis affecting adults may be due to cigarette smoking. Relative risk for smokers is 3.97 and for former smokers is 1.68.
Smoking diminishes the capability for repair to an equivalent level of a non-smoker 36 years older.
Smoking as a risk factor for periodontitis-significant factor for developing periodontal disease. Primary effect may be interference with wound healing.
Surgical and non-surgical treatments are less successful in smokers than in non-smokers. Clinical studies suggest that the healing outcome is less favorable in smokers.
Microbial factors- Not clear if smoking selects specific bacterial populations in periodontal pockets.
Gingival inflammatory response- Not clear what effects result from alterations in pro-inflammatory factors due to smoking. Neutrophil elastase activity and MMP-8 were reported to be increased in smokers with refractory periodontitis. Bostrom et al reported higher levels of TNF-a in the GCF of current and former smokers in comparison to non-smokers.
Genetic polymorphism- Not clear what role polymorphisms play
Effect of nicotine- May affect cells involved in periodontal repair. Nicotine adversely affects the proliferation, attachment and chemotaxis of PDL cells.
Effect of cotinine -May affect cells involved in periodontal repair. Cotinine enhances the effects of toxins from periodontopathogens.
Topic: Tobacco related disease
Author: Bergstrom J. NO ARTICLE
Title: Tobacco smoking and risk for periodontal disease.
Source: J Clin Periodontol 2003;30:107-113.
Type: Discussion
Rating: Good
Keywords: smoking, tobacco, relative risk, non-smoker, definition of disease
Purpose: To investigate the relationship between definition of disease, prevalence and relative risk associated with smoking.
Methods: Samples from previous study; 133 smokers and 242 non-smokers 20-69 years old. All smokers were current smokers. Pocket depth and radiographic measurement of bone height were recorded and used for the purpose of disease definition (PD and Bone loss). Cutoff points were designated (1, 5, 10, 15% for 5 mm PDs; and 1, 5, 10% for 6 mm; Bone loss 30th, 25th, 20th percentile). The smoking exposure was expressed in terms of consumption (cigarettes/day), duration (number of years of smoking), and lifetime exposure (cigarette-years). The relative risk was estimated from the odds ratio.
Results: Disease definition had an impact on the prevalence and the relative risk. At 1% of pocket > 5 mm., the prevalence for smokers was twice the prevalence for non-smokers. A narrower definition such as 15% of pocket > 5 mm resulted in decreased prevalence for both smokers and non-smokers. Increasing exposures correlated with greater magnitudes of risk. Heavy exposure was associated with greater risk than light exposure.
Conclusion: Smoking-associated relative risk is dependent on definition of disease. A narrower definition of disease will result in a low prevalence and a high risk and a broader definition will give an increased prevalence and a decreased risk associated with smoking. When combining a narrow definition of disease and heavy exposure to smoking, the smoking-associated risk of attracting periodontal disease is considerable. The results give an explanation as to why there is variation reported in the literature concerning the magnitude of risk for periodontal disease attributed to smoking.
Topic: Systemic Effects of Periodontitis
Title: Influence of tobacco smoking on peridontal bone height. Long – term observations and hypothesis.
Source: J Clin Periodontol 2004; 31:260-266
Type: Clinical study
Rating: Good
Keywords: bone height, bone loss, periodontal disease, smoking, tobacco
Purpose: To determine the periodontal bone height changes related to the premolar regions in smokers, former smokers and non-smokers over 10 years.
Methods: 3 groups include: 1) 19 continuous smokers (14.9cig/day), B) 28 former smokers (stopped smoking 10.9 years before baseline and C) 44 non-smokers (20-60y.o). Radiographs were obtained at 2 time points with interval of 10yrs. Height of bone measured using bitewings of the 1st and 2nd of maxillary and mandibular region and measured from CEJ to bone crest mesially and distally.
Results: NSSD in number of missing teeth between groups at baseline or follow-up. Mean CEJ-bone crest distance at baseline was 1.82 grp 1, 1.65 grp 2, 1.16 for grp 3. The mean bone height reduction was .74 grp 1, .26 for grp 2, and .27 for grp 3. Age had no role in the process of bone height reduction.
Discussion: Bone height reduction in smokers was 2.7 times greater than non smokers suggesting three fold bone height reduction rate under influence of smoking.
Conclusion: From the observations of the study it was hypothesized that 1) bone height reduction in non-smokers occurs at a modest constant rate, 2) bone height in smokers is accelerated, and 3) the smoking induced acceleration will return toward the non-smoker rate following cessation of smoking.
Topic: smoking
Authors: Giovanni E et al ARTICLE
Title: Experimental gingivitis in cigarette smokers: A clinical and microbiological study.
Source: J Clin Periodontol 2005; 32: 441-447
Type: clinical
Rating: good
Keywords: bacterial challenge; cigarette smoking, experimental gingivitis, gingiva, gingivitis, inflammation, pathogenesis, subgingival microbiota
Purpose: To assess clinical and microbiological changes occurring during the development of experimental gingivitis in periodontally health young cigarette smokers and to compare these findings with those of periodontally healthy (never) non-smokers.
Methods: Controlled experimental gingivitis following the model proposed by Loe et al. 11 subjects in each group.
Inclusion criteria: age up to 30 years old, cigarette smoking 5 or more years, no relevant medical conditions, dentition with 24 or more permanent teeth, PD less than 4mm, willingness to comply with study requirements.
Exclusion criteria: pregnant or lactating females, AL, incipient carious lesions that could exacerbate during the study, antibiotic therapy within 3months of baseline, chronic medication known to affect periodontium within 4 weeks of the baseline examination, alcohol or drug abuse, stomatological diseases.
Third molars were excluded from the analysis.
Subgingival plaque samples were collected from one site in each quadrant at Days 0, 21 and 35. Statistical analysis was performed.
Results: No statistical significant difference between smokers and non-smokers with respect to age, race, gender and the number of teeth present.
Both smokers and non-smokers displayed a statistically significant increase in the mean PI, GI during 3 weeks of undisturbed plaque accumulation and decrease after re-institution of mechanical plaque control. No statistical difference between two groups at any observation period.
D. How does smoking affect systemic health? Periodontal tissues?
Topic: Smoking
Author: Palmer RM ARTICLE
Title: Mechanisms of action of environmental factors—tobacco smoking
Source: J Clin Periodontol. 2005;32 Suppl 6:180-95
Type: Review
Rating: Good
Keywords: smoking; periodontitis; bacteria; neutrophils; lymphocytes; fibroblasts
Purpose: To review potential biological mechanisms underlying the effects of tobacco smoking on periodontitis
Discussion:
- While nicotine is the primary psychoactive component, tobacco smoke contains thousands of different compounds, many of these are directly noxious/poisonous to living organisms and cells, and nicotine may be unfairly blamed for most of these properties.
- The harmful effects of tobacco products will result from systemic exposure through absorption in the lungs rather than topical absorption in the oral cavity
- Tobacco smoking affects the oral environment and ecology, the gingival tissues and vasculature, the inflammatory response, the immune response and the homeostasis and healing potential of the periodontal connective tissues.
Effect of smoking on plaque:
-There are now a number of studies that suggest a trend for smokers to harbour more or greater numbers of potential periodontal pathogens than non-smokers without increasing the amount of plaque.
Effect of Smoking on the Periodontal Tissues:
- Smoking has a long-term chronic effect, impairing the vasculature of the periodontal tissues rather than a simple vasoconstrictive effect following a smoking episode
- The suppressive effect on the vasculature can be observed through less gingival redness, lower bleeding on probing and fewer vessels visible clinically and histologically
- This may also have relevance to the healing response with impairment of revascularization.
