Odontogenic infections caused by anaerobes

PULPITIS

Pulpitis is an inflammation of the dental pulp that can result from thermal, chemical, traumatic, or bacterial irritation. The most frequent inducer of pulpitis is dental caries that leads to destruction of enamel and dentin resulting in bacterial invasion. Secondary infection of the pulp by supragingival anaerobes occurs frequently in teeth with longstanding caries. Invasion of the pulp and spread of infection to the periapical areas can promote spreading of infection to other anatomical areas.

Pulpitis

Microbiology

Organisms isolated from an inflamed pulp and root canal are aerobic and facultative anaerobic organisms. Streptococcus salivarius generally constitutes less than 8% of the microorganisms of the infected root canal. Enterococcus faecalis has been reported in 10% to 30% of inflamed root canals. ¹ Other recovered microorganisms are yeasts and Gram-negative bacteria, mostly neisseriae and Gram-negative rods, such as Proteus vulgaris and Escherichia coli.   These bacteria may be difficult to eliminate from contaminated root canals.

Studies of the bacteriology of root canals have detected anaerobic bacteria. The quality of these studies varies considerably, however, and the anaerobic techniques generally are not always optimal. Most of these studies do not avoid contamination of the root canal specimen by oral flora. A variety of anaerobes have been recovered, accounting for 25% to 30% of the root canal isolates. These include anaerobic streptococci, anaerobic Gram-negative bacilli, actinomyces, propionibacteria, veillonellae, and others.²

Used PCR Rolph et al. ¹ detected of clones related to the genera Capnocytophaga, Cytophaga, Dialister, Enterococcus, Eubacterium, Fusobacterium, Gemella, Lactobacillus, Mogibacterium, Peptostreptococcus, Prevotella, Propionibacterium, Selenomonas, Solobacterium, Streptococcus, and Veillonella.

Several PCR studies have revealed new endodontic pathogens. ³ These organisms include  Tannerella forsythensis (formerly Bacteroides forsythus), Prevotella tannerae,  Porphyromonas endodontalis, Porphyromonas gingivalis, Fusobacterium nucleatum, Treponema  spp. (Treponema denticola, Treponema socranskii,  Treponema vincentii  ),  Dialister pneumosintes, Slackia exigua (formerly Eubacterium exiguum), Mogibacterium timidum (formerly Eubacterium timidum), Eubacterium saphenum. 

The bacterial complex composed of T. forsythensis, P. gingivalis, and T. denticola, termed the ‘red complex’, has been implicated in severe forms of periodontal disease. ⁴

Pathogenesis

The dental pulp is normally protected from infection by oral microorganisms by the enamel and dentin. This barrier may be breached allowing entrance of bacteria into the pulp or periapical areas. This can occur through a cavity caused by dental caries, trauma, or dental procedures; through the tubules of cut or carious dentin; in periodontal disease by way of the gingival crevice and by invasion along the periodontal membrane; by extension of periapical infection from adjacent teeth that are infected; or through the bloodstream during bacteremia.

Potentially virulent bacteria can migrate from the root canal into the apical regions. Toxic products from the pulp also may have a pathogenic role in the response to the inflammation. As the abscess progresses, more tissue may become involved, as well as adjacent teeth; the pressure of the accumulated pus can generate a sinus tract to the surface of the skin or to the oral or nasal cavity.

The most important route of pulp invasion is through the tubules of carious dentin. This may take place even before the pulp is exposed directly to the oral environment by cavitation. The bacteria that penetrate the dentin prior to cavitation are mostly facultative anaerobes and include streptococci, staphylococci, lactobacilli, and filamentous microorganisms.⁵

After the pulp becomes necrotic, bacteria can proceed through the necrotic root canal tissue, and inflammation (apical periodontitis) develops in the periapical area.

The organisms that predominate in this stage of the infection are Prevotella, Porphyromonas, Fusobacterium, and Peptostreptococci. However, the primary microorganism causing pulpitis is difficult to determine because of the technical difficulties associated with obtaining samples for culturing, and because the exact time of the initial infection is difficult to ascertain.

Diagnosis

The symptoms of acute suppurative pulpitis include low-grade fever, pain, soreness of the tooth, and facial swelling. Pain is usual induced by hot liquids, a reaction believed to be caused by expansion of gases produced by gas-forming bacteria trapped inside the root canal. Sampling from the root canal for recovery of organisms, before treatment, during treatment and at the end of therapy to insure eradication of the infection is useful, and can differentiate between infectious and non-infectious pulpitis.

The patient may experience intense pain that may be difficult to localize. It may be referred to the opposite mandible or maxilla or to areas supplied by common branches of the fifth cranial nerve. X-rays, pulp testers, percussion, and palpation are helpful aids in confirming the diagnosis.

Treatment

Cleansing of the cavity to remove debris and packing the cavity with zinc oxide-eugenol cement usually will afford relief in early pulpitis. Once pulpitis developed the infected pulpal tissue should be removed and root canal therapy instituted, or the tooth should be extracted.

Antimicrobial therapy supplementing the dental care should be considered, especially when local or systemic spread of the infection is suspected. Penicillin or amoxicillin are generally effective against most of the aerobic and anaerobic bacteria recovered. However, a growing number of patient harbor penicillin-resistant organisms and should be considered for treatment with drugs effective against these organisms. These agents include amoxicillin-clavulanate, clindamycin or the combination of metronidazole plus amoxicillin or a macolide.⁶

DENTOALVEOLAR ABSCESS

An alveolar or apical abscess may be either acute or chronic. The acute alveolar abscess is an extension of necrotic or putrescent pulp into the periapical area, which induces bone and tissue necrosis and accumulation of pus. It may also occur after trauma to the teeth or from periapical localization of organisms. As the abscess growth, more tissue may be involved, including adjacent teeth, and the pressure within the abscess may produce a fistula to the gingival surface or to the oral or nasal cavities.⁷

