CHAPTER 17 309

ea pig t o artificially

induced inflammation, J Dent Res

1948. lickrrran I, Stoller M: The periodontal tissues of the albino Dent Res 27:758, I9AQ deficiency, t in vita min A d e c Irl, ency, e n e s effect of f_1 TN: , .,,,,an 1, Stone 1C, iaw a : The e ec o cortisone cetate upon the periodontium of white mice, I Periodontol 24A61, 1953. Goetz ! EJ : Enhancement of random migration and che mo t actic response of human leukocytes by ascorbic cid, I Clin Invest 53:813, 1974. ;Idmar. HM: Acute aleukemic leukemia, Am J Orthod

~89, 1940. man MH: Perleche: a consideration of its etiology and !'} iology, Bull Johns Hopkins Hosp 51:263, 1943. ,ttsegen R: Dental and oral considerations in diabetes ellitus, NY J Med 62:389, 1962. vier WM, Grieg ME: Prevention of oral lesions in B1 ic rii1tarnincit dogs, Science 98:216, 1943. g.yr,reenberg MS, Cohen SB, Boosz B, et al: Oral herpes infections in patients with leukemia, J Am Dent Assoc 114:483, 1987. 9. Grossi SG, Zambon JJ, Ho AW, et al: Assessment of risk for }periperiodontal disease. 1. Risk indicators for attachment loss, o d o n t a l Periodontol 65:260, 1994. usberti F, Grossman N, Loesche W: Puberty gingivitis in insulin-dependent diabetes, J Dent Res 61:201, 1982 (abstract). VI,' yden P, Buckley LA: Diabetes mellitus and periodontal #

318

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LDL

Periodontal Medicine: Impact of Periodontal Infection on Systemic Health CHAPTER

18

319

Periodontal infection

MO+ phenotype

Periodontal pathogens

Gram-negative bacteremia/LPS Periodontitis

Endothelial damage Platelet adhesion/aggregation Monocyte infiltration/proliferation

Chronic bacterial challenge Proinflammatory cytokines Acute phase reactants

Cytokine/growth factor production Thrombus formation

Risk factors for atherosclerosis

`" Vascular effects

Atheroma formation Vessel wall thickening Thromboembolic events

Hypercoagulability Atheroma formation Thromboembolism

320

PART 5 Relationship between Periodontal Disease and Systemic Health

BOX 18-2
Co mpl i ca ti o ns of Dia betes Mel l i tus

From: We H: Diabetes Care I 6(5uppi 1):329, 1993.

Periodontal Medicine: Impact of Periodontal Infection on Systemic Health C H A P T E R 1 8

321

'diabetic complications in these subjects.

with reduced probing depths and bleeding on

B.O.P. N=5

B.O.P.

unchanged
N = 4

310

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between Periodontal Disease and Systemic Health

Influence of Systemic Disorders and Stress on the Periodontium CHAPTER 17

311

l nse to non-surgica periodontal treatment in subjects ji"diabeteS mellitus, I Clin Periodontol 18:65, 1991. T, Sal edt E, Koppang HS: The effect of immunoSsivc agents on periodontal disease in man, I ontal Res 13:240, 1978. hopping NH, Fraser HE: Mouth lesions associated with dietary deficien c i es in monkeys, Public Health Rep 54:416,

4319, ~9, 6'1

S, Fisher B, Glickman I: A histochemical study of e attached gingiva in pregnancy, I Dent Res I936. 6gel, R: Relationship of fol ic acid to phenytoin-induced n,Vgival overgrowth. In Hassell TM, Johnson M, Dudley K, F'editors: Phenytoin-induced teratology and gingival pathology, rew York, 1980, Raven Press. ogel R, Deasy M, Alfano M, et at: The effect of folic acid n g i rigival health of women taking oral contraceptives, Prey Dent 6:221, 1980.

11 r esky

CHAPTER OUTLINE

312

Periodontal Medicine: Impactof Periodontal Infection on Systemic Health CHAPTER 18

313

a t i o i t n a n d p o r g e r s o i n s i c e l a y l r e c o g n z i e d .

BOX 1 8 pathogenic bacteria are necessary for periodontal Systems and Conditions Possibly Influenced ~-Jfey are not sufficient alone to cause -eptible to disease, the disease. Infection Periodontal Infection m e t s y S pathogenic bacteria may have 8 a ~ ; e f c C . t o n v e r s e l y h t , e s u s c e p b i t e l h o s e t x p e i r A t h e o r s c e l o r s i e nical signs of periodontitis in the presence of Coronary heart disease (CHD) 4 i c bacteria. Angina l i d r a c o y M ) I M ( t f n i l u c s a v o r b ) k o s ( t n d i c a r e C d e f i r f" u g h o u t h e s c i e n t i f c l i t e r a t u r e B . e c a u s e o f E n d o c r i n e S y s t e m
#

u l m s t e b a i D
d s i j l r j , s p a t i e n t s m a y n o t n e c e s s a r i l y h a v e s i m i l a r R e p r o d u c t i v e S y s t e m i tession despite the presence of similar bacteria. Preterm low-birth-weight (LBW) infants Wise, the response to periodontal treatment may vary Preeclampsia
p

