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Bacterial Mouth Infections

  • Author: Talib Najjar, DMD, MDS, PhD; Chief Editor: William D James, MD  more...
 
Updated: Aug 02, 2015
 

Overview

The oral cavity contains some of the most varied and vast flora in the entire human body and is the main entrance for 2 systems vital to human function and physiology, the gastrointestinal and respiratory systems. Several diseases involve these 2 systems and manifest in the oral cavity. In addition, a specific pathologic condition, such as periodontitis (ie, inflammation of the periodontal attachment of the teeth and the alveolar bone), may be present in the oral cavity. These specific conditions in the oral cavity may create foci of infection that can affect many other vital systems, such as the cardiovascular and renal systems. Foci of infection in the oral cavity arising from chronic periodontitis or chronic periapical abscesses (ie, inflammation and abscess of the tissue attached to the apex of the root) may lead to subacute bacterial endocarditis (BE) and glomerulonephritis (GN).

In addition to bacterial organisms, oral microorganisms can include fungal, protozoal, and viral species. The bacteria include hundreds of types of organisms of which only "22 predominant ones have been identified."[1] A variety of organisms in the microenvironment of the oral cavity adhere to the teeth, the gingival sulcus, the tongue, and the buccal mucosa. Each site has a unique way of allowing the organisms to establish their residency. The normal flora in healthy individuals maintains similar patterns. When a local or systemic disease process or concomitant use of medications alters this overall pattern, atypical organisms begin to predominate and some normal organisms with a benign nature, such as Candida albicans, become pathogenic.

The microenvironment of the oral cavity changes with the age of the patient, the eruption or loss of teeth, and the appearance of disease states (eg, caries, periodontal disease). Systemic changes, such as pregnancy or drug intake, also alter the number and proportion of flora. These changes are due to alterations in the flow and composition of salivary fluid and in the levels and activity of defense components (eg, immunoglobulins, cytokines) in the saliva.

Increasing evidence indicates that oral microbiota participate in various systemic diseases. Periodontal disease permits organisms to enter deep systemic tissues, such as the carotid atheroma. An association between periodontal pathogens, such as Porphyromonas gingivalis, and atherosclerosis has been suggested because of the pathogen's possible direct effect on atheroma formation. P gingivalis has also been found in carotid and coronary atheromas. It may also invade and proliferate within heart and coronary artery endothelial cells, and, along with Streptococcus sanguis, it may also induce platelet aggregation associated with thrombus formation. Oral microorganisms may also enter the deeper tissue after trauma or surgery, which contributes to the disease process, particularly when they cause BE.

Periodontitis is a common chronic bacterial infection of the supporting structures of the teeth. The host response to this infection is an important factor in determining the extent and severity of the disease. Systemic conditions may modify the extent of periodontitis principally through their effects on normal immune and inflammatory mechanisms.

Several systemic diseases, such as diabetes mellitus, may increase the prevalence, incidence, or severity of gingivitis and periodontitis. Medications such as phenytoin, nifedipine, and cyclosporin are known to predispose to gingival overgrowth and to increase the severity of plaque formation. Immunosuppressive drug therapy and any disease (eg, HIV infection) resulting in suppression of the normal inflammatory and immune mechanisms can cause or enhance severe periodontal diseases. Smoking, which has an adverse effect on periodontal health, also affects this overall disease condition. Specific diseases, such as histiocytosis, may result in necrotizing ulcerative periodontitis.

The severity and prevalence of periodontitis are increased in persons with diabetes and are worse in persons with poorly controlled diabetes. Periodontitis may exacerbate diabetes by decreasing glycemic control. This effect indicates a degree of synergism and a link between the 2 diseases.

The relative risk of cardiovascular disease is doubled in persons with periodontal disease. Periodontal and cardiovascular disease share many common risk and socioeconomic factors, particularly smoking, which is a powerful risk factor for both diseases. The actual underlying etiology of both diseases is complex, as are the potential mechanisms whereby the diseases may be causally linked. The chronic inflammatory state and microbial burden in persons with periodontal disease may predispose to cardiovascular disease in ways proposed for other infections, such as with Chlamydia pneumoniae.

A 72-year-old man with severe periodontal disease A 72-year-old man with severe periodontal disease (same patient as in Media Files 2-6).
Radiographically evident severe alveolar bone loss Radiographically evident severe alveolar bone loss and periodontitis (same patient as in Media Files 1 and 3-6).
Carotid duplex ultrasonogram exhibits severe ather Carotid duplex ultrasonogram exhibits severe atherosclerosis/stenosis of the left carotid artery (same patient as in Media Files 1-2 and 4-6).
Status post left carotid endarterectomy (same pati Status post left carotid endarterectomy (same patient as in Media Files 1-3 and 5-6).
Gross pathologic specimen shows carotid plaque as Gross pathologic specimen shows carotid plaque as cause of stenosis (same patient as in Media Files 1-4 and 6).
Dissected pathologic carotid plaque with bacterial Dissected pathologic carotid plaque with bacterial contents similar to periodontal plaque surrounding existing dentition (same patient as in Media Files 1-5).

For patient education resources, see the Teeth and Mouth Center, as well as Gingivitis and Periodontal (Gum) Disease. Also of interest may be the articles Viral Infections of the Mouth and Noncandidal Fungal Infections of the Mouth.