Dental abscess

Microbiology

Anaerobic bacteria were recovered from most cases of dentoalveolar abscesses that were cultured using proper methods for their isolation.⁴ Studies done at the turn of the century of acute and chronic alveolar abscesses described the recovery of predominantly aerobic streptococci; however, fusiform bacilli and Bacteroides spp. were found in some abscesses, sometimes in pure culture. ⁴ More recent studies report the isolation of a variety of anaerobes in periodontal abscesses, including anaerobic cocci, anaerobic Gram-negative bacilli, and anaerobic Gram-positive bacilli. ⁴ The microflora associated with dentoalveolar abscesses was also recently determined and characterized by molecular methods.⁸ A quantitative and qualitative study of 50 dentoalveolar abscesses reported the presence of 3.3 isolates per abscess.⁹ Twenty (40%) abscesses harbored anaerobes only, and 27 (54%) abscesses had a mixture of both aerobes and anaerobes. Three fourths of the isolates were strict anaerobes, the most common Peptostreptococcus spp., Prevotella oralis, and Prevotella melaninogenica.

Anaerobes were the predominant isolates, outnumbering aerobes eight to one in periodontal abscesses in 12 children.¹⁰ Anaerobes were recovered in all patients; in two thirds of the patients, they were the only organism isolated, and in the rest they were mixed with aerobes. There were 53 anaerobic isolates (4.4/specimen), 20 Gram-negative bacilli (including nine P. melaninogenica, three P. oralis), 17 anaerobic Gram-positive cocci, 5 Fusobacterium spp., and 3 Actinomyces spp. There were 6 aerobic isolates (0.5/specimen), 3 S. salivarius,2 alpha-hemolytic streptococci, and one gamma-hemolytic Streptococcus. Beta-lactamase production was noticed in 4 isolates 3 P. melaninogenica, and one P. oralis.

Brook et al ¹¹ who studied 39 periapical abscesses detected bacterial growth 32 specimens. A total of 78 bacterial isolates (55 anaerobic and 23 aerobic and facultative) were recovered (2.4 isolates/specimen). Anaerobic bacteria only were present in 16 (50%) patients, aerobic and facultatives in 2 (6%), and mixed aerobic and anaerobic flora in 14 (44%). The predominant anaerobic isolates were Gram-negative bacilli (23 isolates, including 13 Pigmented Prevotella and Porphyromonas spp.), Streptococcus spp. (20), anaerobic cocci (18), and Fusobacterium spp. (9). Beta-lactamase-producing organisms were recovered from 7 of the 21 (33%) tested specimens.

Similar organisms were isolated from aspirate of pus from 5 periapical abscesses of the upper jaw and their corresponding maxillary sinusitis. ¹²  Polymicrobial flora were found in all instances, where the number of isolates varied from 2 to 5. Anaerobes were recovered from all specimens. The predominant isolates were Prevotella spp., Porphyromonas spp., Fusobacterium nucleatum, and Peptostreptococcus spp. Concordance in the microbiological findings between periapical abscess and the maxillary sinus flora was found in all instances. However, certain organisms were only present at one site and not the other.

Diagnosis

An abscess can be focal or diffuse and present as red tender fluctuant gingival swelling. Pain from an acute abscess usually is intense and continuous. The involved tooth is painful when percussed. Hot or cold foods may increase the pain.

A chronic periapical abscess presents few clinical signs, since it is essentially a circumscribed area of mild infection that spreads slowly. In time, the infection may become granulomatous. Radiographic studies of the involved tooth can be helpful, and free air eventually can be observed in the tissues.

 X ray of a dental  abscess

Complications

Complications can occur by direct extension or hemotogenous spread. If treatment is delayed, the infection may spread directly through adjacent tissues, causing cellulitis (phlegmona), varying degrees of facial edema, and fever. The infection may extend into osseous tissues or into the soft tissues of the floor of the mouth. Local swelling and gingival fistulas may develop opposite the apex of the tooth, especially with deciduous teeth.

Serious complications from periapical infections are relatively. The infection can spread to tissues in other portions of the oral cavity, causing submandibular or superficial sublingual abscesses; abscesses may be produced also in the submaxillary triangle or in the parapharyngeal or submasseteric space.¹³

In the maxilla, periapical infection may affect only the soft tissues of the face, where it is less serious. It may extend, however, to the intratemporal space including the sinuses and then to the nervous system, where it can cause serious complications such as subdural empyema, brain abscess, or meningitis.^4,14

Other potential complications include mediastinitis, suppurative jugular thrombophlebitis (Lemierre Syndrome), maxillary sinusitis, carotid artery erosion, and osteomyelitis of the mandible and maxilla.^{15, 15a}

The finding of anaerobic bacteria in periodontal abscesses is of importance because of the association of anaerobes with many serious infections arising from dental foci, such as bacteremia, endocarditis, sinusitis, meningitis, subdural empyema, brain abscess, and pulmonary empyema. The spread of dental infections into the central nervous system via the sinuses has been documented.^4,15

Intracranial suppuration following tooth extraction or dental infection is an uncommon but extremely serious complication. Intracranial infections of buccodental origin may evolve cavernous sinus thrombosis, at times associated with brain abscess or subdural empyema.^4,16 Isolated brain abscesses occur much less frequently, and subdural empyema of odontogenic origin is quite rare. Infections of the molar teeth are more likely to cause intracranial complications because pus arising in the back of the jaw tends to collect between the muscles of mastication and spread upward in the fascial planes, whereas infection arising in the front of the jaw has free access to the oral cavity.¹⁷

Management

Extraction or root canal therapy and drainage of pus usually are indicated. Antibiotic prophylaxis is recommended if extraction or drainage is contemplated in patients at risk of developing endocarditis. Penicillin and erythromycin have been used. However, although the incidence of bacteremia caused by aerobic and anaerobic oral flora is reduced by such therapy, antimicrobial therapy does not prevent it.¹⁸ If high fever persists, antibiotics should be administered. Antibiotic should also be given if drainage is not adequate or when the infection perforates the cortex and spread into surrounding soft tissue. Most of the aerobic and anaerobic pathogens isolated from the abscesses are sensitive to penicillin. Some strains of Fusobacterum and pigmented Prevotella and Porphyromonas recovered from patients with periodontal abscesses may be resistant to penicillin, however.¹⁹ In patients who require therapy, the recovery of these penicillin-resistant organisms may require the administration of antimicrobial agents also effective against these organisms. These include clindamycin, chloramphenicol, cefoxitin a combination of a penicillin and a beta-lactamase inhibitor or a carbapenem.³¹ Metronidazole should be administered with an agent effective against the aerobic or facultative streptococci. Although the need for judicious selection of antimicrobial agents must be emphasized, it is essential to note that the treatment of periapical abscess may require surgical intervention and that surgical drainage of these cases is, therefore, an integral part of the management.