Smoking and Neutrophil Function
-Tobacco smoke exposure increases the number of neutrophils, despite this, tobacco smoking does not seem to affect the numbers of neutrophils entering the gingival sulcus and oral cavity
- These findings imply that neutrophil transmigration across the periodontal microvasculature is impeded in tobacco smokers.
- Tobacco smoke is capable of affecting neutrophil function both directly and indirectly
- Tobacco may contribute to the progression of periodontal disease at least in part through the induction of protease release from periodontal neutrophils.
- The respiratory burst represents the combined oxygen-dependent processes by which neutrophils kill phagocytosed bacterial cells through the generation of multiple reactive oxygen and reactive nitrogen species
- Cigarette smoke constituents may inhibit the respiratory burst of neutrophils
- Early studies suggested detrimental effects of tobacco smoke extract on migration of oral neutrophils. The results showed a dose- dependent suppression of both chemo- taxis and phagocytosis.
- The priming capacity of TNF-a, measured as generation of oxygen radicals from stimulated neutrophils, is higher in neutrophils from smokers compared with neutrophils from non-smokers.
- There are many studies that show leucocytosis in smokers.
- The effects of tobacco smoking on T cell function/proliferation are controversial. Some studies show significant reductions in T cell proliferation compared with controls when lymphocytes are stimulated with mitogens, while others show no significant differences between lymphoproliferative responses of smokers and non-smokers.
- Tobacco smoke has been found to affect both humoral immunity and cell-mediated immunity
- Serum IgG levels are reduced in smokers
- Non-smokers have higher levels of IgG2 compared with smokers
- B cell numbers are similar in smokers and non-smokers
- That B cell function is impaired in smokers. On cessation of smoking, B cell function returns to normal
- Reduced NK cytolytic activity has been reported in smokers
- There are inconsistencies and variations in findings reflecting the complex relationship between smoking, race, periodontal diagnosis and age.
- Smoking may result in lower resting GCF flow rate 5 days post- quitting.
- For the most part, research has demonstrated that there are lower levels of have demonstrated detrimental effects, which could have significant impact in the inflammatory destructive process and the healing response
- Smoking has a detrimental effect on clinical healing of non-surgical and surgical treatment modalities in periodontology
- The biological basis for this is undoubtedly multifactorial as smoking affects the vasculature and revascularization, the inflammatory response and fibroblast function, as outlined above
Tobacco smoking has widespread systemic effects, many of which may provide mechanisms for the increased susceptibility to periodontitis and the poorer response to treatment.
Topic: Smoking
Authors: Buduneli N et al. ARTICLE
Title: Saliva concentrations of RANKL and osteroprotegerin in smoker versus non-smoker chronic periodontits patients
Source: J Clin Periodontol 2008; 35(10):846-52
Type: Clinical research study
Rating: Good
Keywords: Chronic periodontitis, cotinine, maintenance, osteoprotegerin, RANKL, saliva, smoking
Purpose: (1) to evaluate the concentrations of sRANKL and OPG in saliva samples of a smoker and non-smoker and a non-smoker chronic periodontitis patients, and (2) to investigate whether these salivary parameters change during the maintenance phase of treatment.
Methods: 111 subjects were included in this study. 67 were untreated patients (smokers and non-smokers) with chronic periodontal disease, and 44 patients (smokers and non-smokers) treated who had been on maintenance therapy for 3 years. Saliva samples were obtained in the morning following an overnight fast. A clinical exam followed measuring PI, PD, CAL, recession, BOP, and PA radiographs. Third molars were excluded. ELISA kits for human sRANKL and hOPG were used for enzyme detection. Cotinine kits were used to confirm smoking status.
Results: Age, number of teeth present, PDs >5 mm, PI, and recession did not differ among the 4 groups. The untreated smoker chronic periodontitis group had significantly higher values of PD and CAL compared with the untreated non-smoker group. Untreated and maintenance smokers had significantly lower OPG concentrations than untreated non-smokers with periodontitis. RANKL levels appeared to be greater in the smokers, but not a significantly so.
Untreated non-smoker patients had significantly greater concentrations of RANKL than the non-smokers on maintenance. Smokers on maintenance had significantly lower OPG levels and increased RANKL/OPG ratios than the non-smokers on maintenance.
OPG concentration in the untreated group showed a statistically significant positive correlation with PD, CAL, and BOP. Pack year also correlated with PD, CAL, and gingival recession in untreated smokers as well. OPG concentration significantly correlated positively with probing depth, clinical attachment level and bleeding on probing and negatively with pack-year, and cotinine level.
Discussion: OPG concentrations in saliva are affected by smoking and the significantly increased RANKL/OPG ratio in smokers provides further support for the hypothesis that smoking increases the risk for periodontitis.
Topic: RANKL and OPG
Authors: David F, Lappin et al. NO ARTICLE
Title: Effect of smoking on serum RANKL and OPG in sex, age, and clinically matched supportive-therapy periodontitis patients.
Source: J Clin Periodonto 2007; 34:271-277
Type: clinical study
Rating: Good
Keywords: RANKL, OPG, RANKL/OPG, smokers, nonsmokers, periodontal disease
Background: The RANK system contributes to bone resorption by inducing production of a cysteine proteinase, cathepsin K, by activated osteoclasts and this enzyme is involved in bone matrix solubilization. In periodontal disease, increased concentrations of RANKL are found in diseased tissues, and the upset balance with OPG concentrations is associated with disease severity.
OPG is a member of the TNF receptor family that is expressed by osteoblasts. It inhibits bone resorption by high-affinity binding to RANKL and prevents RANKL from coupling with the RANK receptor.
It is known that some factors involved in the pathogenesis of periodontal disease, such as prostaglandin-E2 (PGE2), increase RANKL expression and decrease OPG expression.
Purpose: To investigate the effects of cigarette smoking on the serum concentrations of RANKL and OPG in chronic periodontitis patients.
Methods: Patients with CPITN (Community Periodontal Index of Treatment Needed) of 4 in at least 1 sextant, who had undergone Phase 1 and then were provided with maintenance by their general practitioner, and former patient who had received treatment 3 and 5 years previously were contacted for a screening. During the screening patients were regarded as eligible if they had chronic periodontitis, at least 16 teeth including 4 molars and in two different quads, at least 2 PD ≥ 5mm. Patients were grouped in smokers (35) and non-smokers (123) and healthy controls (9 smokers, 10 non-smokers) and were matched according to gender, age, or severity of disease. At baseline complete perio-exam was done and blood samples were taken. OPG and RANKL concentrations were assessed by ELISA. Statistical analysis was done.
Results: Smokers yielded a concentration of 406.9±37.8ng.ml, compared to non-smokers 29.5±9.5 ng/ml. There was NSSD in any of the clinical parameters. RANKL concentration was higher for the smokers but NSSD. There was a SS lower concentration of OPG in the sera of smoker patients compared to non-smokers. Smokers had a higher ratio of RANKL/OPG 1.16 than non-smokers 0.95. Smokers demonstrated an excess of RANKL in the serum and non-smokers had an excess of OPG. There were NSS correlations between pack years and RANKL concentration or the RANKL/OPG ratio. There was a SS inverse relationship between the use of tobacco and the serum concentrations of OPG in smokers.
Conclusion: This study suggests that one mechanism of periodontal disease progression could be suppression of OPG production and increase of bone resorption by smoking.
Topic: Smoking
Authors Thomson W, Broadbent J, et al. ARTICLE
Title: Cigarette smoking and periodontal disease among 32 year – olds: A Prospective study of a representative birth cohort.