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Bacterial Endocarditis Secondary to Oral Foci of Infection

Dental manipulation has been proven to cause transient bacteremia. Patients who have congenital or acquired cardiovascular defects are at risk for BE. Before the antibiotic era, these infections were fatal. Today, even with the best medical treatment, this disease has a mortality rate of 10-80%. The lesion of BE is a vegetation that develops on a heart valve. BE is relatively rare, with a worldwide incidence of 10-60 cases per 1 million persons per year.[2] However, this rate is low considering the more susceptible group of patients with rheumatic fever and those with a previous history of endocarditis; these patients have a 10-30% risk of developing BE. However, only 200 cases of streptococcal endocarditis following dental and genitourinary tract procedures have been reported in the literature.

Etiology

Infective endocarditis occurs when microorganisms enter the bloodstream and infect damaged endocardium or endothelial tissue. It most commonly involves the heart valves (either native or prosthetic), but it may also occur at the site of a septal defect, on the chordae tendineae, or on the mural endocardium.[3] The prototypic lesion is at the site of the infection; the vegetation is a mass of platelets, fibrin, microcolonies of microorganisms, and scant inflammatory cells.[4] Endocarditis is classified as acute or subacute, which applies to the features and the progression of infection until diagnosis.

Of BE cases, 8-10% are possibly associated with oral infections in the absence of dental manipulation, and a synergistic effect could exist between the presence of periodontal or periapical disease and dental manipulation favoring BE.[5] Brushing teeth, chewing gum, or even eating may provoke bacteremia because of the production of micromovements of the teeth within the sockets.[6] Oral bacteremia manifesting after tooth extractions is usually transient, lasting less than 15-30 minutes.[7]

Epidemiology

In developed countries, the incidence of BE varies from 1-5 cases per 100,000 population per year.[8] and has increased in recent years, notably in elderly persons. The cumulative rate of prosthetic valve endocarditis is 1.5-3% one year after valve replacement. This risk is greatest during the first 6 months after replacement.[4]

The rate of endocarditis occurring in an at-risk patient after receiving dental treatment can vary from 0-1 case in 533.9 population. Numerous studies have demonstrated that bacteremia after dental procedures can cause bleeding in 50-90% of patients.[9] Patients with oral bacteremia who do not receive antibiotic treatment can have a mortality rate of 100%. Those treated have a mortality rate of 10-80%; patients with early prosthesis valve endocarditis have the highest mortality rate. Morbidity can include congestive heart failure, renal disease, stroke, and scarred heart valves.

Pathology

The oral cavity, the skin, and the upper respiratory tract are the primary portals for Streptococcus viridans; Staphylococcus species; and Haemophilus aphrophilus, Aggregatibacter (formerly Actinobacillus) actinomycetemcomitans,[10] Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae (HACEK) organisms,[11] with streptococcal and staphylococcal organisms responsible for more than 80% of cases of BE.

The lesions usually manifest as cardiac, embolic, or general lesions. Cardiac lesions are usually valvular, with vegetative lesions occurring on the line of contact with damaged valve cusps. The mitral valve is usually the most commonly affected, involving 28-45% of patients with BE.[4] Endothelial injury causes aberrant flows and allows either direct infection by virulent organisms or the development of an uninfected platelet-fibrin thrombus (nonbacterial thrombotic endocarditis). This thrombus serves as a site of bacterial attachment during transient bacteremia.

Pathogenesis

The microorganisms in the blood adhere to the thrombi, leading to further proliferation, increased platelet fibrin deposition, and vegetative formation. Embolizations of these friable lesions are vegetations that detach and lodge in distal arterioles of every organ system, causing infection and infarction of remote tissues, including the extremities, the spleen, the kidneys, the bowel, or the brain.[4]

Clinical presentation

Septic emboli can manifest as congestive heart failure with infection-induced valvular damage and splenomegaly and splenic abscesses. Neurologic manifestations, such as delirium, headache, and meningeal irritation, may be caused by mycotic aneurysms. Other generalized lesions can cause myalgias, anorexia, backache, fever, chills, sweats, Osler nodes, Janeway lesions, and splinter hemorrhages with clubbing of the fingers. Persons at greatest risk are patients with prosthetic heart valves, previous infective endocarditis, cyanotic congenital heart disease, aortic valve disease, mitral regurgitation, patent ductus arteriosus, ventricular septal defect, or coarctation of the aorta and those who use intravenous drugs.

Diagnosis

The diagnosis is based on clinical, laboratory, and echocardiographic findings. Transthoracic echocardiography is rapid and noninvasive, and it has excellent specificity (98%) for vegetations.[12] However, transthoracic echocardiography may be inadequate as much as 20% of the time because of emphysema or body habitus, and it only has a sensitivity of 65% for detecting vegetations. Transesophageal echocardiography detects vegetations in more than 90% of patients with definite endocarditis,[4] and it is the optimal method for the diagnosis of prosthetic valve endocarditis and the detection of a myocardial abscess.[3]

Outcome

The outcome varies according to the causative organism, time to diagnosis, involvement of the prosthetic valves or the aortic valve, intracardiac complications, and major neurologic complications. The overall survival rate for patients with native valve endocarditis caused by S viridans, HACEK organisms, or enterococci ranges from 85-95%. For Staphylococcus aureus native valve endocarditis, the mortality rate is 55-70% in persons who do not abuse intravenous drugs and is 85-90% in those who do. Prosthetic valve endocarditis beginning within 2 months of valve replacement results in mortality rates of 40-50%.[4]

Treatment

Because of the high morbidity and mortality rates associated with BE, antibiotic prophylaxis is recommended before selective procedures likely to produce bacteremia and endocarditis, as is maintaining good dental hygiene and aggressively treating local infections.[4] The benefits of antibiotic prophylaxis are not established, and, in fact, only 50% of patients with native valve endocarditis know they have a valve lesion predisposing to infection. Organisms not targeted by prophylaxis cause more than 35% of infections.