GINGIVITIS AND PERIODONTITIS

Pathogenesis and complications

The healthy gingiva is a pink, keratinized mucosa, attached to the teeth and alveolar bone, that forms the interdental papilla between the teeth. A 1-2 mm deep cervice of free gingiva surrounds each tooth. The gingival cervice is heavily colonized by anaerobic Gram-negative bacilli and spirochetes.

Periodontal disease is a term referring to all diseases involving the supportive structures of the teeth (periodontium). It most commonly begins as gingivitis and progresses to periodontitis. How rapidly these infections progress depends on the type of bacteria present and the resistance and self-care of the patient. Although children are more resistant to gingivitis as compared to adults, it is the most common periodontal disease during childhood and peaks in adolescence.²¹

The host response to the inflammation varies and depends on many factors including the type of the bacterial insult and it’s duration, the local and environmental contributing factors, immunological and inflammatory responses, predisposing genetic factors, and association with systemic diseases.²²

 ^Gingivitis

Purulent gingival pockets or gingival abscesses may complicate periodontal disease. Gingivitis results from accumulation of plaque and bacteria in the gingival crevice. Gingivitis is an inflammation of the gingivae, characterized by swelling, redness, change of normal contours, and bleeding. Swelling deepens the crevice between the gingivae and the teeth, forming gingival pockets. Although the patient usually experiences no pain, a mild foul smell may be noticed.^21,23,24 Gingivitis may be acute or may be chronic with remissions and exacerbations.

Peridontitis

Subgingival plaque is associated with periodontal diseases. The bacteria that colonize the area are primarily anaerobic. Both Gram-negative and Gram-positive species are regularly isolated. Most of these bacteria utilize protein and other nutrients provided in the subgingival environment by the gingival fluid. Once established in the subgingival areas, periodontal infections usually drain into the oral cavity via a periodontal pocket. If the drainage of the periodontal pocket is obstructed, an acute process results.

Abscess formation is usually limited to the alveolar process. In some cases, spread to adjacent spaces may be noted. Focal or diffuse periodontal abscesses can develop. They appear as red fluctuant swelling of the gingiva or mucosa, which are tender. As the underlying tissues are affected, a complete destruction of the periodontium occurs, with subsequent loss of teeth.

Dental abscess

Aspiration pneumonia and lung abscess can develop as a complication of gingival disease, especially in individuals with poor dental hygiene. This has been noted especially following aspiration of the contents of a spontaneously drained periodontal abscess, in the neurologically impaired, who constantly aspirate their oral secretions and in those with gingivitis associated with Dilantin therapy.25

Epidemiological studies have indicated that untreated periodontal disease could be a risk factor to preterm delivery of low birth infants, coronary heart disease, and cerebral vascular accidents. This is explained by the production of lipopolysaccharides, heat-shock proteins, and proinflammatory cytokines by the anaerobic Gram negative bacilli that cause periodontal disease. ²⁶

Classification and manifestations of periodontal diseases

Until recently, the accepted standard for the classification of periodontal diseases was the one agreed upon at the 1989 World Workshop in Clinical Periodontics. This classification system, however, had its weaknesses as some of the criteria for diagnosis were unclear, disease categories overlapped, and patients did not always fit into any one category. Additionally, over emphasis was placed on the age of disease onset and the rate of progression, which are commonly difficult to determine. In 1999, an International Workshop for a Classification of Periodontal Diseases and Conditions was created by the American Academy of Periodontology to revise the classification system.²⁷ (Table 2)

Gingivitis: The most fulminate form of gingivitis is nercotizing ulcerative gingivitis (NUG) (previously called-acute nercotizing ulcerative gingivitis, "trench mouth" or "Vincent's infection") It is a very painful, fetid, ulcerative disease that occurs most often in persons under severe stress with no or very poor oral hygiene. It is manifested by acutely tender, inflamed, bleeding gums associated with the interdental papillae necrosis and loss. Halitosis and fever are often present. Microbiological examinations of the bacterial biofilms found in NUG revealed high numbers of spirochetes and fusobacteria. ^28-30

        Another form of fulminate gingivitis is acute streptococcal gingivitis.  It is caused by Group A beta-hemolytic streptococci ( Streptococcus pyogenes) and is generally associated with acute streptococcal tonsillitis.

Periodontitis: Periodontitis often develops as a progression of gingivitis to the point that loss of supporting bone has begun because of destruction of alveolar bone. Tooth mobility, bleeding gingivae, and increased spaces between the teeth are common but are not necessarily signs of advanced disease. In some cases purulent exudate is present. Periodontal infection tends to localize to intraoral soft tissue but can spread to adjacent sites.

The two main forms of periodontitis are chronic and aggressive periodontitis (Table 2).

Chronic periodontitis ( replaced adult periodontitis ) occurs mostly in adults, but can be also seen in younger individuals.  Destruction is consistent with the amount of plaque present and other local factors (i.e., anatomic and other factors that retain plaque next to a tooth such as overhanging restorations, open contacts and palato-radicular grooves); subgingival calculus is also commonly found. The disease progresses slowly but there may be bursts of destruction. Local factors, systemic diseases and extrinsic factors such as smoking can modify the rate of disease progression. 

