Dentoalveolar infections can be defined as pus-producing (or pyogenic) infections associated with the teeth and surrounding supporting structures, such as the periodontium and the alveolar bone. Other terms for these conditions include periapical abscess, apical abscess, chronic periapical dental infection, dental pyogenic infection, periapical periodontitis and dentoalveolar abscess. The clinical presentation of den- toalveolar infections depends on the virulence of the causative microorganisms, the local and systemic defence mechanisms of the host and the anatomical features of the region. Depending on the interactions of these factors, the resulting infection may present as:
■ an abscess localized to the tooth that initiated the infection
■ a diffuse cellulitis that spreads along fascial planes
■ a mixture of both.
Initiating events of dentoalveolar infections: pulpitis and apical periodontitis
In health, the dental pulp and the apical periodontium are sterile. The dental pulp can become infected due to dental caries, dental trauma, or via extra-radicular root canals from deep periodontal pockets. Most frequently, the dental pulp infection is transmitted through dentinal tubules due to a carious lesion. Inflammation of the pulp tissue is called pulpitis.
If early pulpitis is left untreated, the inflammation develops into an irreversible condition and the pulp gradually becomes necrotic. As the disease develops, the microflora in the root canal becomes more complex and a biofilm will develop on the inner surfaces of the root canals. When the dental pulp is fully necrotic, the biofilm may extend through the apical foramen of the root to the outer wall of the apical part of the tooth, resulting in an inflammation in the periapical tissue to become a dentoalveolar abscess.
Source of microorganisms
Endogenous oral commensals, usually from the apex of a necrotic tooth or from periodontal pockets as a result of either caries or periodontal disease (Fig. 34.1).
A dentoalveolar abscess usually develops by the extension of the initial carious lesion into dentine, and spread of bacteria to the pulp via the dentinal tubules (Figs 34.1 and 34.2). The pulp responds to infection either by rapid acute inflammation involving the whole pulp, which quickly becomes necrosed, or by development of a chronic localized abscess with most of the pulp remaining viable. Other ways in which microbes reach the pulp are:
■ by traumatic tooth fracture or pathological exposure due to tooth wear
■ by traumatic exposure during dental treatment (iatrogenic)
■ through the periodontal membrane (periodontitis and pericoronitis) and accessory root canals
■ rarely by anachoresis, that is, seeding of organisms directly into pulp via the pulpal blood supply during bacteraemia (e.g., tooth extraction at a different site).
Once pus formation occurs, it may remain localized at the root apex and develop into either an acute or a chronic abscess, develop into a focal osteomyelitis, or spread into the surrounding tissues (Figs 34.2 and 34.3).
Fig. 34.1 The pathways by which microorganisms may invade the pulp and periapical tissues: (1) from the apical foramen, (2) via the periodontal ligament and (3) via the blood stream (anachoresis).
1. Spread into the superficial soft tissues may:
• localize as a soft-tissue abscess (Fig. 34.4)
• extend through the overlying oral mucosa or skin, producing a sinus linking the main abscess cavity with the mouth or skin
• extend through the soft tissue to produce a cellulitis.
2. Spread may occur into the adjacent fascial spaces, following the path of least resistance; such spread is dependent on the anatomical relation of the original abscess to the adjacent tissues (Table 34.1). Infection via fascial planes often spreads rapidly and for some distance from the original abscess site, and occasionally may cause severe respiratory distress as a result of occlusion of the airway by oedema (e.g., Ludwig's angina).
3. Infection may extend into the deeper medullary spaces of alveolar bone, producing a spreading osteomyelitis; this may occur in compromised patients.
4. In maxillary teeth, odontogenic infection may directly spread into the maxillary sinus, especially if the sinus lining and the tooth apex are subjacent, leading to acute or chronic secondary maxillary sinusitis (as opposed to primary sinusitis due to direct sinus infection). Such infection, if not arrested, may rarely spread to the central nervous system, causing serious complications such as subdural empyema, brain abscesses or meningitis.