Dental treatments are the procedures most widely accepted as predisposing to endocarditis; however, they are no more frequent during the 3 months preceding this diagnosis than in uninfected matched controls.[4] The administration of antibiotic prophylaxis to at-risk patients who are undergoing dental manipulations is a reasonably well-accepted clinical practice.[13] The most frequently used guidelines are those of the American Heart Association (see Endocarditis Prophylaxis Information) and the British Society of Antimicrobial Chemotherapy.

Numerous studies have demonstrated that antibiotics can reduce the prevalence and the magnitude of bacteremia.[14] Patients who are susceptible may be able to reduce the risk of endocarditis by maintaining good dental hygiene and aggressively treating local infections. The antibiotic regimen for prophylaxis of endocarditis in adults at moderate or high risk is as follows:

  • Oral cavity, respiratory tract, esophageal, or minor surgical procedures
    • Standard regimen (low-to-moderate risk) - Amoxicillin at 2 g orally 1 hour before the procedure
    • Inability to take oral medication - Ampicillin at 2 g intravenously or intramuscularly within 30 minutes of the procedure
    • Penicillin allergy
      • Clarithromycin at 500 mg orally 1 hour before the procedure
      • Cephalexin or cefadroxil at 2 g orally 1 hour before the procedure
      • Clindamycin at 600 mg orally 1 hour before the procedure
    • Inability to take oral medication
      • Cefazolin at 1 g intravenously or intramuscularly 30 minutes before the procedure
      • Clindamycin at 600 mg intravenously 30 minutes before the procedure
    • Patients at high risk
      • Ampicillin at 2 g intravenously or intramuscularly plus gentamicin at 1.5 mg/kg intravenously or intramuscularly (not to exceed 120 mg) within 30 minutes of the procedure; repeat ampicillin at 1 g intravenously or intramuscularly or amoxicillin at 1 g orally 6 hours later
      • Penicillin allergy - Vancomycin at 1 g intravenously over 1-2 hours plus gentamicin at 1.5 mg/kg intravenously or intramuscularly within 30 minutes before the procedure, no second dose used
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Cardiovascular and Cerebrovascular Disease Secondary to Oral Foci of Infection

Periodontitis has been shown to be associated with atherosclerosis and coronary heart disease. Periodontal disease is common in persons with these conditions, and it may account for a significant portion of infection-associated risk of cardiovascular disease.[15]

Etiology

Oral infections may directly contribute to atherogenesis and thromboembolic events by providing repeated systemic vascular challenges of proinflammatory cytokines, periodontal pathogens, and lipopolysaccharide (LPS). The proinflammatory cytokines may be more closely associated with the more chronic aspects of cardiovascular disease, such as the formation and the progression of arterial plaques, whereas the microbial and the LPS exposures may be associated with the more acute aspects of coronary heart disease and stroke, such as thrombus formation.

As with chronic infections elsewhere in the human body, chronic periodontal infections are associated with systemic changes to the blood and blood-forming organs, such as increases in plasma fibrinogen and white blood cells. Other chronic infections, such as Helicobacter pylori gastritis and C pneumoniae pneumonitis, have also been associated with an increased risk of ischemic heart disease. One can postulate that changes to the blood and blood-forming organs (eg, hyperfibrinogenemia) and chronic inflammatory conditions may be mechanisms through which infections promote an increased risk of ischemic diseases. Microorganisms can infect vascular endothelial cells directly, initiating the inflammatory response needed for the initial process of inducing atherosclerosis.[16]

Epidemiology

Acute episodes of an infectious disease may play a role in precipitating an acute cardiovascular event.[16] The infection with the largest body of evidence to support an association with cardiovascular disease and cerebrovascular disease is infection with C pneumoniae. Most of the 30 retrospective and cross-sectional studies show an association between C pneumoniae antibodies and cardiovascular disease. Sufficient evidence from biological mechanisms and animal models warrant interventional studies on periodontitis and the development of cardiovascular events.