        Chronic periodontitis has been further classified as localized or generalized depending on whether < 30% or > 30% of sites are involved. Severity is based on the amount of clinical attachment loss (CAL) and is designated as slight (1-2 mm CAL), moderate (3-4 mm CAL) or severe (> 5 mm CAL).     

          Aggressive periodontitis ( replaced early onset, destructive and juvenil periodontitis ) is diagnosed based on clinical, radiographic and historical findings which show rapid attachment loss and bone destruction, and possible familial aggregation of disease. Except for periodontal disease, patients are healthy. Other features that may be present are periodontal tissue destruction that is greater than would be expected given the level of local factors.

Aggressive peridontitis

Microbiology (table1)

Gingivitis: The healthy gingival sulcus contains relatively few organisms, usually Streptococci and Actinomyces. The development of gingivitis is associated with a significant increase in Gram negative anaerobes (F.  nucleatum, P. intermedia and Bacteroides spp.), spirochetes and motile rods.

NUG is known to be caused by synergistic infection between unusually large spirochetes and fusobacteria,^28-30 which are part of the normal oropharyngeal flora. Loesche et al.²⁹ found that the bacteria associated with the infection are fairly constant and include oral Treponemes and Selenomonas spp., which represent these Spirochete and Spirochete-like organisms, and P. intermidia and Fusobacterium spp.

      
 Periodontitis: All forms of periodontitis are polymicrobial aerobic-anaerobic bacterial infection. Periodontal disease develops usually because of two events in the oral cavity: an increase in bacterial quantity of anaerobic Gram negative bacteria and a change in the balance of bacterial types from harmless to disease causing bacteria. sease-causing bacteria. Among the bacteria most implicated in periodontal disease and bone loss are Actinobacillus actinomycetemcomitans and P. gingivalis. Other bacteria associated with periodontal disease are B. forsythus , T.denticola, T. sokranskii and P. intermedia .^21,31

          
Bacteria listed in Table 1 have been implicated in chronic periodontitis.  Those most prevalent can be identified with cultures and DNA probes.  These include  P. intermedia, B. forsythus, Actinomyces spp. , Capnocytophaga , and Peptostreptococcus micros.

        
Examinations of subgingival biofilms with a phase contrast microscope can be helpful with patient education and motivation and with follow-up. Following the prevalence of spirochetes provides insight into patient compliance and the adequacy of their self-care. The microorganisms involved are generally acquired from another person’s saliva, possibly over a period of years, and the self-care the patients have used has not controlled them.


Aggressive periodontitis is now recognized as a contagious infection that can be passed between family members. A. actinomycetemcomitans and P. gingivalis, are believed to play a major role in this infection.
       

The role of anaerobic organisms in this infection is strengthened by the finding of elevated levels of serum IgG antibodies specific for these organisms in patients with periodontitis.³² This immunoserologic observation is strongly supportive of several bacteriologic studies^33,34 that have indicated that P. gingivalis is a predominant isolate from advancing chronic periodontitis lesions. Several oral anaerobes and streptococci including P. gingivalis, P. intermedia, P. melaninogenica, Capnocytophaga spp; S. sanguis and Streptococcus mitis, produce IgA proteases,³⁵ that may impair local immunity.

Management

Gingivitis: Treatment of gingivitis involves removing dental plaques and maintaining good oral hygiene. Personal plaque/calculus control and professional debridement, oral hygiene care, correction of plaque retentive sites, and if these are unhelpful, chlorhexidine gluconate 0.12% mouthwash or baking soda plus hydrogen peroxide rinses should be used.

       
Antibiotics are generally not recommended for gingivitis. The types of gingivitis that require systemic antimicrobial therapy include streptococcal gingivitis and NUG .

      
Local and systemic antimicrobials are used in the therapy of NUG. Some of the agents that can be used topically in the dental office include a 3% solution of hydrogen peroxide mixed with sodium bicarbonate, and a 0.12 % solution of chlorhexidine gluconate. Systemic antibiotic therapy is very beneficial because it provides continuous bacterial control.(Table 3)

Priodontitis therapy of chronic periodontitis  should include debridement and thorough scaling and root planing to remove the subgingival and supergingival deposits of calculus and plaque (bacterial biofilm) are first-line interventions.^21,36   When pockets are more than 5 mm deep, local therapy rarely adequately suppresses the involved pathogens. Therefore, subgingival irrigation to disinfect the gingival crevices can be accomplished with the use of either ultrasonic scalers or individual irrigating syringes. Effective antiseptic solutions are povidone iodine, chlorhexidine, chloramine-T, or salt water. Helpful measures may include twice-daily rinsing with chlorhexidine-gluconate 0.12% mouthwash, brushing with a mixture of baking soda plus hydrogen peroxide, and/or frequent salt-water rinses. Local therapy with antimicrobial delivery systems is to be considered as adjunctive therapy and not as an alternative to instrumentation. Since there is negligible calculus and firm plaque in aggressive periodontitis , traditional scaling and root planing is not needed. Pockets may be irrigated with an antibacterial solution and the patient receives systemic antibiotics (Table 3).

The use of systemic antimicrobials is especially indicated in aggressive periodontitis and is sometimes needed in chronic periodontitis (Table 3). Appropriate systemic antibiotic regimens should be based on culture and susceptibility testing of the subgingival flora whenever possible. Cultures should also be taken after therapy to insure eradication of pathogens. 


Periodontal Abscess: Treatment includes drainage of pus and debridement. Antimicrobial therapy is necessary whenever local or systemic spread occurs (Table 3). Extraction of the involved tooth may be needed if antimicrobial therapy fails. 

General guidelines for use of antimicrobial agents: Periodontal infections are generally mixed anaerobic and facultative anaerobic infection. Identifying the causative organisms in the subgingival flora and determining their antimicrobial susceptibility is helpful in selecting the proper antimicrobial therapy. Identification can be done by culture or DNA probing methods.³⁴ Cultures should be also taken after therapy to insure eradication of pathogens.