Other sequelae entail indirect spread via:
■ lymphatic routes, to regional nodes in the head and neck region (submental, submandibular, deep cervical, parotid and occipital). Usually, the involved nodes are tender, swollen and painful, and rarely may suppurate, requiring drainage
Table 34.1 Sites of contiguous spread of dentoalveolar infection (see also Fig. 34.3)
Site of spread
Palatal roots of premolars and molars; also, lateral incisors with a palatally curved root
Canines, premolars and molars
Canines, premolars and molars
Infraorbital/ periorbital region
Canines, premolars and molars
Central and lateral incisors
Masseteric space, pterygomandibular space, lateral pharyngeal space
Lower third molars
Incisors and canines
Root apices below insertion of mylohyoid; usually molars but can also be premolars
Incisors and canines
Root apices above mylohyoid/ geniohyoid; usually incisors, canines and premolars; rarely molars
■ haematogenous routes: to other organs such as the brain (rare).
Clinical signs and symptoms depend on the:
■ site of infection
■ degree and mode of spread
■ virulence of the causative organisms
■ efficiency of the host defences.
Clinical features may include a non-viable tooth with or without a carious lesion, a large restoration, evidence of trauma, swelling, pain, redness, trismus, local lymph node enlargement, sinus formation, raised temperature and malaise. The latter two symptoms are a direct consequence of increased levels of systemic inflammatory cytokines such as interleukins and tumour necrosis factor in response to bacterial products such as lipopolysaccharides (i.e., endotoxins).
Fig. 34.2 Prequelae and sequelae related to a dentoalveolar abscess.
Microbiologically, the dentoalveolar abscess is characterized by the following features:
■ infection is usually polymicrobial (endogenous), with a mixture of three or four different species
■ monomicrobial (endogenous) infection (i.e., with a single organism) is unusual
■ strict anaerobes are the predominant organisms, and the viridans group streptococci are less common than once thought.
The common species isolated from dentoalveolar abscesses are Prevotella, Porphyromonas and Fusobacterium spp., and anaerobic streptococci; facultative anaerobes are the second largest group, for example, Streptococcus milleri (Table 34.2). There is evidence that some strictly anaerobic bacteria, especially Porphyromonas gingivalis and Fusobacterium spp., are more likely to cause severe infection than other species, and that synergistic microbial interactions play an important role in the severity of dentoalveolar abscesses.
Collection and transport of pus samples
1. Wherever possible, pus should be collected by needle aspiration or in a sterile container after external incision. Care must be exercised during re-capping the syringe after needle aspiration, and a safety device must be used. In addition, it is important to drain the residual pus, once the aspirate has been obtained via an appropriate incision (see Chapter 6).
Fig. 34.3 Pathways by which pus may spread from an acute dentoalveolar abscess (coronal section, at the first molar tooth level).
Fig. 34.4 Extension of periapical infection from the left upper canine tooth to the infraorbital region in a teenager.
Table 34.2 Bacteria commonly isolated from dentoalveolar abscesses
2. If swabs must be used, then a strict aseptic collection technique is required (because of the indigenous flora on mucosal surfaces, it is difficult, if not impossible, to collect uncontaminated samples when intraoral swabs are used for pus collection). When the pus sample is contaminated with saliva or dental plaque during collection, this information must be recorded on the request form.
The specific treatment for any given individual will vary. The major management guidelines entail:
1. draining the pus
2. removing the source of infection
3. prescribing antibiotics, probably not required for the majority of localized abscesses, although it may be necessary:
• when drainage cannot be established immediately
• if the abscess has spread to the superficial soft tissues
• when the patient is febrile.
Standard antibiotics include:
■ phenoxymethylpenicillin (penicillin V) or short-course, high-dose amoxicillin
■ in penicillin-hypersensitive patients: erythromycin or metronidazole (as most infections are due to strict anaerobes).
Ludwig's angina is a spreading, bilateral infection of the sublingual and submandibular spaces.
In the vast majority of cases (about 90%), Ludwig's angina is precipitated by dental or post-extraction infection; uncommon sources of infection include submandibular sialadenitis, infected mandibular fracture, oral soft-tissue laceration and puncture wounds of the floor of the mouth. The infection is essentially a cellulitis of the fascial spaces rather than true abscess formation.