A series of case-control and cross-sectional studies has shown a significant association between various indexes of poor dental health and coronary heart disease.[15] The odds of having a history of heart attack increase with the severity of periodontal disease.[17] The association between specific subgingival periodontal organisms and myocardial infarction (MI) has been evaluated, and 2 periodontopathic organisms, Bacteroides forsythus and P gingivalis, are associated with MI.[18] Another study reported that 921 men free of cardiovascular for 18 years had high levels of alveolar bone loss at baseline (measure of periodontal disease) and noted that this was a significant predictor of total cardiovascular disease and stroke.[19]

Pathology and pathogenesis

The disease mechanism for atheroma formation and thrombosis has been linked to platelet aggregation. The oral gram-positive bacteria, S sanguis, and the gram-negative periodontal pathogen, P gingivalis, found in dental plaque, enter the bloodstream during bacteremic episodes. These bacteria may induce platelet activation and aggregation through the expression of collagenlike platelet aggregation–associated proteins, playing a role in the formation of atheroma and thrombosis.[20]

Studies suggest that periodontal pathogens may be present in arteriosclerotic plaques and, similar to other infectious organisms (eg, C pneumoniae), may play a role in the development and progression of atherosclerosis. The infection with the largest body of evidence supporting an association with cardiovascular and cerebrovascular association is infection with C pneumoniae. An acute episode of infectious disease may play a role in precipitating an acute cardiovascular event via an acute thrombus dislodging a vulnerable plaque.[16]

Several studies have found P gingivalis capable of invading the coronary and carotid endothelium in cell cultures.[21] Animal studies have suggested that infection with P gingivalis activates the acute-phase response, increasing lipemia and atheroma formation.[22] C pneumoniae has proven, in vitro, capable of infecting vascular endothelial cells, smooth muscle cells, and macrophages of human origin.[23]

Periodontal infections may stimulate the release of cytokines, such as tumor necrosis factor-alpha, interleukin (IL)–1, IL-6, and IL-8. One of these potential stimuli, the endotoxin LPS, is present in the subgingival plaque of patients with severe periodontal disease. LPS and other bacterial components can activate an impressive cascade of inflammatory cytokines, which, in turn, can play a role in atherosclerotic heart disease either through direct action on the vessel wall or by inducing the liver to produce acute-phase proteins.[24]

C pneumoniae and its LPS can enhance low-density lipoprotein accumulation in human-derived monocytes to form foam cells, which are a key component of atherosclerosis. Microorganisms can infect vascular endothelial cells directly, initiating the inflammatory response needed for the initial process of inducing atherosclerosis and for accelerating or enhancing this process.

Acute-phase proteins, such as C-reactive protein (CRP) and fibrinogen, affect coagulation, platelet activation, and aggregation, contributing to atheroma formation. The LPS and inflammatory cytokines present in periodontal pathogens may also increase the expression of leukocyte adhesion molecules, such as intercellular adhesion molecules or vascular cell adhesion molecules, by endothelial cells. Intercellular adhesion molecules and vascular cell adhesion molecules are associated with atheroma formation.[25] Studies have also provided evidence that periodontal disease is associated with cardiovascular risk factors, including CRP and plasma fibrinogen levels, which are systemically increased in people with periodontitis. One study demonstrated that CRP levels are highest in patients infected with periodontal pathogens.[26]

CRP is also an independent risk factor for cardiovascular disease. CRP localizes with complement in human hearts during MIs, suggesting that CRP binds to diseased muscle tissue, fixes complement, and triggers complement-mediated inflammation that contributes to atheroma formation.[27] Periodontal infections may be associated with an increased risk of atherosclerotic processes, such as coronary artery disease and strokes, because of the association of periodontal infections with elevated levels of CRP.

The accumulation of epidemiologic, in vitro, and animal evidence suggests more than just a casual role of periodontal infections as a risk factor for cardiovascular disease and stroke. People with severe periodontitis have the strongest link to cardiovascular disease and cerebrovascular disease. These people also have the greatest amounts of pathogenic bacteria and systemic factors that may contribute to an altered immunoinflammatory response.

A study aimed to identify further shared genetic risk factors between coronary artery disease (CAD) and periodontitis. The study concluded that PLASMINOGEN is the third replicated shared genetic risk factor of atherosclerosis and periodontitis. All known shared risk genes of CAD and periodontitis are members of transforming growth factor-β signaling.[28]

Treatment

According to the discussion of the etiology and pathogenesis of atheroma in patients with severe periodontal disease, the goals of treatment are to treat hypercholesterolemia and lower low-density lipoprotein levels via any of the new statin medications in conjunction with a low-fat, low-cholesterol diet. Maintaining good oral hygiene and eliminating the oral foci of infection and bacterial diseases are additional methods used to eliminate the oral cause of atheroma formation.

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Glomerulonephritis Secondary to Oral Foci of Infection

In patients with poor oral hygiene and in the presence of oral foci of infection, renal involvement is characterized by the abrupt onset of hematuria and proteinuria and is often association with edema, hypertension, and mild-to-moderate renal insufficiency. The disease usually develops several days after Streptococcus mitis or Streptococcus mutans bacteremia. However, several reported cases indicate that renal disease is not caused by streptococci but is associated with a bacteremic state or with viral or parasitic diseases.

GN is the most common primary renal disease in developing countries; however, it is becoming uncommon in the Western world. This suggests that the development of GN is associated with low socioeconomic status and poor hygienic conditions. This suggestion is bolstered by the observation that cases occur in clusters and epidemics, which, at times, may even be cyclic. GN can affect persons of any age; however, most patients are aged 2-12 years. Proliferative GN is twice as common in males as in females.