      

Antimicrobials utilized in odontogenic infections can be divided into broad and narrow spectrum.

Many patients can be treated with narrow spectrum antimicrobials. However, two categories of patients need to be treated with broad spectrum antimicrobials to prevent failure and complications: patients infected by resistant bacteria, ^37,38 and those with underlying serious medical conditions or are suffering from a severe dental infection.  The risk factors for failure of narrow spectrum agents are listed in Table 4.

Narrow spectrum antimicrobials include penicillin, amoxicillin , cephalexin, the macrolides ( erythromycin, clarithromycin and azithromycin) and the tetracyclines ( including doxycycline ). These agents have a limited antimicrobial efficacy as they are not effective against aerobic and anaerobic betal-lactamase producers as well as other specific organisms. 

Broad spectrum antimicrobials or antimicrobial combinations include clindamycin, and the combination of a penicillin ( i.e. amoxicillin ) plus a beta-lactamase inhibitor ( i.e. clavulanate ), and the combination of metronidazole plus penicillin, amoxicillin or  a macolide. ²⁰ These possess a broad spectrum of activity against most odontogenic pathogens  including aerobic and anaerobic betal-lactamase producers. Furthermore some of these agents ( clindamycin and amoxicillin-clavulante ) provide better pharmacokinetic and pharmacodynamic indexes against the odontogenic pathogens compared to the other agents. ^37,38  Pharmacokinetic and pharmacodynamic indexes of each antimicrobial can predict their clinical efficacy by considering their concentrations at the site of the infection and the susceptibility of the pathogens.

The choice between broad and narrow spectrum antimicrobials should be individualized in each patient. Utilization of broad spectrum antimicrobial can insure efficacy against all potential pathogens especially those resist to antimicrobials.

       Anti-infectives should be given a chance to work. Improvement may take time and therefore therapy should not be changed until it is given for at least 48-72 hours.

An antimicrobial need to be taken for sufficiently time to be successful. The short-term use of an anti-infective, effective as it may be, may not produce long-term results because the patient may become re-infected.

PERICORONITIS

Pericoronitis is an infection of the pericoronal soft tissue associated with gum flaps (opercula) that partially overlie the crown of the tooth. The teeth most often involved are the third mandibular molars. The infection is caused by microorganisms and debris that become entrapped in the gingival pocket between the tooth and the overlying soft tissue. If the overlying soft tissue becomes swollen, the drainage is obstructed and inflammatory exudate is entrapped and will spread to other anatomical sites. Pericoronitis is usually accompanied by swelling of the soft tissues and marked trismus. However, the underlying alveolar bone is not usually involved. In most cases, antibiotic treatment is necessary to avoid spread of the infection. The microorganisms most often isolated from acute pericoronitis are anaerobic cocci, Fusobacteria spp. and anaerobic gram negative bacilli.³⁹  

Pericoronitis 

Treatment of pericoronitis also includes gentle debridement and irrigation under the tissue flap. Excision of the gum flap may be considered. Antibiotics and incision and drainage may be needed if fascial plains cellulitis develops.

REFERENCES

1.   Rolph H.J., Lennon A., Riggio M.P.,. Saunders W.P,. MacKenzie D, Coldero L., Bagg J., Molecular identification of microorganisms from endodontic infections. Journal of Clinical Microbiology 39: 3282–3289, 2001.

2.   Liljemark W.F., Bloomquist C.: Human oral microbial ecology and dental caries and periodontal diseases. Crit Rev Oral Biol Med. 7:180-98. 1996.

3.   Siqueira J.F. Jr, Rocas I.N. PCR methodology as a valuable tool for identification of endodontic pathogens. J Dent. 2003 ;31:333-9.

4.   Socransky S.S., Haffajee A.D., Cugini M.A., Smith C., Kent, Jr R.L, Microbial complexes in subgingival plaque. Journal of Clinical Periodontology 25:134–144.1998.

5.   Siqueira Junior JF. Aetiology of root canal treatment failure: why well-treated teeth can fail.  Int. Endod. J.  ;34:1-10,2001.
5a. McClelland S, Hall WA. Postoperative central nervous system infection: incidence and associated factors in 2111 neurosurgical procedures. Clin Infect Dis;45:55-9.2007.

6.   Kinder, S.A., Holt S.C, Korman K.S.: Penicillin resistance in the subgingival microbiota associated with adult periodontitis. J. Clin. Microbiol. 23:1127-33, 1986.

7.   Johnson B.R., Remeikis N.A., Van Cura J.E. Diagnosis and treatment of cutaneous facial sinus tracts of dental origin. J Am Dent Assoc  ;130:832-6, 1999.

8.   Dymock, D., Weightman A.J., Scully C., Wade W.G.: Molecular analysis of microflora associated with dentoalveolar abscesses. J. Clin. Microbiol. 34:537-42, 1996.

9.   Lewis, M.A.O., MacFarlane, T.W., McGowan, O.A.: Quantitative bacteriology of acute dentoalveolar abscesses. J. Med. Microb. 21:101-4, 1986.

10. Brook, I., Grimm, S., Kielich, R.B.: Bacteriology of acute periapical abscess in children. J. Endodontics 7:378-80, 1981.

11. Brook, I., Frazier EH, Gher ME.: Aerobic and anaerobic microbiology of periapical abscess. Oral. Microbiol. Immunol. 6:123-5, 1991.

12. Brook, I., Frazier E..H, Gher M.E. Jr.: Microbiology of periapical abscesses and associated maxillary sinusitis. J Periodontol  ;67:608-10, 1996.

13. Brook, I., Friedman E.M., Rodriguez W.J., Controni G.: Complications of sinusitis in children. Pediatrics 66:568-72, 1980.

14. Brook, I., Friedman E.: Intracranial complications of sinusitis in children - a sequela of periapical abscess. Ann. Otol. Rhinol. Laryngol. 91:41-3, 1982.