The infection of sublingual and submandibular spaces raises the floor of the mouth and tongue and causes the tissues at the front of the neck to swell. The brawny swelling has a characteristic board-like consistency, which can barely be indented by the finger. There is severe systemic upset with fever. Complications include:
■ airway obstruction due to either oedema of the glottis or a swollen tongue blocking the nasopharynx
■ spread of infection to the masticator and pharyngeal spaces
■ death due to asphyxiation is a certainty without immediate intervention.
Surgical drainage may yield little pus.
Oral commensal bacteria are common agents, especially Porphyromonas and Prevotella spp., fusobacteria and anaerobic streptococci; it is a mixed endogenous infection. Because of the
severity of the condition, samples for microbiology assessment should always be obtained, if possible.
1. Ensure that the patient's airway remains open (surgically, if necessary).
2. Maintain fluid balance.
3. Institute high-dose, empirical antibiotic therapy (usually intravenous penicillin, with or without metronidazole) immediately.
4. Collect a sample of pus before antibiotic therapy, if the patient's condition permits, or immediately afterwards.
5. Change the prescribed antibiotic if necessary, once the bacteriological results are available.
6. Institute surgical drainage as soon as possible.
7. Eliminate the primary source of infection (e.g., a non-vital tooth).
Pericoronitis (see Chapter 33)
Alveolar osteitis (dry socket)
This extremely painful condition is a localized form of alveolar osteitis, which is a complication of wound healing following the extraction of a tooth. Alveolar osteitis is seen after approximately 3% of routine extractions and in almost one in five surgical extractions, although these figures may vary in different locales.
Not fully understood; thought to be due to the fibrinolysis of blood clot by anaerobic flora; smoking and oral contraceptives are thought to predispose the condition.
■ More common in females.
■ More common in mandible than maxilla.
■ Symptoms: severe, throbbing pain, halitosis.
■ An extraction socket devoid of granulation tissue.
Possibly a polymicrobial opportunistic infection with a predominance of anaerobic flora; other causative reasons have been proposed.
■ Debridement of socket with chlorhexidine or saline.
■ Control the pain with analgesics.
■ Metronidazole may be an option in recalcitrant cases.
A periodontal abscess is caused by an acute or chronic destructive process in the periodontium, resulting in localized collection of pus communicating with the oral cavity through the gingival sulcus and/or other periodontal sites (and not arising from the tooth pulp).
The abscess probably forms by occlusion or trauma to the orifice of a periodontal pocket, resulting in the extension of infection from the pocket into the supporting tissues. These events might result from impaction of food such as a fish bone, or of a detached toothbrush bristle, or from compression of the pocket wall by orthodontic tooth movement or by unusual occlusal forces. Normally, the abscess remains localized in the periodontal tissues, and its subsequent development depends on:
■ the virulence, type and number of the causative organisms
■ the health of the patient's periodontal tissues
■ the efficiency of the specific and non-specific defence mechanisms of the host.
1. Onset is sudden, with swelling, redness and tenderness of the gingiva overlying the abscess.
2. Pain is continuous or related to biting and can be elicited clinically by percussion of the affected tooth.
3. There are no specific radiographic features, although commonly associated with a deep periodontal pocket.
4. Pus from the lesion usually drains along the root surface to the orifice of the periodontal pocket; in deep pockets, pus may extend through the alveolar bone to drain through a sinus that opens on to the attached gingiva.
5. Because of intermittent drainage of pus, infection tends to remain localized, and extraoral swelling is uncommon.
6. Untreated abscesses may lead to severe destruction of periodontal tissues and tooth loss.
Endogenous, subgingival plaque bacteria are the source of the microorganisms in periodontal abscesses; infection is polymicrobial, with the following bacteria being commonly isolated:
■ anaerobic Gram-negative rods, especially black-pigmented Porphyromonas and Prevotella spp., and fusobacteria
■ streptococci, especially haemolytic streptococci and anaerobic streptococci
■ others, such as spirochaetes, Capnocytophaga spp. and Actinomyces spp.