Pathology

In the early phases of bacterial infection, diffuse glomerular, mesangial, and endothelial cell proliferation is present and is associated with infiltration of the capillary lumens by polymorphonuclear leukocytes and mononucleotide cells. Extracapillary proliferation may involve a few glomeruli, whereas diffuse and extensive circumferential crescent formation is uncommon, although possible. Inflammatory cells expressing IL-8 and transforming growth factor-beta (TGF-beta) appear to increase the expression of intercellular adhesion molecules, which can be found in both glomerulus and interstitial sites. IL-8 levels are correlated with glomerular neutrophil infiltration, whereas TGF-beta levels are correlated with mesangial matrix proliferation.[29] The tubulointerstitial compartment is usually normal, but, in most proliferative forms, acute cellular infiltrates can be seen.

The typical immunohistologic pattern is characterized by abundant and well-defined granular deposits of C3 along the outer aspects of the glomerular capillary walls. These deposits confer the appearance known as starry sky. Immunoglobulin G and immunoglobulin M are present in 60-70% of cases. C1q and C4 are generally lacking. Fibrinogen is seen only in crescents. With electron microscopy, coarse electron-dense subepithelial deposits are the distinguishing feature of GN. Because of their shape, the deposits are defined as humps. However, intramembranous and subendothelial deposits and mesangial deposits can also be found.

In later phases of the disease, endocapillary proliferation and polymorphonuclear infiltration are less evident and prominent mesangial deposits can be observed. In other cases, subepithelial deposits are confluent, so that apparently elongated deposits, which confer a flarelike pattern immunohistologically, replace the humps. In cases without complete resolution, the typical endocapillary disease can transform over time into a mesangiocapillary pattern.

Pathogenesis

Some data suggest that GN is an immune-complex disease in which some components of nephritogenic streptococci likely act as antigens. Cell membrane antigens, streptococcal cationic proteinase, extracellular plasmin-binding protein, and endostreptosin or preabsorbing antigen have been proposed as possible triggers for the formation of the immune complexes. On the other hand, antiimmunoglobulin antibodies could be involved in the pathogenesis of GN, as demonstrated by the high titers of rheumatoid factor and by the presence of antiimmunoglobulin deposits in renal biopsy specimens of some patients.

An important role in conferring antigenicity to immunoglobulins can be played by another streptococcal component, the neuraminidase. In fact, this component can cause consequent modifications of autologous immunoglobulins; moreover, neuraminidase can alter leukocytes and favor their deposition in the glomeruli and the interstitium.

Cellular immunity may also be involved in the pathogenesis of GN, as suggested by glomerular and interstitial infiltration of granulocytes, monocyte/macrophages, and T lymphocytes; increased IL-8 and TGF-beta levels in the kidneys; and increased IL-6 and tumor necrosis factor-alpha levels in the circulation.

Clinical presentation

The typical patient with GN presents with an acute nephritic syndrome (ie, oliguria, edema, hypertension, gross hematuria) 10-21 days after the onset of bacteremia. Nonspecific symptoms, such as malaise, weakness, and nausea, are frequent. Dull lumbar pain is present in 5-10% of patients.[30] Although rare, an extrarenal disease is possible in patients with GN, as demonstrated by the association with oliguria, scleritis or cerebral palsy in elderly patients, and vasculitis.

Decreased glomerular filtration and salt and water retention are the main causes of edema and hypertension, as documented by the finding of increased plasma volume and cardiac output in most patients with GN. In children, edema is usually generalized, while in adolescents and adults, it is more frequently confined to the face and the legs. Hypertension is observed in 80% of patients, but only 50% of patients require treatment. However, in rare cases, hypertension may be severe and cause hypertensive encephalopathy.[31] Especially in elderly patients, oliguria and fluid retention can cause heart failure and death. Proteinuria is common in persons with GN; however, nephrotic proteinuria is rare, especially in children.[32]

In other patients, GN can be asymptomatic and cause only a transient serum complement decrease and/or mild urinary abnormalities, such as isolated microscopic hematuria, with or without hypertension.[33] Prospective studies in families have shown that this presentation is more common than the overt clinical presentation described above. Very rarely, GN is associated with urinary abnormalities in spite of clinical symptoms and the presence of endocapillary GN at biopsy.

Outcome

Usually, the nephritic symptoms spontaneously reverse 4-7 days after the onset; however, urinary changes, mild renal function impairment, or hypertension can persist or develop months or years after the acute episode. These abnormalities can be found in approximately 20% of patients 1-2 decades after the onset. Usually, children do better than adults. Patients with a nephrotic syndrome at presentation and those with extensive deposits in the peripheral capillary loops have a worse prognosis. Patients with crescentic disease may recover spontaneously. However, the prognosis is poor when crescents involve 60% of glomeruli.[34] In some patients with a subclinical presentation, persistent or intermittent microscopic hematuria may be seen at long-term follow-up examinations.

Diagnosis

GN results in increased antistreptolysin titers and decreased C3 levels. Increased antistreptolysin titers are observed in 40-90% of patients with GN. With GN, more than 90% of patients have a decrease in C3 levels and normal C4 serum levels, indicating an activation of the alternative pathway of complement. In most cases, C3 levels return to normal in less than 8 weeks, even though a prolonged decrease of C3 levels is possible. The behavior of complement distinguishes GN from other renal diseases, such as lupus nephritis, in which both C3 and C4 levels are usually reduced in active phases. In type 2 cryoglobulinemic nephritis, usually only the C4 level is strongly decreased.

Usually, no extrarenal symptoms are present in persons with GN besides edema and hypertension. These features differentiate GN from systemic diseases that cause acute nephritic syndrome. However, keep in mind that in occasional patients with GN, extrarenal symptoms (eg, scleritis, cerebral vasculitis) may be present.