Source: J Clin Periodontol 2007; 34: 828-834
Type: Prospective study
Rating: Good
Keywords: Smoking, cessation
Purpose: To describe and quantify the association between long-term smoking and periodontitis by age 32, and to determine the effects of recent smoking cessation on age-32 periodontal status.
Method: Periodontal examinations of two quadrants were conducted at ages 26 and 32 in a longstanding prospective study of a birth cohort born in Dunedin (New Zealand) in 1972/1973. Three sites (mesiobuccal, buccal and distolingual) per tooth, gingival recession and probing depth were examined. Longitudinal categorization of smoking exposure was undertaken using data collected at ages 15, 18, 21, 26 and 32. Questionnaire:
Have you ever smoked for as long as a year? (“No” means <20 packs of cigarettes in your lifetime or less than one cigarette/day for as long as a year).
How old were you when you started smoking regularly?
Have you cut down or stopped smoking?
How long ago did you cut down or stop smoking?
How many cigarettes per day did you smoke (on average) before the change?
How many cigarettes per day do you now smoke on average?
Results:
810 individuals of whom 48.9% had ever smoked (31.5% were current smokers). Compared with never-smokers, long-term smokers (and other age-32 smokers) had very high odds ratios (ORs of 7.1 and 5.7, respectively) for having 1 +sites with 5 +mm AL, and were more likely to be incident cases after age 26 (ORs of 5.2 and 3.2, respectively). Two-thirds of new cases after age 26 were attributable to smoking. There were no significant differences in periodontal health between never-smokers and those who had quit smoking after age 26.
Conclusion: Long-term (and current) smoking is detrimental to periodontal health, and quitters may be associated with a relatively rapid improvement in the periodontium.
E. Does smoking affect outcome of periodontal therapy? Wound healing?
Topic: Dental implants and cigarette smoking
Authors: Bain C, May P ARTICLE
Title: The association between the failure of dental implants and cigarette smoking.
Source: J Oral and Max Impl 8:609-615, 1993
Type: Review
Rating: Good
Keywords: Branemark implants, failure, implant length, implant location, osseointegration, smoking/adverse effects
Purpose: To evaluate the influence of smoking on the failure rate of Branemark dental implants by one of the authors over a 6 year period.
Methods: A total of 2,194 implants were placed in 540 patients between 1984 and 1990. This included single tooth placements and overdentures. 311 women, 229 men. Average age 55. Follow up time was up to 81 months. An implant was considered to be a failure if 1. It had to be removed, or 2. If it had > 50% bone loss. The study does show if the patients smoked or not, but does not state how much each patient smoked.
Results: A total of 1804 implants were placed in nonsmokers, and 390 were placed in smokers. There were 44 failures in smokers (11.3%), and 86 failed in non-somkers (4.8%). After evaluating the different areas of the mouth – smoking failure rates were higher in all areas of the mouth, but there was no statistical difference found in the posterior mandible. See chart:
Region Smokers Non-Smokers
Post Maxilla 19.1% 10.9%
Ant Maxilla 16.8% 3.6%
Post Mandible 4.6% 3.8%
Ant Mandible 4.7% 0.3%
This study also looked at implant lengths with the failures. % failure rate was better as implant length increased.
Conclusion: Smokers – 11% failure rate, Non-Smokers – 5% failure rate.
Topic: Smoking
Authors: Strietzel F et al ARTICLE
Title: Smoking interferes with the prognosis of dental implant treatment: A systematic review and meta-analysis
Source: J Clin Periodontol 2007; 34:523-544
Type: Review
Rating: Good
Keywords: dental implants; meta-analysis; odds ratio; smoking; success rate; survival rate
Purpose: Meta-analysis and systematic review focused on the question, if there is a significant increased risk of implant failures in smokers compared to non-smokers.
Methods: A systematic electronic and hand-search (articles published between 1989 and 2005) was performed to identify publications providing numbers of failed implants, related to the number of smokers and non-smokers for meta-analysis. Of the 139 publications, 29 were considered for meta-analysis and 35 for systematic review.
Results: Meta-analysis revealed a significantly enhanced risk for implant failure among smokers compared to non-smokers, expressed by odds ratio of 2.4 considering all included studies providing implant-related data or 2.6 considering all included studies providing patient-related data. Systematic review revealed significantly enhanced risk for peri-implant inflammatory complications in periodontally compromised smokers. Smoking was also found to have a significant impact on the marginal bone level at implants with machined or TPS- or HA- coated surfaces, which was not confirmed by 2 studies on implants with particle-blasted and acid-etched or dual acid- etched or anodic-oxidized surfaces. Significant enhanced risk with OR of 3.6, of implant failures for smokers undergoing augmentation procedures.
Conclusion: Smoking is a significant risk factor for dental implant therapy and augmentation procedures accompanying implantations.
Topic: Oral systemic connection
Author: Tonetti M, Pini-Prato G, Cortellini P NO ARTICLE
Title: Effect of cigarette smoking on periodontal healing following GTR in infrabony defects. A preliminary retrospective study.
Source: J Clin Periodonto 22:229-234, 1995
Type: RCT
Rating: Good
Keywords: guided tissue regeneration, smoking, clinical attachment gain, regeneration complications
Purpose: To assess the effect of smoking status on periodontal regeneration following GTR in deep infrabony defects.
Methods: Retrospective study of 71 infrabony defects in 51 subjects (27M, 24 F; 18-59 years old) that were treated with GTR. Defects were interproximal with at least ≥6mm CAL loss and radiographic evidence of infrabony component. Initial therapy with SRP and OHI completed. PD, CAL, BOP, recession and defect configuration were assessed 3 months after Phase 1. 1 week later, GTR was performed using Gore-Tex e-PTFE membranes with tetracycline HCl 250 qid and 0.2% CHX rinse with weekly prophylaxis. Membranes were removed after 4-6 weeks postop. Patients were placed in a monthly recall for 1 year and re-evaluated at year 1. Subjects were divided in 2 groups. Group 1 were smokers (>10 cigarettes/day) contributing 32 defects and group 2 were non-smokers contributing 39 defects. Light/occasional smokers (<10 cigarettes/day) were excluded from the study.
Results: PD, PAL and CEJ-base of defect were significantly deeper in defects of non-smokers, but total infrabony component and defect subcomponents were NSSD between groups.
At baseline and at 1 year follow up, full mouth plaque scores were SS higher in smokers vs nonsmokers.
At membrane removal: PAL gain was 7.6±2mm for smokers and 6.0±1.5mm for non-smokers, NSSD in percent gain between the two groups. A SSD decrease in PD from 8.7±2.1mm to 2.3±0.8mm was observed in non-smokers and from 7.3±2.1mm to 3.0±1.5mm for the smokers group. A significant increase in recession was observed for both groups.
At 1 year follow up: PAL gain was 2.1 ±1.2 mm for smokers vs 5.2±1.9 mm of PAL gain in non-smokers, the difference was SS. The relative risk for a site to be a loser was determined during the maturation stage, which qualified as losing >3 mm of newly formed granulation tissue between the time of membrane removal and 1 year follow up. Smokers had a 4.3 fold increase to be a “loser” and 3.4 fold increase for patients with ≥12% plaque scores. A combination of both parameters increased the risk at 11.4 times higher than non-smoking patients with low plaque scores.
Conclusion: Smoking and poor plaque control individually contribute to losing attachment after GTR. Together, they provide a relative risk of 11.4 fold higher chance of being a loser site. Smoking is associated with a reduced healing response following GTR in deep infrabony pocket.
Topic: Systemic Effects of Periodontitis
Authors: Souza s et al. NO ARTICLE
Title: Subetpithelial connective tissue graft for root coverage in smokers and non-smokers: A clinical and histologic controlled study in humans.