1. Make a thorough clinical assessment of the patient, including a history of systemic illnesses (e.g., diabetes).
2. If the prognosis is poor, owing to advanced periodontitis or recurrent infection, and it is unlikely that treatment will achieve functional periodontal tissues, then extract the tooth. If the abscess is small and localized, extraction may be carried out immediately; otherwise, extraction should be postponed until acute infection has subsided.
3. Drainage should be encouraged, and gentle subgingival scaling should be performed to remove calculus and foreign objects.
4. Irrigate the pocket with warm 0.9% sodium chloride solution and prescribe regular hot saline mouthwashes.
5. If pyrexia or cellulitis is present, antibiotics should be prescribed: penicillin, erythromycin and metronidazole are the drugs of choice.
Suppurative osteomyelitis of the jaws
Suppurative osteomyelitis is a relatively rare condition that may present as an acute or chronic infection, depending on a variety of factors.
An inflammation of the medullary cavity of the mandible or the maxilla, with possible extension of infection into the cortical bone and the periosteum as a sequela.
Osteomyelitis of the head and neck region is much rarer than dentoalveolar infections, probably because of the good vascular supply to the bone. Conditions that tend to reduce the vascularity of bone predispose to osteomyelitis (e.g., radiation, osteoporosis, Paget's disease, fibrous dysplasia and bone tumours). A wide range of organisms have been associated with osteomyelitis of the jaws, including endogenous bacteria (described in the following text) and, rarely, exogenous organisms such as Treponema pallidum and Mycobacterium tuberculosis.
1. The source of infection is usually a contiguous focus, or haematogenous seeding of bacteria may occur infrequently.
2. Bacteria multiply in bony medulla and elicit an acute inflammatory reaction.
3. This results in increased intramedullary pressure leading to venous stasis, ischaemia and pus formation.
4. Pus spreads through the haversian canal system, breaching the periosteum, with resultant sinus formation and appearance of soft-tissue abscesses on the oral mucosa or skin.
5. If there is no intervention, chronic osteomyelitis results, with new bone (involucrum) formation and separation of fragments of necrotic bone (sequestra).
Clinical features include pain, mild fever, paraesthesia or anaesthesia of the related skin; loosening of teeth; and exudation of pus from gingival margins or through sinuses or fistulae in the affected skin.
In chronic osteomyelitis, there is minimal systemic upset, chronic sinuses with little pus, and tender and indurated skin.
As the majority of osteomyelitis cases begin as a dentoalveolar infection, the causative organisms of both diseases are similar. Anaerobes are the most common isolates, for example, Tan- nerella, Prevotella and Porphyromonas spp., fusobacteria and anaerobic streptococci; rarely enterobacteria may be present. Staphylococcus aureus, the most common agent of osteomyelitis in long bones, is infrequently isolated from jaw lesions.
The management of osteomyelitis is complex. The main principles are:
1. rapid diagnosis of the disease
2. empirical prescription of antibiotics (to prevent further bone destruction and surgical intervention)
3. collection of a pus sample, if feasible, for investigations: collect pus with care when it is exuding from the gingival sulcus, to prevent contamination with commensal bacteria; aspirate pus from contiguous soft-tissue lesions
4. send the sample immediately to the laboratory in anaerobic transport medium for identification and sensitivity testing of causative bacteria
5. drugs of choice are penicillin, penicillinase-resistant penicillins (e.g., flucloxacillin) and, in penicillin-allergic patients, clindamycin and erythromycin
6. other treatment options include tooth extraction, sequestrectomy and resection and reconstruction of the jaws.
Actinomycosis (see Chapter 13) is an endogenous, granulomatous disease that may occur in the following sites:
■ cervicofacial region, most common (60%-65%)
■ abdomen (10%-20%)
In humans, the main infecting organism is Actinomyces israelii, which is a common oral commensal present in plaque, carious dentine and calculus. Trauma to the jaws, tooth extraction and teeth with gangrenous pulps may precipitate infection (e.g., calculus or plaque becoming impacted in the depths of a tooth socket at the time of extraction).