15. Brook,I. Brain abscess in children: microbiology and management.J. Child. Neurol. ;10:283-8.1995. 
15a.Dixon, O.J.: Dental infection as a cause of cavernous sinus thrombosis. Dental Cosmos 71:121, 1929.

16. Corson M.A, Postlethwaite K.P., Seymour R.A.: Are dental infections a cause of brain abscess? Case report and review of the literature. Oral Dis  ;7:61-5, 2001.

17. Colville A., Davies W., Heneghan M., Goodwin A., Griffiths T.: A rare complication of dental treatment: Streptococcus oralis meningitis.  Br. Dent. J.21;175:133-4,1993.

18. Josefsson, K., Heimdahl A., von Konow L., Nord C.E.: Effect of phenoxymethyl-penicillin and erythromycin prophylaxis on anaerobic bacteremia after oral surgery. J. Ant. Chemoter. 16:243-51, 1985.

19. Brook, I., Calhoun, L.,  Yocum, P.: Beta lactamase producing isolates of Bacteroides species for children. Antimicrob. Agents Chemother. 18:164-6, 1980.
20. Brook I , Douma M. Antimicrobials Therapy Guide for the Dentist. Handbooks in Health Care Co. Newtown, Pennsylvania. 2004.

21 Oh TJ, Eber R, Wang HL.: Periodontal diseases in the child and adolescent.

 J Clin Periodontol; 29:400-10, 2002.

      22. Van Dyke TE, Tohme ZN. Periodontal diagnosis: evaluation of current concepts and future needs. J Int Acad Periodontol. 2:71-8, 2000.

     23. Loesche, W.J.: Bacterial mediators in periodontal disease. Clin. Infect. Dis. 16:S203-10, 1993.

     24. Kureishi, K., Chow, A.W.: The tender tooth-dentoalveolar, pericoronal, and periodontal infections. Infect. Dis. Clin. North Am. 2:163-82 , 1988.

25. Brook, I., Finegold, S.M.: Bacteriology of aspiration pneumonia in children. Pediatrics 65:1115-20, 1980.

26..Loesche W.J. Association of the oral flora with important medical diseases. 

       Curr Opin Periodontol. 4:21-8,1997.

       27. 1999 International Workshop for Classification of Periodontal Diseases and Conditions.         Ann Periodontol. 4:, 1-112,1999.

       28. Stammers, A.F.: Vincent's infection: observations and conclusions regarding the aetiology and treatment of 1017 civilian cases. Br. Dent. J. 76:147-53, 1944.

29. Loesche, W.J., Syed SA, Laughon BE, Stoll J..: The bacteriology of acute necrotizing ulcerative gingivitis. J. Periodont. 53:223-30, 1982.

30. Socransky, S.S., Haffajee, A.D.: Evidence of bacterial etiology: a historical perspective. Periodontol 2000 5:7-25, 1994.

31.  Darby I, Curtis M.. Microbiology of periodontal disease in children and young adults. Periodontol. 2000; 26:33-53 , 2001.

32. Kinane DF, Mooney J, Ebersole JL.: Humoral immune response to Actinobacillus actinomycetemcomitans and Porphyromonas gingivalis in periodontal disease. Periodontol 2000;20:289-340 ,1999.

33. Slots, J.: Microbial analysis in supportive periodontal treatment. Periodontol 2000.;12:56-9. 1996.

34. Conrads G. DNA probes and primers in dental practice. Clin Infect Dis  1;35(Suppl 1):S72-7, 2002.

35. Gronbaek Frandsen E.V.: Bacterial degradation of immunoglobulin A1 in relation to        periodontal diseases. APMIS Suppl. 87:1-54, 1999.

36. Slots J, Ting M. Systemic antibiotics in the treatment of periodontal disease. Periodontol 2000; 28:106-76, 2002.

37. Heimdhal, A., Von-Konow, L., Nord, C.E.: Isolation of beta-lactamase producing Bacteroides strains associated with clinical failures with penicillin treatment of human orofacial infections. Arch. Oral. Biol. 25:689-92, 1980.

38.  Brook, I.: Beta-lactamase-producing bacteria recovered after clinical failure with various penicillin therapy. Arch. Otolaryngeal 110:228-31, 1984.

39.  Rajasuo, A., Jousimies-Somer, H., Savolainen, S., Leppanen, J., Murtomaa, H., Meurman, J.H.: Bacteriologic findings in tonsillitis and pericoronitis. Clin. Infect. Dis. 23:51-60, 1996.

Table 1. Microorganisms Associated with Periodontal Infections

Aerobic and Facultative anaerobic

Anaerobic

I. Gram-positive cocci         Streptococcus spp.         Beta-hemolytic streptococci         Streptococcus milleri group (viridans)         Streptococcus mutans group II. Gram-positive bacilli         Rothia dentcocariosa         Lactobacillus spp. III. Gram-negative cocco-bacilli         Actinobacillus spp.         Actinobacillus              actinomycentemcomitans†         Campylobacter spp.         Campylobacter rectus         Capnocytophaga spp.         Eikenella spp. IV. Gram-negative rods          Pseudomonas spp.‡          Enterobactericeae‡

I.   Gram-positive cocci         Peptostreptococcus spp.         Peptostreptococcus micros II.  Gram-negative bacilli         Veillonella spp. III. Gram-positive bacilli         Actinomyces spp.         Eubacterium spp.         Propionibacterium spp.         Lactobacillus spp. IV.  Spirochetes           Treponema denticola           Treponema sokranskii V.   Gram-negative bacilli          Prevotella spp.          Prevotella intermedia          Prevotella nigrescens          Porphyromonus spp.          Porphyromonus gingivalis          Bacteriodes spp.          Bacteriodes forsythus          Fusobacterium spp.          Fusobacterium nucleatum          Selemenomas sputigena

† = Common in juvenile periodontitis.

‡ = Rare.