Source: J Periodontol, 2008; 79(6):1014-1021
Type: Clinical study
Rating: Good
Keywords: Connective tissue, gingival recession/surgery, grafts, plastic surgery, smoking/adverse effects
Purpose: To evaluate root coverage of gingival recessions and to compare graft vascularization in smokers and non-smokers.
Methods: Thirty subjects, 15 smokers and 15 non-smokers, were selected. Each subject had one Miller Class I or II recession ≥ 3mm and, ≤ 3mm of KG in a non-molar tooth. Clinical measurements of probing depth (PD), relative clinical attachment level (CAL), gingival recession (GR), and width of keratinized tissue (KT) were determined at baseline and 3 and 6 months after surgery. An acrylic stent was used for the clinical measurements. The recessions were treated surgically with a coronally positioned flap associated with a subepithelial connective tissue graft. A small portion of this graft was prepared for immunohistochemistry. Blood vessels were identified and counted by expression of factor VIII–related antigen–stained endothelial cells.
Results: Intragroup analysis showed that after 6 months there was gain in CAL, a decrease in GR, and an increase in KT for both groups, whereas changes in PD were not statistically significant. Smokers had less root coverage than non-smokers (58.02% ± 19.75% versus 83.35% ± 18.53%; P <0.05). Furthermore, the smokers had more GR (1.48 ± 0.79 mm versus 0.52 ± 0.60 mm) than the non-smokers (P <0.05). Histomorphometry of the donor tissue revealed a blood vessel density of 49.01 ± 11.91 vessels/200× field for non-smokers and 36.53 ± 10.23 vessels/200× field for smokers (P <0.05).
Discussion: The graft survival depends on an avascular plasmatic circulation but within 4 days, anastomoses between vessels of the periosteal bed and preexisting vessels in the graft take place. By day 7, there is a network of smaller, tortuous vessels characteristic of capillary budding throughout the graft. Our results showed that smokers had ;30% less BVD (blood vessel density) in the SCTG than non-smokers. The reduced availability of blood vessels may retard the revascularization of the SCTG. Adequate blood supply is critical for healing of the graft, and this reduction could have contributed to the clinical differences in root coverage between smokers and non-smokers.
Conclusion: Root coverage with subepithelial connective tissue graft was negatively affected by smoking, which limited and jeopardized treatment results.
F. Can quitting smoking reverse the effects on the periodontium or are changes from smoking irreversible?
Topic: smoking
Authors: Morozumi T et al ARTICLE
Title: Smoking cessation increases gingival blood flow and gingival crevicular fluid.
Source: J Clin Periodonto, 2004, 31:267-272
Type: clinical
Rating: good
Keywords: gingival blood flow; gingival crevicular fluid; smoking cessation
Purpose: To investigate the alteration of gingival microcirculation due to smoking cessation for 8 weeks, by measuring GBF (gingival blood flow) level and GCF volume.
Methods: 16 smokers (22-39 yo) and 11 non-smokers (23-27 yo) with no clinical signs of systemic or periodontal diseases. Exclusion criteria less than 24 teeth, antibiotics, anti – inflammatory or immunosuppressive during the previous 8 weeks, or perio therapy in the past 6 months. Smokers have smoked at least 10 cigarettes/day for minimum 5 years, non – smokers have never smoked. GI, PPD, PAL were recorded 1 month prior to starting the study.
GBF and GCF in smoker subjects were monitored over an 8 – week period at baseline, 1, 3, 5 days and 1, 2, 4 and 8 weeks. They were instructed not to brush, gargle or eat and drink anything for 30min prior to taking measurements. Smoking cessation was verified by CO concentration, by serum nicotine and cotinine concentration. Blood flow was evaluated with laser Doppler flowmeter. GCF was collected with sterile paper strip. Statistical analysis was performed.
Results: 5 smokers dropped out during the study. CO concentration in smokers was statistically low at day 1 after smoking cessation compared to baseline. It was significantly higher than non-smokers only at baseline. There was a decreasing tendency in nicotine and cotinine concentration after smoking cessation.
GBF rate was statistically significantly increased at 3 days after smoking cessation. GCF volume was statistically significantly increased compared to the baseline at 5 days after smoking cessation, but until 2 weeks after, it was significantly lower compared to non-smokers.
Conclusion: GBF and GCF significantly increased within 5 days after smoking cessation. Study also found that GCF after 2 weeks of smoking cessation was comparable to that of non-smokers.
Data suggest that the gingival microcirculation may recover in the early stages of smoking cessation, which is beneficial for the prevention and treatment of periodontal disease.
Topic: Smoking
Title: Smoking-attributable periodontitis in the United States: findings from NHANES III. National Health and Nutrition Examination Survey
Source: J Periodontol. 2000 May;71(5):743-51.
Type: Survey
Reviewer: Phillip Crum
Rating: Good
Keywords: National Health and Nutrition Examination Survey; periodontal disease/epidemiology; periodontitis/epidemiology; smoking/adverse effects; risk assessment; tobacco/adverse effects
Purpose: 1) to investigate the association between cigarette smoking and periodontitis in a nationally representative sample in the US. 2) To estimate the proportion of total periodontitis cases attributable to smoking.
Methods:
-Data was taken from the third National Health and nutrition examination survey NHANES III
- Participants received standardized dental examinations and were interviewed about tobacco use.
-The analysis was limited to 13,650 dentate adults who received a periodontal examination and provided data on their cigarette smoking.
-The periodontal examination included measurement of PD and CAL in two randomly selected quadrants. Measurements were made at two sites per tooth.
Results:
-The analysis was on 12,329 patients
-In 1988 to 1994, 27.9% of dentate US adults were current smokers and 23.3% former smokers
-9.2% of dentate adults in the US had periodontitis. Of this, 15.6% were current smokers, 10.5% former smokers and 4.9% never smokers
-The crude association (ORp) between cigarette smoking and periodontitis was 3.58 (95% CI 2.94-4.36)
-After adjusting for age, race income level and educational attainment, current smokers were 4 times as likely as never smokers to have periodontitis
-There was a dose response relationship between cigarettes smoked per day and the likelihood of periodontitis, the ORp rose from 2.79 for those smoking 9 cigarettes per day to 5.88 for those smoking >9 cigarettes per day.
-Former smokers were more likely than never smokers to have periodontitis
-It is estimated that 74.8% of the cases of periodontitis in the US among current smokers were attributable to their smoking, from 64.2% among those smoking 9 cigarettes per day to 83.0% among those smoking 31 cigarettes daily
-It is also estimated that 55.2% of periodontitis cases in the US occurred among former smokers
-In the entire US population its estimated that 52.8% of periodontitis was attributable to smoking
Discussion:
-Those who had quit in the previous 2 years were 3 times as likely as never smokers to have periodontitis.
-The strong association between cigarette smoking and periodontitis in this study is consistent with the findings of many other studies.
-Smoking cessation appears to improve the likelihood that periodontal therapy will be successful and reduce the risk of disease progression.
Does smokeless tobacco have the same effects on the periodontal tissues?
Topic: Smokeless tobacco
Authors: Bergstrom J et al. ARTICLE
Title: Smokeless tobacco (snuff) use and periodontal bone loss
Source: J Clin Periodontol 2006;33:549-554
Type: cross-sectional study
Rating: Good
Keywords: nicotine, periodontal bone, periodontal disease, periodontitis, smokeless tobacco, snuff, tobacco
Purpose: To investigate the possible association between the use of moist snuff and periodontal bone loss in subjects with moderate to long-term duration of use.