Predominantly a disease of younger people, although all ages may be affected, the infection can present in an acute, subacute or chronic form. There is usually a history of trauma, such as a tooth extraction or a blow to the jaw. Most infections start as an acute swelling indistinguishable on clinical grounds from a dentoalveolar abscess. The chronic form of the disease follows, due to either inadequate or no therapy, or subacute infection related to trauma.
Swelling is common and is either localized or diffuse; if untreated, it may progress into discharging sinuses. Classically, this discharge of pus contains visible granules, which may be gritty to touch, yellow and known as 'sulphur granules' (a descriptive term, as sulphur is not found in the granules). These granules in pus are almost pathognomonic of the disease.
The submandibular region is most commonly affected; rarely the maxillary antrum, salivary glands and tongue may be involved. Pain is a variable feature. Other features, depending on the site of infection, are multiple discharging sinuses, trismus, pyrexia, fibrosis around the swelling, and the presence of infected teeth.
The most common agent is Actinomyces israelii, although Actinomyces bovis and Actinomyces naeslundii may occasionally be isolated. In a minority, Aggregatibacter actinomycetemcomitans may be isolated in mixed culture with Actinomyces israelii.
If a fluctuant abscess is present, collect fluid pus by aspiration using a syringe, or in a sterile container if drainage by external incision is performed. Examine the pus for the presence of 'sulphur granules'; Gram films are made from any part with a lumpy or granular appearance. The granules are washed and crushed in tissue grinders and cultured on blood agar under anaerobic conditions at 37°C for 7 days. Colonies often produce a typical 'molar tooth' morphology (see Fig. 13.1). Pure cultures are then identified using biochemical techniques. A Gram film of a colony will reveal moderate to large clumps of Gram-positive branching filaments.
1. Removal of any associated dental focus.
2. Incision and drainage of facial abscess.
3. A 2- to 3-week course of antibiotics; penicillin is the drug of choice.
Subacute or chronic lesions
1. Surgical intervention, as in (1) and (2) above.
2. A longer antibiotic course, 5-6 weeks on average.
If penicillin cannot be given because of hypersensitivity, erythromycin, tetracycline and clindamycin are good alternatives. The latter drugs penetrate bony tissues well.
On occasions, facial soft-tissue wounds, owing to traumatic or similar injuries, may get infected.
Commensal skin flora such as Staphylococcus aureus, Staphylococcus epidermidis and Corynebacterium acnes.
■ Debridement with saline.
■ Close wound by suturing or adhesive strips, if necessary.
■ Tetanus vaccine/antibody, if the wound is contaminated, as appropriate.
■ If infected, swab sample taken for culture and sensitivity.
■ If infected, antibiotics with known activity against staphylococci (e.g., Flucloxacillin).
■ Topical application of mupirocin or fucidin cream.
Endodontic infections (syn. root canal infections; intraradicular infections)
Most common diseases that affect the dental pulp and periapical tissues are bacterial infections originating from the commensal microbiota of the oral microbiome, and hence they are called endogenous infections, as opposed to exogenous infections caused by bacteria from external sources (e.g., tuberculosis). Root canal or intraradicular or endodontic infections are classic endogenous infections.
Note: Microbiology of endodontic infections is a complex subject and only a thumb sketch is provided here; readers are urged to consult reference texts in further reading list for fuller accounts of the subject.
Source and routes of infection of pulp and periapical tissue: see above and Fig. 34.1.
Pathogenesis of pulp and periapical infections
Once bacteria gain access into the sterile pulp chamber, it is extremely difficult for the host defences to completely eliminate them. Resultant acute or chronic inflammation of the pulp, which of course is encased in its mineralized 'tomb', inevitably leads to stasis of the blood supply owing to compressive forces on pulpal blood vessels entering through a narrow apical foramen. Natural pulpal defences on its own cannot cope with this outcome, and in a majority of cases pulpal necrosis is the end result. This, in turn, sets in motion a cascade of events shown in Fig. 34.5.