GN can be easily diagnosed in epidemic or family cases, even when only transient and minor clinical and urinary changes are present. However, for sporadic cases with only persistent urinary abnormalities, distinguishing between immunoglobulin A nephropathy, thin basement membrane disease, and other conditions can be difficult without performing a renal biopsy. However, a typical history and clinical picture in most patients with acute nephritic syndrome caused by GN make diagnosis easy; thus, a confirmatory biopsy is not needed. Renal biopsy may be indicated for patients with an atypical history or presentation and especially for patients with severe or prolonged renal failure, which can be caused by crescentic disease.

Treatment

The primary goals of treatment are to eliminate oral foci of infection and to manage oliguria, edema, and hypertension. Renal management includes restriction of sodium and fluid intake. Furosemide or other loop diuretics are frequently needed. In many patients, hypertension reverses with the correction of fluid overload and edema. However, in some patients, antihypertensive agents are needed.

Antistreptococcal antibiotics, such as penicillin, cephalosporins, erythromycin, or derivatives, should be given. Corticosteroids or immunosuppressive agents are not indicated in persons with GN because the disease spontaneous resolves in most cases. However, in patients with extensive crescent formation and slow resolution of symptoms, a short course of high-dose glucocorticoids may be considered.

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Conclusion

Maintaining good long-term oral hygiene is required in patients with GN and in patients with BE and atherosclerotic cardiovascular disease. Elimination of oral foci of infection as potential sources of bacterial seeding is essential for persons with any of the conditions discussed.

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Contributor Information and Disclosures
Author

Talib Najjar, DMD, MDS, PhD Professor of Oral and Maxillofacial Surgery and Pathology, Rutgers School of Dental Medicine

Talib Najjar, DMD, MDS, PhD is a member of the following medical societies: American Society for Clinical Pathology

Disclosure: Nothing to disclose.

Coauthor(s)

Robert A Schwartz, MD, MPH Professor and Head of Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, Rutgers New Jersey Medical School; Visiting Professor, Rutgers University School of Public Affairs and Administration

Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, New York Academy of Medicine, American Academy of Dermatology, American College of Physicians, Sigma Xi

Disclosure: Nothing to disclose.

Torin W Rutner, DMD, MD Consulting Staff, Oral and Maxillofacial Surgery, Joseph D DeMaio, DDS

Torin W Rutner, DMD, MD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Association of Oral and Maxillofacial Surgeons, American Dental Association, American Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

David F Butler, MD Section Chief of Dermatology, Central Texas Veterans Healthcare System; Professor of Dermatology, Texas A&M University College of Medicine; Founding Chair, Department of Dermatology, Scott and White Clinic

David F Butler, MD is a member of the following medical societies: American Medical Association, Alpha Omega Alpha, Association of Military Dermatologists, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Phi Beta Kappa

Disclosure: Nothing to disclose.

Drore Eisen, MD, DDS Consulting Staff, Department of Dermatology, Dermatology Research Associates of Cincinnati

Drore Eisen, MD, DDS is a member of the following medical societies: American Academy of Dermatology, American Academy of Oral Medicine, American Dental Association

Disclosure: Nothing to disclose.

Chief Editor

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology, Society for Investigative Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Noah S Scheinfeld, JD, MD, FAAD Assistant Clinical Professor, Department of Dermatology, Weil Cornell Medical College; Consulting Staff, Department of Dermatology, St Luke's Roosevelt Hospital Center, Beth Israel Medical Center, New York Eye and Ear Infirmary; Assistant Attending Dermatologist, New York Presbyterian Hospital; Assistant Attending Dermatologist, Lenox Hill Hospital, North Shore-LIJ Health System; Private Practice

Noah S Scheinfeld, JD, MD, FAAD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Serve(d) as a speaker or a member of a speakers bureau for: Abbvie<br/>Received income in an amount equal to or greater than $250 from: Optigenex<br/>Received salary from Optigenex for employment.

References
  1. Topazian RG, Goldberg MH, Hupp JR, eds. Oral Maxillofacial Infections. 4th ed. Philadelphia, Pa: WB Saunders; 2002.

  2. Little JW, Miller CS, Rhodus NL, Falace D, eds. Dental Management of the Medically Compromised Patient. 6th ed. St. Louis, Mo: Mosby; 2002.

  3. Mylonakis E, Calderwood SB. Infective endocarditis in adults. N Engl J Med. 2001 Nov 1. 345(18):1318-30. [Medline].

  4. Braunwald E, Fauci AS, Kasper DL, et al, eds. Harrison's Principles of Internal Medicine. 15th ed. New York, NY: McGraw-Hill; 2001.

  5. Drangsholt MT. A new causal model of dental diseases associated with endocarditis. Ann Periodontol. 1998 Jul. 3(1):184-96. [Medline].

  6. Hogevik H, Olaison L, Andersson R, Lindberg J, Alestig K. Epidemiologic aspects of infective endocarditis in an urban population. A 5-year prospective study. Medicine (Baltimore). 1995 Nov. 74(6):324-39. [Medline].

  7. Everett ED. Complications and residuals of meningococcal disease. Mil Med. 1971 Jul. 136(7):612-6. [Medline].

  8. Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association. JAMA. 1997 Jun 11. 277(22):1794-801. [Medline].