Methods: The study was carried out on 84 healthy men in the age range 26–54 years consisting of 25 current snuff users(3.2 boxes/week, 16.9 years), 21 former snuff users (3.1 boxes/week, 12.9 years), and 38 never users of moist stuff. The periodontal bone height was evaluated from bitewing radiographs measuring the distance from the cement–enamel junction (CEJ) to the bone crest (BC). Bone height measurements were performed from two bilateral pairs of bitewings in each subject (CEJ to bone crest) in interproximal areas in molars and premolars in all quadrants. Periodontal condition was assessed by BOP, PD, and GI. Photographs were also taken.
Results: The mean CEJ-BC distance was 1.00 mm, 1.12 mm, and 1.06 mm for current users, former users, and never-users, respectively. The association between snuff use and bone height level controlling for age was not statistically significant. There was no significant difference between light and heavy exposure users controlling for age. No significant differences existed between groups for periodontal parameters, however clinical photographs revealed a mucosal lesion in current users not found in former and never users.
Discussion: The findings of this study suggest that the use of moist snuff is not associated with periodontal bone loss or other disease parameters measured.
Cr: Recession?
Is alcohol use a risk factor for periodontitis?
Topic: Alcohol
Authors: Tezal M et al. ARTICLE
Title: Alcohol consumption and periodontal disease. The NHANES III Survey.
Source: J Clin Periodonto, 2004 Jul;31(7):484-8
Type: Survey
Rating: Fair
Keywords: alcohol, periodontal disease, survey
Background: 90% of people consume alcohol in the US, although the amount, frequency and pattern varies
Purpose: To evaluate the effect of alcohol consumption on the severity of periodontal disease
Methods: secondary analysis of 13,198 subjects from NHANES III, >20 yrs old with at least 6 natural teeth. From questionnaire, number of drinks in the past 12 months and then calculated to number of drinks/week. The dental exam included PD and CAL, BOP at the particular sites. No plaque index available.
Results: Number of drinks/week broken into >5,>10,>15,>20. CALoss increases as number of drinks/week increases, suggesting dose dependent, but results NSD. Regression analysis for CAL adjusted for age, gender, race, education, income, smoking, diet, diabetes, number of remaining teeth, and gingival bleeding showed odds ratio of 1.22, 1.39, 1.54 & 1.67 using 5, 10, 15, 20 drinks/wk standards
Discussion: The effect of alcohol consumption on periodontal disease is usually explained by poor OH of chronic alcohol users. Alcohol consumption can adversely effect the host defense (deficient complement and defective PMN function), clotting mechanism (factors produced in the liver), bone metabolism, healing and direct toxic effect on perio tissues.
Conclusion: As the number of drinks/week increases, the odds ratio for periodontal disease also increases, however the greatest odds ratio for >20 drinks/week was 1.67. The researches consider this a moderate but consistent dose-dependent relationship between alcohol consumption and periodontal disease.
Topic: Alcohol
Authors Amaral, C eta al. ARTICLE
Title: The relationship between alcohol dependence and periodontal disease.
Source: J Periodontol 2008; 79: 993-998
Type: Clinical study
Rating: Good
Keywords: Alcohol, risks
Purpose: To evaluate the relationship between alcohol dependence and periodontal dz..
Method: 50 alcoholics and 49 non-alcoholics were selected for this cross-sectional study. Medical and smoking hx as well as socio demographic data (age, education, income, and smoking, living status) were collected. CAGE (Cut-down, annoyed, guilty, eye opener) was used to screen alcohol dependence in both groups. Periodontal clinical parameters (PD, AL, visible plaque [VP]) were collected.
Results: A linear relationship was found between alcohol dependence and mean CA and mean PD after controlling for the % of sites with VP, age, income, education, living condition and smoking.
Conclusion: Alcohol dependence may be associated with the increase severity of the CAL and PD. Further investigations are necessary to understand the role of alcohol dependence as a putative risk factor for period dz.
Is diabetes a risk factor for periodontitis? How does it affect the body locally? Systemically? Does it matter if it is controlled or uncontrolled?
Topic: Diabetes mellitus and periodontal disease
Authors: Mealey BL, Oates TW NO ARTICLE
Title: AAP Commissioned Review: Diabetes mellitus and periodontal diseases
Source: J Periodontol. 77:1289-303, 2006
Type: Review
Rating: Good
Keywords: Diabetes mellitus, inflammation, insulin resistance, obesity, periodontal disease
Purpsoe: To discuss the relationship b/w diabetes and periodontal disease.
Discussion:
Mechanism by which diabetes affects the periodontium:
- Some suggest that periodontitis should be listed among the classic complications of diabetes (CVD, neurpathy, nephropathy, retinopathy)
- Fxn of immune cells including neutrophils, monocytes, and macrophages is altered in diabetes. Neutrophil adherence, chemotaxis, and phagocytosis are often impaired.
- The monocyte/macrophage cell line may however be upregulated in response to bacterial antigens. This hyperresponsiveness leads to increased production of pro-inflammatory cytokines and mediators. Peripheral blood monocytes from diabetics produce elevated levels of TNF-α in response P.g.
- Studies have shown that levels of inflammatory cytokines in gingival crevicular fluid are also increased in pts w/ HbA1c levels > 8%
- CT metabolism has been shown to be altered and impaired osseous healing and bone turnover.
- Irreversible glycation of proteins (AGE’s) accumulate in tissue due to their resistance to normal enzymatic degradation. They thicken blood vessels and narrow lumen. AGE-modified vascular collagen as an affinity for LDL which also accumulates in vessel wall contributing to atherosclerotic changes characteristic of macro-vascular complications in diabetes.
- AGE’s also activate a receptor (RAGE) on the surface of smooth m. cells, endothelial cells, neurons, and monocyte/macrophages. Receptor is found in the periodontium and a 50% increase in mRNA for RAGE was found in gingival tissue of pts with type II diabetes.
- AGE-RAGE interaction in periodontal tissues leads to elevated levels of of IL-1β, TNF-α, and prostaglandin E2
- Not very clear the impact of periodontal treatment on glycemic control of diabetes.
Conclusion: Diabetes increases the risk of periodontal diseases. Less clear is the impact of periodontal disease on glycemic control of diabetes and the mechanisms through which this occurs. Inflammatory periodontal disease may increase insulin resistance in a way similar to obeisity, thereby aggravating glycemic control.
Topic: Diabetes
Authors: Taylor GW, Burt BA, et al ARTICLE
Title: Non-insulin dependent diabetes mellitus and alveolar bone loss progression over 2 years.
Source: J Periodontol 69:76-83, 1998
Type: Clinical
Rating: Good
Keywords: Periodontitis; diabetes mellitus; diabetes mellitus, non-insulin dependent; longitudinal studies; epidemiology; alveolar bone loss.
Purpose: To test the hypothesis that persons with non-insulin dependent diabetes mellitus (NIDDM) have a greater risk of more severe alveolar bone loss progression than those without NIDDM over a 2-year period.