The time required for complete necrosis of the pulp is variable. In some cases, this may happen within days or weeks. However, in others localized, subacute, chronic insidious infection may be present for many months or even years before the pulp eventually succumbs. The sequelae of this chronic process are (Fig. 34.5):
1. spread of bacteria via lateral canals or the periapical foramen to cause a granuloma
2. development of a periapical cyst
3. development of a periapical abscess
4. development of a sinus.
Host defence mechanisms
The host attempts to foil the microbial invasion into pulpal tissue by a variety of mechanisms:
■ acute pulpal inflammation with phagocytosis in acute stages and antibody-mediated and cell-mediated immune response at a late stage
■ deposition of irregular or sclerotic dentine with minor breaches of defence
■ necrosis of the pulp.
Microbiology of endodontic infections
There is a vast literature on this subject and only a summary is given in the following sections.
Endodontic biofilm: properties
Endodontic infections are essentially caused by a complex polymicrobial biofilm adherent to the root canal surface and formed by microorganisms that have invaded the pulpal space.
Conditions under which biofilms develop in root canals are not well understood, and histological data indicate that endodontic biofilm morphology varies between cases, with the following properties:
■ biofilms of primary endodontic infections have higher contents of endotoxins (lipopolysaccharides) by virtue of its complex Gram-negative bacterial community (compare with the secondary infections that ensue after treatment)
■ the severity of bone destruction in periapical tissues of infected root canals is related to levels of biofilm endotoxins
■ bacteria from infected roots canals resist alkaline stress better in biofilm phase than in planktonic phase cultures
■ older endodontic biofilms are more resistant than younger biofilms to antimicrobials.
Microbiota of endodontic infections
There appears to be a significant difference in the microbiota in primary and secondary endodontic infections as will be described in the following sections. Primary endodontic infection refers to the initial infection of the root canal system, whereas secondary infection refers to the infection that ensues after endodontic therapy.
Microbiota of primary endodontic infections
The microbiota of primary endodontic infections is shown in Table 34.3. Primary root canal infections are complex polymicrobial diseases with 10-30 bacterial species, and a predominance of obligate anaerobic bacteria. Recent 16S ribosomal RNA (rRNA)-based molecular biological studies have shown uncultivable bacteria such as species of the genera Dialister, Olsenella, and unnamed clones of Synergistes in the infected root canals. Clearly, therefore, a vast number of organisms can colonize and inhabit the breached pulp chamber, and some organisms are more important and common etiological agents of infection than others.
In general, microbial succession from a healthy pulp to a necrotic pulp is as follows:
■ In early pulpitis: microflora is simple, dominated by caries-related bacteria.
■ As the endodontic biofilm advances a growth of proteolytic bacteria such as Gram-negative anaerobic species such as Prevotella, Porphyromonas, Eubacterium, Parvimonas, and Campylobacter species are seen; this is due to the change in the eco system such as its Eh and pH and the ready availability of nutrients within a necrotic pulp chamber.
■ Bacterial ingress to the pulp chamber via extra-radicular accessory root canals via periodontal lesions leads to the development of a microbiome similar to that of chronic periodontitis.
Table 34.3 Microbiota of primary endodontic infectionsa,b
The prevalence of these organisms shown in Table 34.3 is only an approximate estimate and differs widely between studies. One reason for this is the quality of microbiological samples delivered for laboratory studies. Aseptic sampling of the infected canal is critical to obviate commensal contaminants, and the generation of spurious data from many studies may be due to contaminated samples. Additionally, the laboratory culture conditions that are not optimal for growth of fastidious bacteria may generate false data.
Some general features of the primary endodontic microbiome are outlined below:
■ Distribution of microorganisms in the root canal varies according to which part of the root canal system is being sampled:
• Apical areas are generally dominated by slow growing obligate anaerobes.
• Coronal part of the canal is populated by more rapidly growing facultative anaerobes.
■ Gram negative anaerobic rods, (e.g., Porphyromonas, Prevotella and Tannerella spp.) are present in both symptomatic and asymptomatic endodontic infections.