Table 2: Outline of the 1999 Classification of periodontal Disease. ²⁷

1.    Gingival Disease

• Dental Plaque-Induced
• Non-Plaque-Induced

2.    Chronic Periodontitis*¶

• Localized
• Generalized (>30%of Sites Involved)

3.    Aggressive Periodontitis‡

• Localized
• Generalized (>30%of Sites Involved)

4.    Periodontitis Associated with Systemic Diseases ( Hematological, Genetic and    Other)

5.    Necrotizing Periodontal Diseases ( Necrotizing Ulcerative Gingivitis or Periodontitis)

6.    Abscesses of the Periodontium (Gingival, Periodontal and Pericoronal )

7.    Periodontal Diseases associated with Endodontic Lesions (Combined)

8.    Developmental or Acquired Deformities and Conditions (including Trauma)

* Can be further classified on basis of extent and severity

‡  Aggressive periodontitis replaced early onset, destructive and juvenile periodontitis

        

¶  Chronic periodontitis replaced adult periodontitis   

DEEP AND INVASIVE INFECTIONS

Anaerobic bacteria are part of the normal oral flora and outnumber aerobic organisms by a ratio of 1:10 at this site, and therefore predominant in dental infections. There are at least 264 distinct bacterial groups or species that colonize the oral and dental ecologic sites.¹ In the gingival crevice, there are approximately 1.8 ´ 10¹¹ anaerobes/gram. Most odontogenic infections result initially from the formation of dental plaque. Once pathogenes become established, they can cause local and disseminated complications including endocarditis, infection of orthopedic or other prosthesis, pleuropulmonary infection, cavernous sinus infection, septicemia, maxillary sinusitis, mediastinal infection, and brain abscess. 

The organisms most commonly isolated in dental infections are anaerobic streptococci, Cupnocytophaga, Actinobacillus, fusobacteria, Prevotella and Porphyromonas.² Porphyromonas gingivalis and Prevotella intermedia appear to be the most frequently isolated from periodontal lesions.

 VINCENT'S INFECTION

This infection, sometimes called trench mouth, Vincent's infection, or acute necrotizing ulcerative gingivitis, occurs at the gingival papillae between the teeth.

Pathogenesis

Poor oral hygiene, physical or emotional stress, nutritional deficiencies, blood dyscrasias, debilitating diseases, and insufficient rest may predispose to this disease. Vincent's infection may also be seen in patients who are debilitated by conditions such as diabetes, Down's syndrome, or malnourishment.

Microbiology

This condition is known to be caused by synergistic infection between unusually large spirochetes ( Treponemes and Selenomonas sp.), and fusobacteria, which are part of the normal oropharyngeal flora.⁴

Symptoms

Symptoms include, abrupt onset, malaise, regional lymphadenopathy, gum bleeding, blunting and cratering of the interdental papillae, fetid breath, pain, numbness, marginal gingivae and interdental papillae ulcerations (with a characteristic necrotic punched-out appearance and covered by a grayish membrane and bleed on slight pressure or irritation ). Swallowing and talking may be painful. Lesions on the buccal mucosa are rare but may appear as diffuse ulcerations covered with an easily removed pseudomembrane. Rarely, lesions may occur on the tonsils, pharynx, bronchi, rectum, or vagina.

Vincent's infection

Diagnosis

The presence of overwhelming numbers of fusospirochetal forms in stained smears from the lesions confirms the diagnosis. Early differentiation from diphtheria or agranulocytosis is essential when the tonsillar or pharyngeal tissues are involved. Streptococcal or staphylococcal pharyngitis and herpetic stomatitis must be considered .

Management

Gentle debridement, good oral hygiene, adequate nutrition, and rest are essential. Rinsing the mouth with warm normal saline or 3% peroxide solution may be helpful. Analgesics may be required after initial debridement. Therapeutically, the various drugs that are active against anaerobes in general, including penicillin G, are effective in the management of Vincent's angina. Other anti-microbial agents used successfully in the treatment of this infection include clindamycin, or metronidazole and erythromycin.⁵

DEEP FASCIAL SPACE INFECTIONS

Odontogenic infections may extend to fascial spaces of the lower head and upper neck. These space infections can be divided into those around the face (masticator, buccal, cannine, and parotid), the suprahyoid area (submandibular, sublingual, with lateral pharyngeal), with those in the infrahyoid region or lateral neck (retropharyngeal, and pretracheal spaces).⁶ If penetration of the infection occurs above the attachment of the buccinator muscle on the mandible or below the attachment in the maxilla, the pus will drain intraorally. However, penetration above or below these attachments will result in extraoral drainage.

Masticator spaces

Masticator spaces include the masseteric, pterygoid, and temporal spaces, which communicate with each other as well as with the buccal submandibular and lateral pharyngeal spaces, allowing spread of the infection. The molar teeth, especially the third molar, are frequently the source of infection. Patients usually present with trismus and pain in the mandible. Swelling is not always apparent. The infection may spread internally, pressing the lateral pharyngeal wall and causing dysphagia. Deep temporal space infections generally originate from posterior maxillary molars. As the infection progresses, the swelling increases, involving the cheeks, eyelids, and side of the face. Management includes surgical drainage and antimicrobial therapy.

Buccal, canine, and parotid spaces

Buccal space infections generally originate from an intraoral extension of the bicuspid or molar teeth infection. This type of infection is characterized by marked cheek swelling with minimal trismus and systemic symptoms. Often, antimicrobial therapy alone is sufficient. Extraoral superfical drainage may be needed.

Canine space infections generally follow maxillary incisor involvement. The typical swelling involves the upper lip, canine fossa, and periorbital tissues. Extension into the maxillary sinuses may occur. Intraoral surgical drainage and antibiotic therapy are advocated.

Parotid space infections are generally a sequela of masseteric space infection and are characterized by swelling of the angle of the jaw, pain, fever, and chills. These infections have the potential of direct extension into the posterior mediastinum and visceral spaces.

Submandibular and sublingual spaces

Infection of the submandibular and sublingual spaces usually arises from the second and third mandibular teeth. Swelling and minimal trismus are generally present. Sublingual space infection usually originates from the mandibular incisors and is characterized by a brawny, erythematous, tender swelling of the floor of the mouth. In the later stages, tongue elevation may also be noted.