Methods: Data from the longitudinal study of the oral health of residents of the Gila River Indian Community were analyzed for 362 subjects, aged 15 to 57, 338 of whom were free of diabetes at the beginning and did not develop NIDDM during a 2-year follow-up period. The other 24 subjects had NIDDM at baseline. Subjects selected had 20 or more teeth, lost no teeth during the study and had less than 25% bone loss at baseline. Diabetes was defined by a plasma glucose concentration 200mg/dl 2hrs after a 75-g oral glucose load. All oral examinations were conducted by one of two trained examiners who at the time of examination, did not know the diabetes status of examined subjects. Clinical examination was performed on the six index teeth described by Ramfjord. Calculus, plaque, gingival inflammation, PDs and CAL were assessed. Panoramic radiographs were used to assess interproximal bone loss. All panoramic radiographs were made by a single technician on the same radiographic unit. All radiographs were exposed with the patient standing and stabilized with mounted hand grips, head alignment was accomplished using vertical and horizontal light beams in the radiographic unit to position the head with respect to anatomic landmarks. Bone scores (scale 0-4) from panoramic radiographs corresponded to bone loss of 0%, 1%-24%, 25%-49%, 50%-74%, or 75% and greater. Change in bone score category was computed as the change in worst bone score (WBS) reading after 2 years. Additional variables were evaluated for confounding and effect modification in the analyses: alcohol consumption, smoking, obesity, age, gender, blood pressure, coronary artery disease.
Results: NIDDM was positively associated with the probability of a change in bone score when the covariates were controlled. A higher proportion of subjects with diabetes had 1-24% radiographic bone loss (67%) than did non-diabetics (44%). A higher proportion of subjects with NIDDM were experiencing change in WBS (worst bone score) than did non-diabetics. The cumulative odds ratio for NIDDM at each threshold of the ordered response was 4.23. The interaction model suggested that the effect of NIDDM on alveolar bone loss progression may be lower or non-existent at older ages.
Conclusion: In addition to being associated with the incidence of alveolar bone loss, NIDDM increased the risk for more severe progression of alveolar bone loss. The effect of NIDDM on progression of alveolar bone loss may not be constant at all ages.
Topic: Type I Diabetes
Author: Lalla E et al ARTICLE
Title: Periodontal infection profiles in type 1 diabetes.
Source: J Clin Periodontol. 2006 Dec ;33(12) :855-62
Type: RCT
Rating: Good
Keywords: diabetes, cytokines, oral systemic connection
Purpose: To investigate the levels of subgingival plaque bacteria and serum IgG responses in patients with type 1 diabetes and non-diabetic controls of comparable periodontal status.
Methods: 50 type 1 diabetes patients (mean duration 20.3 years, range 6-41) were age-and gender-matched with 50 non-diabetic individuals with similar levels of periodontal disease. Full-mouth clinical periodontal status was recorded (PD, recession, BOP, PI), 10 ml blood sample obtained from each patient, and eight plaque samples/person were collected using sterile curettes and analyzed by checkerboard hybridization with respect to 12 species. Homologous serum IgG titers were assessed by checkerboard immunoblotting. In a sub-sample of pairs, serum cytokines and selected markers of cardiovascular risk were assessed using multiplex technology.
Results: Among the investigated species, only levels of Eubacterium nodatum were found to be higher in diabetic patients, while none of the IgG titers differed between the groups, both before and after adjustments for microbial load. Patients with diabetes had significantly higher serum levels of soluble E-selectin, vascular cell adhesion molecule-1 (VCAM-1), adiponectin and lower levels of plasminogen activator inhibitor-1 (PAI-1).
Cconclusion: After controlling for the severity of periodontal disease, patients with type 1 diabetes and non-diabetic controls showed comparable subgingival infection patterns and serum antibody responses.
Are there any known patient populations who are at greater risk for diabetes and periodontal disease?
Topic: Systemic Effects of Periodontitis
Authors: Emrich LJ, Shlossman M, Genco RJ ARTICLE
Title: Periodontal disease in non-insulin dependent diabetes mellitus.
Source: J Periodontol. 62:123-130, 1991
Type: Clinical study
Rating: Good
Keywords: diabetes, periodontal disease, type II diabetes
Background: 50% of the Pima Indian tribe >35 yrs old have type II diabetes (highest incidence and prevalence in
a given population in the world). 20 yrs after original study, an epidemiologic study was conducted to estimate prevalence and severity of periodontal dz
Purpose: This paper relates to a subset of these individuals to determine whether diabetes mellitus is associated with destructive periodontal disease, or whether the perio dz in this population can be explained by other factors.
Methods: The periodontal AL, alveolar bone loss (measured with Schei ruler on a pan x-ray), age, sex, plaque index, gingival index, fluorosis, DMFT and the diabetic status was assessed in 1,342 Pima Indians who were at least partially dentate. Subjects were recalled 14-21 days for duplicate measurements.
Results: Diabetic status, age, and the presence of sub-g calculus were SS associated with higher prevalence and greater severity of destructive periodontitis in this population. Diabetic status was significantly and strongly related to both the prevalence and severity of disease after adjusting for the effects of demographic variables and several indices of oral health including the plaque index. Subjects with type 2 diabetes have an increased risk of destructive periodontal disease with an odds ratio of 2.81 (95% confidence interval 1.91 to 4.13) when attachment level is used to measure the disease. The odds ratio for diabetic subjects was 3.43 (95% CI 2.28 to 5.16) where bone loss was used to measure periodontal destruction. Bone loss and attachment level correlated in 83.6% of this population. Prevalence of perio dz in subjects over 55 was equal. AL in diabetics (15-24 yrs old) was twice to that of normal subject of the same age group.
Conclusion: Diabetes increased the risk of developing destructive periodontal disease about 3x among the young and middle aged. Diabetes increases the risk of developing perio dz in a manner that cannot be explained by age, sex, and hygiene or other dental measures.
Topic: perio treatment and diabetes
Authors: Grossi S, et al. ARTICLE
Title: Treatment of peridontal disease in diabetics reduces glycated hemoglobin
Source: J Periodonto 68:713-719, 1997
Type: clinical
Rating: good
Keywords: diabetes mellitus; non-insulin dependent/epidemiology, periodontal diseases/therapy; doxycycline/therapeutic use; chlorhexidine/therapeutic use; povidone-iodine/therapeutic use; porphyromonas gingivalis.
Purpose: To test a periodontal treatment incorporating topical and systemic antimicrobials in Native Americans suffering from periodontal disease and NIDDM (non-insulin dependent diabetes mellitus).
Methods: 113 patients with moderate to severe periodontitis, 81 females and 32 males between 25 and 65 years of age, exhibiting severe periodontal disease and a history of diabetes mellitus. Patients on renal dialysis or presenting with diabetics complications which required hospitalization were excluded from the study.
They were stratified by duration of diabetes, insulin use ad gender and randomly assigned to one of the 5 treatment groups. Each of the groups had at least 1/3 males.
All patients received therapy with ultrasonics with continuous irrigation with an antimicrobial solution. The antimicrobial treatments for each group were:
H20 irrigant and doxycycline 100mg/day for 2 weeks
0.12% CHX and doxycycline 100mg/day for 2 weeks
0.05% povidone-iodine and doxycycline 100mg/day for 2 weeks
0.12% CHX and placebo
H2O irrigant and placebo (control group)
Periodontal status was assessed at baseline and at 3 and 6 months after treatment and included plaque and gingival assessment, PD, CAL on all teeth. Plaque sample from 4 sites with the deepest probings were collected and tested for the presence of P. gingivalis. Venous blood samples were collected at baseline and at 3 and 6 months after treatment and assayed for fasting blood glucose. HbA1c was determined using high performance liquid chromatography. Statistical analysis was performed.
Results: Mean PD and AL ranged between 3.5 and 3.7mm and 4.5 and 5.0mm respectively at baseline. Mean HbA1c was above 10% in all 4 test groups and 9.2% in the control, and fasting serum glucose was above 220mg/dl for test groups and 186mg/dl for the control.
At 3 and 6 months all groups showed reduction in plaque scores, gingival bleeding, mean PD.
Although changes did not reach significance, the trend indicated that all 4 test groups showed greater changes in pocket depth compared to the control group at 6 months. Similar pattern was seen in changes in AL.