■ Eukaryotic yeasts may be seen, and Candida albicans is the most common fungus recovered from endodontic infections. Their role in endodontic infections is not clear.
■ Viruses (e.g., Herpes group) have been occasionally isolated from endodontic lesions.
■ Prions causing spongiform encephalopathies are not present in infected pulpal tissue (see Chapter 4).
■ Some archaea and uncultivable bacteria have also been detected in infected pulp.
Microbiota of secondary endodontic infections
Secondary endodontic infection may ensue after unsuccessful treatment of the affected tooth. This usually occurs due to introduction of microbes into the root canal system during endodontic therapy, especially in cases where the tooth is left open, or leakage from temporary fillings during interappointment periods and/or coronal leakage from defective permanent restorations.
During this phase certain, relatively more potent microbe may enter the root canal system from the oral cavity or alternatively bacteria that were lying in a dormant state in the canal may assume a more aggressive role due to ecological changes conducive for their survival. For instance, Enterococcus faecalis, one of the major offenders in secondary endodontic infections, may proliferate within avascular and inaccessible dentinal tubules and evade the action of all antimicrobial components and medicaments (Table 34.4). The reasons why Enterococcus faecalis is common in recalcitrant endodontic infections are:
■ its ability to invade dentinal tubules and adhere to collagen
■ its ability to grow in high and low pH, high salt concentration, high temperatures (45°C)
■ its ability to grow both aerobically and anaerobically
Table 34.4 Microbiota of secondary endodontic infections3
Gram-negative anaerobic rods
Fusobacterium nucleatum, Prevotella spp., Porphyromonas spp., Bacteroides family, Tannerella, coliforms
Enterococcus faecalis, Lactobacillus spp., Streptococcus mitis, Streptococcus oralis, Parvimonas micra, Propionibacterium spp., Bifidobacterium spp., Actinomyces spp., Staphylococcus aureus
Mainly Candida albicans
aMore common isolates are in bold; not an exhaustive list.
■ its resistance to antibiotics as it has plasmids that carry a variety of antibiotic-resistant genes
■ expression of virulence factors (e.g., gelatinase, which mediates its adhesion to particulate dentin).
In general, one to five bacterial species have been isolated from root canals after chemo-mechanical preparation, with the counts ranging from 102- to 105 cells per canal. Apart from Enterococcus faecalis, anaerobic rods such as Fusobacterium nucleatum, Prevotella species, and Campylobacter rectus and various Gram-positive streptococci can be isolated from such lesions (Table 34.4).
To conclude, it is important to note that the outcome of pulp infection is difficult to predict and depends on the net result of a number of interacting factors such as:
1. the source, route and duration of infection
2. the species, number and toxic end products of the organism/s
3. the specific and non-specific defence mechanisms of the host
4. the robustness and asepsis of the endodontic interventional procedure, in the case of secondary endodontic infections.
Role of microbiology in endodontics
It is generally accepted that the role of endodontic therapy is to render the root canal and periapical tissues 'sterile' and thus ensure the success of the root canal filling. Based on this premise, sterility testing is an attractive proposition as it encourages meticulous clinical technique, and assists the clinician in deciding when the canal/s should be filled. Yet, the rationality of the term 'sterile' in the context of endodontics has been questioned. Sterility is an absolute term (like pregnancy!) and indicates absence of living microbes, and even if a single organism remains in the canal it cannot be termed sterile. The question then is the magnitude of bacterial numbers that is compatible with clinical success. There is now clear evidence to show that a few residual bacteria may not cause secondary endodontic infection, and these canals can be filled with good clinical outcomes. Hence the case for routine culture of samples from root canals is poor.
There are, however, a number of clinical situations where the microbiological assessment of root canals is justified and helps the clinician. They are:
■ patients with a dentoalveolar abscess where endodontic treatment is indicated
■ symptomless, non-vital teeth with apical radiolucency
■ root canals undergoing treatment with persistent exudate and clinical symptoms.
Some clinicians prefer to keep root canals open without a temporary filling, to encourage pus drainage from a den- toalveolar abscess associated with the tooth. This should be avoided because a complex mixture of oral microbes may then selectively colonize the canal, and eradicating them will often prove difficult.