  9. Peterson LJ, Peacock R. The incidence of bacteremia in pediatric patients following tooth extraction. Circulation. 1976 Apr. 53(4):676-9. [Medline].

  10. Lampe AS, Schroijen MA, Smith SJ. [Endocarditis due to Aggregatibacter (formerly: Actinobacillus) actinomycetemcomitans, a bacterium that grows in characteristic star-shaped colonies]. Ned Tijdschr Geneeskd. 2008 Apr 5. 152(14):827-30. [Medline].

  11. Beck JD, Slade G, Offenbacher S. Oral disease, cardiovascular disease and systemic inflammation. Periodontol 2000. 2000 Jun. 23:110-20. [Medline].

  12. Shively BK, Gurule FT, Roldan CA, Leggett JH, Schiller NB. Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis. J Am Coll Cardiol. 1991 Aug. 18(2):391-7. [Medline].

  13. Hall G, Nord CE, Heimdahl A. Elimination of bacteraemia after dental extraction: comparison of erythromycin and clindamycin for prophylaxis of infective endocarditis. J Antimicrob Chemother. 1996 Apr. 37(4):783-95. [Medline].

  14. Baltch AL, Pressman HL, Hammer MC, Sutphen NC, Smith RP, Shayegani M. Bacteremia following dental extractions in patients with and without penicillin prophylaxis. Am J Med Sci. 1982 May-Jun. 283(3):129-40. [Medline].

  15. Genco R, Offenbacher S, Beck J. Periodontal disease and cardiovascular disease: epidemiology and possible mechanisms. J Am Dent Assoc. 2002 Jun. 133 Suppl:14S-22S. [Medline].

  16. Fong IW. Infections and their role in atherosclerotic vascular disease. J Am Dent Assoc. 2002 Jun. 133 Suppl:7S-13S. [Medline].

  17. Arbes SJ Jr, Slade GD, Beck JD. Association between extent of periodontal attachment loss and self-reported history of heart attack: an analysis of NHANES III data. J Dent Res. 1999 Dec. 78(12):1777-82. [Medline].

  18. Genco RJ, Wu TJ, Grossi S, et al. Periodontal microflora related to the risk for myocardial infarction: A case control study. J Dent Res. 1999. 78:457.

  19. Beck J, Garcia R, Heiss G, Vokonas PS, Offenbacher S. Periodontal disease and cardiovascular disease. J Periodontol. 1996 Oct. 67(10 Suppl):1123-37. [Medline].

  20. Herzberg MC, Brintzenhofe KL, Clawson CC. Aggregation of human platelets and adhesion of Streptococcus sanguis. Infect Immun. 1983 Mar. 39(3):1457-69. [Medline].

  21. Dorn BR, Dunn WA Jr, Progulske-Fox A. Invasion of human coronary artery cells by periodontal pathogens. Infect Immun. 1999 Nov. 67(11):5792-8. [Medline].

  22. Chung HJ, Champagne CME, Southerland JH, et al. Effects of P. gingivalis infection on atheroma formation in ApoE(+/-) mice [abstract]. J Dent Res. 2000. 7:313.

  23. Gaydos CA, Summersgill JT, Sahney NN, Ramirez JA, Quinn TC. Replication of Chlamydia pneumoniae in vitro in human macrophages, endothelial cells, and aortic artery smooth muscle cells. Infect Immun. 1996 May. 64(5):1614-20. [Medline].

  24. Castell JV, Andus T, Kunz D, Heinrich PC. Interleukin-6. The major regulator of acute-phase protein synthesis in man and rat. Ann N Y Acad Sci. 1989. 557:87-99; discussion 100-1. [Medline].

  25. Lopes-Virella MF, Virella G. Immunological and microbiological factors in the pathogenesis of atherosclerosis. Clin Immunol Immunopathol. 1985 Dec. 37(3):377-86. [Medline].

  26. Noack B, Genco RJ, Trevisan M, Grossi S, Zambon JJ, De Nardin E. Periodontal infections contribute to elevated systemic C-reactive protein level. J Periodontol. 2001 Sep. 72(9):1221-7. [Medline].

  27. Lagrand WK, Niessen HW, Wolbink GJ, Jaspars LH, Visser CA, Verheugt FW, et al. C-reactive protein colocalizes with complement in human hearts during acute myocardial infarction. Circulation. 1997 Jan 7. 95(1):97-103. [Medline].

  28. Schaefer AS, Bochenek G, Jochens A, et al. Genetic evidence for PLASMINOGEN as a shared genetic risk factor of coronary artery disease and periodontitis. Circ Cardiovasc Genet. 2015 Feb. 8 (1):159-67. [Medline].

  29. Rastaldi MP, Ferrario F, Yang L, Tunesi S, Indaco A, Zou H, et al. Adhesion molecules expression in noncrescentic acute post-streptococcal glomerulonephritis. J Am Soc Nephrol. 1996 Nov. 7(11):2419-27. [Medline].

  30. Reichert LJ, Huysmans FT, Assmann K, Koene RA, Wetzels JF. Preserving renal function in patients with membranous nephropathy: daily oral chlorambucil compared with intermittent monthly pulses of cyclophosphamide. Ann Intern Med. 1994 Sep 1. 121(5):328-33. [Medline].