P. gingivalis before treatment ranged from 43-71%. At 3 months it was below detectable levels in all patients in the H20/doxycycline and CHX/doxycycline group. 16 and 17% in the iodine/doxycycline and CHX/placebo group and 22% in the control group were still positive for P. gingivalis. At 6 months the doxycycline treated groups showed a greater antimicrobial effect.
At 3 months the doxycycline – treated groups showed a reduction in HbA1c to a level below 10%, and no significant changes were observed in the other two groups. At 6 months all groups showed HbA1c levels comparable to baseline.
Hyperglycemia was modestly reduced at 3 months after periodontal therapy in H20/doxycycline and iodine/doxycycline groups but was significantly elevated compared to baseline in CHX/placebo and control group.
Conclusion: Study shows that in patients with NIDDM, treatment of periodontal disease incorporating systemic doxycycline and topical antimicrobial results in a significant reduction in periodontal infection and inflammation and a short-term reduction in levels of HbA1c.
How is osteoporosis measured? Is osteoporosis a risk factor for periodontal disease?
Topic: Osteoporosis
Author: Wactawski-Wende NO ARTICLE
Title: The Association Between Osteoporosis and Alveolar Crestal Height in Postmenopausal Women
Source: J Periodontol 2005, Vol. 76, No11: 2116-2124
Type: Cohort study
Rating: Good
Keywords: Bone mineral density; osteoporosis; periodontal disease; postmenopause; women
Purpose: to assess the cross sectional association between alveolar crestal height (ACH) and skeletal bone density in a large group of well characterized postmenopausal women.
Methods:
-1341 postmenopausal women were included in the analysis
-Participants completed physical and oral examinations, had their bone density assessed, and completed study questionnaires
-ACH loss was the primary variable of interest and was assessed using oral radiographs.
-ACH was defined as the distance in mm from the CEJ to alveolar crest.
Results:
-1341 postmenopausal women from age 53 to 85 were examined
-The mean loss of ACH was 2.5mm with approximately half of the women with a mean mouth ACH loss between 2-3 mm
-Only 4.3% of the women had mean mouth ACH loss values 4mm.
-24% were in the no ACH loss group (n = 316), 50% in the mild/moderate group (n = 667), and the remaining 26% (n = 358) in the severe group (Table 2)
-Most women (45.4%) had T scores ranging from -1.0 to -2.5; however, 39.1% had T scores consistent with osteoporosis. Only 15.4% had T scores within the normal range.
-There was a statistically significant trend for worse loss of ACH with decreasing T score
-The trend for increasing association by worsening T score can be seen overall and also in those subjects <70; however, in the 70+ age group the association of ACH to T score is especially dramatic.
Discussion:
-These data from a large cross-sectional study of post- menopausal women show a strong association between bone density and loss of oral bone surrounding the teeth
-Postmenopausal women with T scores consistent with low bone mass and/or osteoporosis have a substantially greater odds of having loss of alveolar crestal bone height than those with T scores in the normal range.
-There was more than a 3-fold increase in the odds of worse ACH subjects with T scores consistent with osteoporosis
-In women ages 70 and older, there was a 2.5- to 4-fold increase in odds of oral bone loss in women with low, moderate, or severe bone loss compared to those with normal bone mass
-These data provide increasing evidence of a positive association between low bone mass and loss of oral bone in older women. These results support the finding that in postmenopausal women there is a strong and consistent association between worsening T score and loss of ACH, and that increasing age is an important modifier of this association that needs careful consideration.
Topic: Postmenopausal women
Authors: Brennan R, Genco R, Hovey K, Trevisan M, Wactawski-Wende J ARTICLE
Title: Clinical Attachment Loss, Systemic Bone Density, and Subgingival Calculus in Postmenopausal Women
Source: J Periodontol 2007, 78; 2104 - 2111
Type: Cross-sectional study
Rating: Good
Keywords: Bone density, dental calculus, osteoporosis, periodontal attachment loss, periodontal diseases, postmenopausal
Purpose: To assess the cross-sectional association between measures of periodontal disease and systemic bone mineral density (BMD) among a large group of postmenopausal women and to assess potential effect modification by subgingival calculus and age.
Methods: 1,329 postmenopausal women were recruited from the Buffalo Women’s Health Initiative Observational Study. Inclusion criteria included: at least six teeth present, no history of bone disease other than osteoporosis, no bilateral hip replacement, no history of cancer in the past 10 years, and no other serious illnesses. Systemic bone density was measured at the spine, hip, forearm, and whole body by dual-energy x-ray absorptiometry. T score groups were defined as follows: normal= T score ≥ -1; osteopenia = T score < -1.0 but >-2.5, osteoporosis = T score ≤ -2.5. T score: the number of standard deviations above or below the mean for a healthy 30 year old adult of the same sex and ethnicity as the patient. Complete oral examination was conducted and included teeth present, calculus assessment (supragingival and subgingival), PD (for CAL). Associations between T scores, CAL, and subgingival calculus were then assessed.
Results: The average age of participants was 66.6 years. 58.8% had subgingival calculus. Among women without subgingival calculus, osteoporotic women had significantly worse CAL than normal T score women. Results were adjusted for age, cigarette smoking, education, and time since last dental cleaning. Among women with subgingival calculus, there were no associations between T score group and CAL.
Discussion: Presence or absence of subgingival calculus was a strong effect modifier of the association between systemic bone density and CAL. Our results provide evidence of an association between osteoporosis and one measure of periodontal disease severity, CAL. The associations between bone density, CAL, and subgingival calculus require further research, particularly in longitudinal studies.
L. Is stress a risk factor for chronic periodontal disease? Is stress a risk factor for any other periodontal diagnosis?
Topic: Stress
Authors: Genco RJ, Ho AW, Grossi SG, Dunford RG, Tedesco LA. ARTICLE
Title: Relationship of stress, distress, and inadequate coping behaviors to periodontal disease.
Source: J Periodontol 70: 711-723, 1999.
Type: Cross-sectional study
Rating: Good
Keywords: Stress, periodontal disease
Purpose: To determine the association of stress, distress, and coping behaviors to periodontal disease
Methods: Cross sectional study of 1,426 subjects between ages 25-74 years. Patients filled a set of 5 psychosocial questionnaires, measuring psychological traits and attitudes, chronic stress or daily strains, distress, coping styles and strategies, hassles and uplifts. Clinical assessment of supragingival plaque, gingival bleeding, subgingival calculus, PD, clinical attach level, and radiographic alveolar crestal height and 8 putative bacteria from subgingival flora.
Results: Logistic regression analysis demonstrated financial strain was significantly associated with greater attachment and alveolar bone loss (OR 1.68). Those with more financial strain who were high emotion-focused copers (inadequate coping) had a higher risk of having more severe attachment loss (OR 2.24) and bone loss (OR 1.91) than those with low levels of financial strain within the same coping group. Subjects with high levels of financial strain who reported high levels of problem-based coping (good coping) had no more periodontal disease than those with low levels of financial strain.
Conclusion: Psychosocial measures of stress associated with financial strain and distress manifest as depression, are significant risk indicators for more severe periodontal disease in adults in an age-adjusted models. Adequate coping behaviors as evidenced by high levels of problem-based coping, may reduce the stress-associated risk.
Topic: Stress
Authors da Silva AMM, Newman HN, Oakley DA. NO ARTICLE
Title: Psychosocial factors in inflammatory periodontal diseases. A review.
Source: J Clin Periodontol 22:516-526, 1995.