The classic Ludwig's angina involves a bilateral infection of both the submandibular and sublingual spaces.⁷ A dental source of the infection usually can be found in most patients, and the second and third mandibular molars are often involved. The infection begins in the floor of the mouth and is a rapidly spreading, indurating cellulitis that often induces abscess formation or lymphatic involvement. The clinical presentation includes a brawny, board like swelling of the mandibular spaces that does not pit on pressure and general toxicity. The mouth is usually held open, and the floor is elevated, which pushes the tongue upward. Eating, swallowing, and respiring may be impaired. Rapid progression can cause neck and glottis edema, which precipitates asphyxiation.

A wide range of microorganisms has been isolated from cases of Ludwig's angina. Anaerobic bacteria predominate, including Fusobacteria spp., Gram negative bacilli, spirochetes and anaerobic cocci. Other organisms include: staphylococci, streptococci, pneumococci, Escherichia col, Haemophilus influenzae, and Candida albicans. Treatment includes high doses of parenteral antibiotics, airway monitoring, early intubation or tracheostomy, soft tissue decompression, and surgical drainage.⁸

Lateral pharyngeal space

The lateral pharyngeal space is continuous with the carotid sheath. Involvement may follow pharyngitis, tonsillitis, parotitis, otitis and odontogenic infection. Anterior compartment involvement is characterized by chills, fever, pain, tremors, and swelling below the angle of the jaw. Posterior compartment infection is characterized by septicemia, with few local signs. Other complications include edema of the larynx, asphyxiation, internal jugular vein thrombosis, and internal carotid artery erosion. Close observation is mandatory and tracheostomy may be needed. Surgical drainage and parenteral antibiotic therapy are needed.

Retropharyngeal and pretracheal spaces

The retropharyngeal space includes the posterior part of the visceral compartment in which the esophagus, trachea, and thyroid gland are enclosed by the middle layers of deep cervical fasci, which extend into the superior mediastinum. Infection of this space may result from direct extension of a pharyngeal space infection or through lymphatics from the nasopharynx. The onset is insidious, although dyspnea, dysphagia, nuchal rigidity, fever, and chills may be present. Posterior pharyngeal wall bulging may be present. Soft tissue radiography or CT scan reveals widening of the retropharyngeal space. Hemorrhage, rupture into the airway, laryngeal spasm, bronchial erosion, and jugular vein thrombosis are the major complications. The pretracheal space that surrounds the trachea usually becomes involved following perforation of the anterior esophageal wall or from an extension of a retropharyngeal infection. Patients usually present with hoarseness, dyspnea, and difficulty in swallowing. Prompt surgical drainage is mandatory to prevent mediastinal extension.

Radiological image of a retropharyngeal infection

Other complications of odontogenic infections

Complications can result from hematogenic or direct spread. Transit bacteremia often occur after dental procedures. A documented relationship exists between this bacteremia and subsequent bacterial endocarditis, and cardiovascular prosthetic and orthopedic prosthetic device infections. The oral bacteria most often associated with subacute bacterial endocarditis are S. mutans and Streptococcus sanguis, isolated also from acute orofacial infections.

Lymphatic, hematogenic, or direct extension septic complications can induce cavernous sinus thrombosis. Complications that arise following local extension include suppurative jugular thrombophlebitis, carotid erosion, maxillary sinusitis, and osteomyelitis of the jaws.⁶ Management of these complications involves surgical and medical procedures.

Odontogenic infections are usually self-limited, however, they tend to form abscesses and cause necrotic tissue. Treatment of the primary dental origin of the infection (i.e. pulpitis, dental absces) is of primary importance. Surgical drainage and removal of necrotic material and infected teeth are crucial. As soon as the infection has been localized, incision should be made and drainage established. Premature incision into a cellulitis may disrupt the normal barriers and facilitate the spread of the infection. Therefore, needle aspiration is valuable both in establishing the presence of pus and collecting samples of microbiologic specimens.

Antibiotic therapy can prevent local and systemic extension. Although penicillin is often useful, the growing resistance of many of the aerobic and anaerobic floras is of concern.⁹ In patients who are seriously ill or who have had unfavorable response to penicillin, adding metronidazole or therapy with clindamycin, A carbapenem or the combination of a penicillin plus a beta-lactamase inhibitor (clavulanic acid or sulbactam) may be warranted.

                      

REFERENCES

1.   Socransky, S.S.: Microbiology of periodontal disease: present status and future consideration. J. Periodontol. 48:497, 1977. 2.      Evaldson, G., et al.: The normal anaerobic microflora. Scand. J. Infect. Dis. (Suppl.) 35:9, 1982.

2.   Finegold, S.M.: Anaerobic bacteria in human disease. New York, 1977, Academic Press.

3.   Loesche, W.J.: Bacterial mediators in periodontal disease. Clin. Infect. Dis. 16:S203, 1993.

4.   Socransky, S.S., Haffajee, A.D.: Evidence of bacterial etiology: a historical perspective. Periodontol 2000 5:7-25, 1994.

5.   Davis, A.H., McFadzean, J.A., and Squires, S.: Treatment of Vincent's angina with metronidazole. Br. Med. J. 1:1149, 1964.

6.   Baker, A.S., Montgomery, W.W.: Oropharyngeal space infections. Curr. Clin. Top. Infect. Dis. 8:227, 1987.

7.   Finch, R.G., Snider, G.E., Sprinkle, P.M.: Ludwig's angina. JAMA. 243:1171, 1980.

8.   Hartmann, R.W., Jr.: Ludwig's angina in children. Am. Fam. Physician 60:109-12, 1999.

  9.  Lemierre, A.: On certain septicemias due to anaerobic organisms. Lancet 2:701-703, 1936.

  10. Brook, I.: Beta-lactamase-producing bacteria recovered after clinical failure with various penicillin therapy. Arc. Otolaryngol, 110: 228-31, 1984.