the host to further disease progression. The i any of the systemic conditions discussed n Chapters Respiratory Syste of the oral infection and the individual's degree of resisof host I'd susceptibility clearlythe evident the 17 serve tois modify host'sin susceptibility to Chronic obstructive pulmonary disease (COPD) specific He also believed that oral organisms had specific m -Acute bacterialpatients pneumonia tiaiontitis. For example, with immune sup acted on different 0 o r g a n s i m s a c e t d don may not be able to mount an effective host by producin g toxins, resulting in low-grade "subinfection,#' rise to subgingival microorganisms, resulting in which produced systemic effects over prolonged periods. (rapid and severe periodontal destruction. Although between Hunter believed that the connection between otential impact of many systemic disorders on the be sepsis and resulting systemic conditions could be 6dontilim is well documented, recent evidence suggests tooth by removal of the causative sepsis throu gh tooth 'periodontal infection may significantly enhance the extraction and observation of the improvement in systeor certain systemic diseases or alter the natural health. Because it explained a wide range of disorders se of systemic conditions .66 Conditions in which for which there was no known explanation at the time, nfluences of periodontal infection are documented and theory became widely accepted in Britain and ~de coronary heart disease (CHD) and CHD-related wholesale the United States, leading to wholesale is such as angina and infarction, atherosclerosis, extraction of teeth. e, diabetes mellitus, preterm labor, low-birth-weight thefocal infection theory fell into disrepute in the very, and respiratory conditions such as chronic of and 1950s when widespread extraction, often of I. F u h t r m e h t , e r o m i p n a t r o h f e c n i t s o tractive pulmonary disease" , '9 (Box 18-1). the entire dentition, failed to reduce or eliminate the are of the precepts of the focal infection theory are W s y e t m c i o n d o t i n o t s w h i c t h e s u p o e s d l y n i f e c t d being revived today in light of recent research demonC ALI N FE CTI ONTHEO R YRE VI SI TEDden ti ti onh a dbeenlink e d.Th ethe ory ,w hil eof f e ringap o b i s e l x p a l n o i t n o f r A p e p r l x i n g s y e t m c i d o s i d r e , s r archintheareaofperiodontalmedicinemarksahadbeenbasedonverylittle,ifany,scientificevidence. rgenceintheconceptoffocalinfection.In1900,Hunterandotheradvocatesofthetheorywereunable s i t u e s a n d h t a t h e s e

"x `1111 Qsses, Hunter also identified gingivitis and periodon-immunology. ti*as foci of infection. He advocated extraction of teeth with these conditions to eliminate the source of sepsis. EVIDENCE-BASED CLINICAL PRACTICE Hunter believed that teeth were liable to septic infection i Pr marily because of their structure and their relationship I Al ' veolar bone. He stated that the degree of systemic effect produced by oral sepsis depended on the virulence

Type of Study

Strength of Evidence

Comments

Case report Cross-sectional study

+/ +

Longitudinal study intervention trial

++ +++

Provides relatively weak, retrospective anecdotal evidence. May suggest further study is needed. Compares groups of subjects at a single point in time. Stronger than case report. Fairly easy to conduct. Relatively inexpensive to conduct. Follows groups of subjects over time. Stronger than cross-sectional study. Studies with control group are much stronger than studies without controls More difficult and expensive to conduct. Examines effects of some interventions. Studies with control group (i.e., placebo) much stronger than studies without controls. Strongest form of evidence is randomized controlled intervention trial. Difficult and expensive to conduct.

Periodontal Medicine: ltnpact of Periodontal Infection on Systemic Health CHAPTER 18

315

no. evidence. Only the occasional case report and k~ .1 tl to the 11 cdotes were availablesubstantiate e L theory. I planatory mechanisms were proposed, none dated with scientific research. Unfortunately, ry predated current concepts of evidence-based leading to unnecessary extraction of ,practice, teeth. Currently, in reexamining the potential oral infections and systemic co Lions between J i mp o r t a n tto d e t er mi n e crLant what evidence (1) s t is I t fey( ) is still needed to substantiate the associaa n d validates the possible mechanisms of assojjon 4i , , is chapter reviews current knowledge relating o al infection to overall systemic health. BGINGIVAL ENVIRONMENT AS RESERVOIR
I"

fiBACTERIA 1,; f in with micro u a n patients w periodontitis des a s gnificant and persistent grain-negative k~w.* ial challenge to the host (see Chapters 9 and 13). A their products, and F I suchas l have i ready p oaccess p too the lperiodontal y chan e (LPS), sues and to the circulation via the sulcular epithelium, i is frequently ulcerated and discontinuous. Even 0ireatment, complete eradication of these organisms "difficult, and their reemergence is often rapid. The al surface area of pocket epithelium in contact with bgingival bacteria and their products in a patient with neralized moderate periodontitis has been estimated . approximately the size of the palm of an adult an even larger areas of exposure in cases of more y 4hced periodontal destruction.78 Bacteremias are *-G? !ynon after mechanical periodontal therapy and also frequently durin g normal dail y function and oral 0 giene procedures .26,33,65 Just as the periodontal tissues bunt an immunoinflammatory response to bacteria and eir products, systemic challenge with these agents also duces a major vascular response. This host response ay offer explanatory mechanisms for the interactions tween periodontal infection and a variety of systemic
diub gingivai
i
I

"tilers.

ERIODONTAL DISEASE AND MORTALITY

.e ultimate medical outcome measure is mortality.

316

PART 5 Relationship between Periodontal Disease and Systemic Health

pathogenic mechanisms.

Periodontal Medicine: Impact of Periodontal Infection on Systemic Health - CHAPTER 18

317

Coronary heart disease (CHID) risk factors Chronic Acute Thromboembolism

Systemic or periodontal infection

Fibrinogen White blood cell count 't' von Willebrand factor Blood viscosity

Occlusion of coronary arteries

Myocardial ischemia Isc h e mic hear t disease Angina Myocardial infarction ure 18-1 Acute and chronic pathways to ischemic heart CHID-related events such as angina or myocardial '%'firction may be precipitated by either pathway or both .;pathways.
Isease.

figure 18-2 Factors affecting blood viscosity in health.

ewise been associated with the risk of ischemic heart disease.82