Type: Clinical study
Rating: Good
Keywords: Antibiotics, GCF
Purpose: To review the literature concerning the possible role of psychosocial factors in the etiology of inflammatory periodontal diseases
Discussion: There are well known etiologies of periodontal disease, but often there are variance that cannot only be explained by these known factors. If a pt’s resistance is lowered by an inability to cope with stressful life events, then overt perio dz symptoms may manifest.
ANUG: most studied perio dz w/a psychosocial predisposing factor. ANUG predisposing factors in susceptible individuals: smoking, g-vitis, or local trauma, compounded w/stress. Examples that have been studied include new induction into the army or academic exams. Several military studies exist (high stress environment) on ANUG. It is possible that the high levels of cortisol released influence the onset of ANUG, but research inconclusive.
Perio onset during psychological disturbances: neglect of OH, changes in diet, increase in smoking and other pathogenic oral behaviors, bruxism, alterations in gingival circulation, changes in saliva, endocrine imbalance and lowered host resistance.
Excessive stress and due to life-changing events or other psychosocial factors can alter immune function and make a person more vulnerable to illness. Stress can lower NK cell activity (Kiecolt-Glaser 84), and both helper and cytotoxic T cell function (Kemeny 89). Stress has been found to increase vulnerability to common colds and respiratory infections.
Intervention through relaxation, hypnosis, physical exercise, therapy (classical conditioning, self-disclosure, and cognitive-behavioral) can all modify the effect of stress on the body, and therefore possibly on periodontal disease severity.
Conclusion: Emotional disturbances including stress and depression can alter both a person’s immune function and behavioral habits, thereby becoming a factor of their periodontal disease.
Is obesity a risk factor for periodontal disease? How does obesity relate to inflammation?
Topic: Overweight and obesity
Authors: Vecchia C, Susin C ARTICLE
Title: Overweight and obesity as risk indicators for periodontitis in adults.
Source: J Periodontol 2005; 76(10) 1721-1728
Type: Clinical study
Rating: Fair
Keywords: Obesity, periodontal attachment loss, periodontal disease/epidemiology, risk factors, smoking
Purpose: To assess the association of being overweight and obese with periodontitis in Brazilian adults
Methods: 706 patients 30-65 years old from South Brazil were examined clinically and with structured interview & questionnaire. BMI was calculated according to WHO criteria. Individuals with >30% teeth with attachment loss >5 mm were classified as having periodontitis. Multiple examiners were trained and calibrated.
Results: Underweight BMI <18.5, normal BMI 18.5-24.9, overweight BMI 25-29.9 and obese BMI >30. 60% of males and 65% of females were overweight or obese. 50.7% of men and 35.3% of females met the qualifications of periodontitis. There was no significant associations between BMI categories and periodontitis among males, but obese females were more likely to have periodontitis than normal (OR=2.1). When separate analyses were performed among smokers and non-smokers, the association of BMI and periodontitis appeared to be more pronounced in non-smokers. Among non-smoker females, the obese group was 3.4 times more likely to have periodontitis than the normal BMI group. No significant association was observed in males.
Discussion: NHANES III showed a sig association between CAL and obesity among US adults after adjusting for age, gender, diabetes, smoking and socioeconomic status. Mechanisms by which obesity may affect the periodontium have not yet been determined, but obesity has been associated with an impaired immune response and increased risk for infectious diseases in some studies. DM is a known risk factor for periodontal diseases, so is likely a confounding factor in the relationship between obesity and periodontitis.
Conclusion: The only sig relationship in this population was between BMI and periodontal disease for non-smoking women.
Topic: Body Mass Index
Authors: Haffajee AD, Socransky SS NO ARTICLE
Title: Relation of body mass index, periodontitis and Tannerella forsythia.
Source: J Clin Periodontol. 2009 Feb;36(2):89-99
Type: Clinical
Rating: Good
Keywords: BMI; periodontal; subgingival plaque; Tannerella forsythia
Purpose: To examine whether being overweight or obese was associated with an increased risk of having periodontitis after adjusting for factors such as gender, age and smoking status. Also, to examine whether there was a shift in the sub-g microbiota in obese subjects that mat account for an increased risk of periodontitis.
Methods: 121 periodontally healthy/gingivitis and 574 patients with chronic periodontitis were included. Clinical parameters were assessed (plaque, gingival redness, BOP, PD, CAL). Periodontally healthy/gingivitis subjects had at least 24 teeth and <2% of sites with PD4mm and CAL4mm. Periodontitis subjects had at least 20 teeth and >5% of sites with PD4mm and/or CAL 4mm. Exclusion criteria: periodontal or antibiotic therapy in the previous 6 months, systemic conditions (diabetes, HIV), need for antibiotic prophylaxis. Also, height, weight and total body fat were measured. Blood pressure was measured, smoking history was recorded by means of a questionnaire and age was recorded. Sub-g samples were taken from mesial surface of each tooth using individual sterile Gracey curettes and analyzed for their content of 40 bacterial species. Logistic regression analysis was performed to examine the association and periodontal status after adjusting for age, gender and smoking status.
Results: There were far greater proportions of overweight and obese individuals in the subjects with periodontitis compared with periodontally healthy/gingivitis individuals. Individuals who were overweight or obese were 3.07 and 5.31 times respectively more likely to have periodontitis than subjects with normal BMI. Logistic regression analysis indicated an OR of 2.3 for an obese subject to exhibit periodontitis after adjusting for age, gender and smoking status. Younger, female subjects exhibited the strongest relationship between obesity and periodontal status. Only T.forsythia differed significantly in proportions among BMI groups and was significantly higher in obese periodontally healthy/gingivitis individuals.
Conclusion: Subjects, particularly younger females who were overweight or obese were at greater risk for periodontitis than subjects with normal BMI after adjusting for age, gender and smoking status. T. forsythia was in greater proportions in gingival sulci in periodontally healthy/gingivitis subjects who were obese, potentially increasing the risk of developing periodontitis.
Topic: Obesity
Author: Suvan J, D'Aiuto F, Moles DR, et al NO ARTICLE
Title: Association between overweight/obesity and periodontitis in adults. A systematic review.
Source: Obes Rev. 2011 May;12(5):e381-404.
Type: RCT
Rating: Good
Keywords: low birth weight babies, pregnancy, oral systemic connection, reproductive system
Purpose: To provide a systematic review of the evidence to date investigating the association between overweight/obesity (as defined by body mass index– BMI) and periodontitis. Systematic review asking the question: What is the relationship between overweight or obesity (based on BMI) associated with excessive body fat and periodontitis in terms of clinical periodontal outcomes in adults?
Background:
Methods: Electronic searching included the search of electronic databases (Ovid MEDLINE, EMBASE, LILACS and SIGLE) to December 2009. Hand searching was comprised of checking bibliographic references of included articles and related review articles. RCTs, cohort, case control and cross-sectional study designs that included measures of periodontitis and body composition were eligible. Duplicate, independent screening and data abstraction were performed. Meta-analyses were performed when appropriate.
Results: 527 titles and abstracts were screened, with 32 full text articles and 1 abstract include in the review. 3 studies reported no evidence of an association between body composition and periodontitis. The remaining 30 studies reported a positive association between body composition and periodontitis. Nineteen studies provided sufficient information for inclusion in meta-analyses. Meta-analyses indicated SS associations between periodontitis and body mass index (BMI) category obese OR 1.81, overweight OR 1.27, and obese and overweight combined OR 2.13.
Conclusion: The overall results indicate evidence of a positive association between overweight and obesity, and/or excessive body fat and prevalence of periodontitis. Additional prospective studies to further quantify, or understand the mechanisms, of this association are needed. There is insufficient evidence to provide guidelines to clinicians on the clinical management of periodontitis in overweight and obese individuals.
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