  31. Remuzzi G, Ruggenenti P, Benigni A. Understanding the nature of renal disease progression. Kidney Int. 1997 Jan. 51(1):2-15. [Medline].

  32. Rodríguez-Iturbe B, Rubio L, García R. Attack rate of poststreptococcal nephritis in families. A prospective study. Lancet. 1981 Feb 21. 1(8217):401-3. [Medline].

  33. Ruiz JG, Lowenthal DT. NSAIDS and nephrotoxicity in the elderly. Geriatr Nephrol Urol. 1997. 7(1):51-7. [Medline].

  34. Savage CO, Pusey CD, Bowman C, Rees AJ, Lockwood CM. Antiglomerular basement membrane antibody mediated disease in the British Isles 1980-4. Br Med J (Clin Res Ed). 1986 Feb 1. 292(6516):301-4. [Medline].

  35. Abozaid S, Peretz A, Nasser W, Zarfin Y. [Rare infection--prolonged A. naeslundii bacteremia caused by severe caries]. Harefuah. 2013 Jul. 152(7):379-80, 435. [Medline].

  36. Benakanakere M, Kinane DF. Innate cellular responses to the periodontal biofilm. Front Oral Biol. 2012. 15:41-55. [Medline].

  37. Calandrini CA, Ribeiro AC, Gonnelli AC, et al. Microbial composition of atherosclerotic plaques. Oral Dis. 2013 Nov 5. [Medline].

  38. Colombo AV, Barbosa GM, Higashi D, di Micheli G, Rodrigues PH, Simionato MR. Quantitative detection of Staphylococcus aureus, Enterococcus faecalis and Pseudomonas aeruginosa in human oral epithelial cells from subjects with periodontitis and periodontal health. J Med Microbiol. 2013 Oct. 62:1592-600. [Medline].

  39. Duval X. Simplification of the prophylaxis of endocarditis: we were right!. Arch Cardiovasc Dis. 2013 Feb. 106(2):69-71. [Medline].

  40. Eberhard J, Stumpp N, Ismail F, et al. The oral cavity is not a primary source for implantable pacemaker or cardioverter defibrillator infections. J Cardiothorac Surg. 2013 Apr 10. 8:73. [Medline]. [Full Text].

  41. Grecchi F, Zollino I, Candotto V, et al. A case of mandible osteonecrosis after a severe periimplant infection. Dent Res J (Isfahan). 2012 Dec. 9:S233-6. [Medline]. [Full Text].

  42. Han YW, Wang X. Mobile microbiome: oral bacteria in extra-oral infections and inflammation. J Dent Res. 2013 Jun. 92(6):485-91. [Medline]. [Full Text].

  43. Hong C, Brennan MT, Kaplan J, Lockhart PB. Infection from an exfoliating primary tooth in a child with severe neutropenia: a case report. Pediatr Dent. 2012 Jan-Feb. 34(1):51-3. [Medline].

  44. Pessi T, Karhunen V, Karjalainen PP, et al. Bacterial signatures in thrombus aspirates of patients with myocardial infarction. Circulation. 2013 Mar 19. 127(11):1219-28, e1-6. [Medline].

  45. Pupe CG, Villardi M, Rodrigues CR, et al. Preparation and evaluation of antimicrobial activity of nanosystems for the control of oral pathogens Streptococcus mutans and Candida albicans. Int J Nanomedicine. 2011. 6:2581-90. [Medline]. [Full Text].

  46. Rodríguez-Iturbe B. Epidemic poststreptococcal glomerulonephritis. Kidney Int. 1984 Jan. 25(1):129-36. [Medline].

  47. Santos AL, Siqueira JF Jr, Rôças IN, Jesus EC, Rosado AS, Tiedje JM. Comparing the bacterial diversity of acute and chronic dental root canal infections. PLoS One. 2011. 6(11):e28088. [Medline]. [Full Text].

  48. Umeda JE, Demuth DR, Ando ES, Faveri M, Mayer MP. Signaling transduction analysis in gingival epithelial cells after infection with Aggregatibacter actinomycetemcomitans. Mol Oral Microbiol. 2012 Feb. 27(1):23-33. [Medline]. [Full Text].

  49. Yagci A, Uysal T, Demirsoy KK, Percin D. Relationship between odontogenic bacteremia and orthodontic stripping. Am J Orthod Dentofacial Orthop. 2013 Jul. 144(1):73-7. [Medline].

  50. Zhang W, Daly CG, Mitchell D, Curtis B. Incidence and magnitude of bacteraemia caused by flossing and by scaling and root planing. J Clin Periodontol. 2013 Jan. 40(1):41-52. [Medline].

 
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A 72-year-old man with severe periodontal disease (same patient as in Media Files 2-6).
Radiographically evident severe alveolar bone loss and periodontitis (same patient as in Media Files 1 and 3-6).
Carotid duplex ultrasonogram exhibits severe atherosclerosis/stenosis of the left carotid artery (same patient as in Media Files 1-2 and 4-6).
Status post left carotid endarterectomy (same patient as in Media Files 1-3 and 5-6).
Gross pathologic specimen shows carotid plaque as cause of stenosis (same patient as in Media Files 1-4 and 6).
Dissected pathologic carotid plaque with bacterial contents similar to periodontal plaque surrounding existing dentition (same patient as in Media Files 1-5).
 
 
 
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