Microbiological sampling of root canals
If an endodontic sample is required, it should be collected under rubber dam using sterile paper points, and a strict aseptic technique. Failure to do so may lead to sample contaminations and interpretation of the microbiological findings difficult or almost impossible (see Chapter 6). The following technique will help the clinician to obtain an optimal sample that yields qualitative and quantitative information of an infected root canal, and the antibiotic sensitivity of the infecting organisms.
■ If the canal is dry, the paper point or the canal should be moistened with a sterile saline prior to sampling.
■ Place the sample in an anaerobic transport medium and send directly it to the microbiology diagnostic laboratory.
■ In the laboratory, the sample is dispersed by vortex mixing, and a standard inoculum is cultured on blood agar to enable a count of bacteria/millilitre of medium to be calculated and to ascertain the degree of infestation of the root canal.
■ The microbes in the sample are identified after 48-72 h, incubation of the medium and after the antibiotic sensitivity of the harvested organisms is assessed.
Management of the infected canal
The most critical part of endodontic therapy is the use of aseptic technique to remove mechanically vital, non-vital or infected tissue, and to prepare the canal to insert a root canal filling material and obturate the canal.
Historically, antimicrobial agents were commonly used as adjunct to endodontic therapy, but their use has declined as the weight of evidence dictates that antibiotics should be used only on the basis of a defined need, such as in cases complicated by severe or recalcitrant infection, as follows.
Systemic antibiotics in endodontics: therapeutic principles
■ The therapeutic use of antibiotics, if at all, must be an adjunct to mechanical treatment.
■ Systemic prophylactic antibiotics are only indicated in medically compromised patients. One exception, however, is the re-implantation of an avulsed tooth.
■ Systemic prophylactic antibiotics, if indicated, must be given preoperatively, preferably as a single high dose.
■ There is no case for using antimicrobials as an adjunct to inadequate and careless clinical technique!
If antibiotics are used in endodontics, then they could be administered in three main ways:
1. as irrigants to wash out canals during mechanical cleaning procedures
2. as topical agents sealed in the root canal for a few days to kill microbes inaccessible to mechanical therapy
3. rarely as systemic agents to destroy microbe within the periapical lesions.
Irrigants in endodontics
The irrigants that are currently used in endodontics for cleaning canals can be divided into:
■ decalcifying agents or their combinations
■ normal saline sometimes laced with a local anaesthetic. Salient features of sodium hypochlorite (NaOCl), chlorhexidine, ethylenediaminetetraacetic acid (EDTA), and a mixture of tetracycline, an acid and a detergent (MTAD) are given in the following sections.
NaOCl: commonly called household bleach, NaOCl is the most popular and the most commonly used root canal irrigant. It is an inexpensive, antiseptic lubricant and is used in dilutions ranging from 0.5% to 5.25%.
■ Advantages of NaOCl include its ability to dissolve organic substances present in the root canal system and its affordability. The major disadvantages of this irrigant are its cytotoxicity when injected into peri-radicular tissues, foul smell and taste, ability to bleach clothes and ability to cause corrosion of metal objects.
■ Depending on the concentration and the freshness of the solution it may not kill all the radicular bacteria nor does it remove all of the smear.
■ Accidental spillover of NaOCl to the peri-apical region is a not an uncommon complication.
Chlorhexidine gluconate: has a broad spectrum of antibacterial action, sustained action and low toxicity. The major advantages of chlorhexidine over NaOCl are its lower cytotoxicity and lack of foul smell and bad taste. However, unlike NaOCl, it cannot dissolve organic debris and necrotic tissues in the root canal system.
EDTA: chelating agents such as EDTA, citric acid and tetracycline are used for removal of the inorganic portion of the smear. EDTA has little or no antibacterial effect.
MTAD (a mixture of a tetracycline isomer, citric acid and a detergent): developed as a final rinse to disinfect the root canal system. It appears to be superior to CHX in antimicrobial activity and has sustained antibacterial activity.
These are used to disinfect root canal system between appointments and reduce inter-appointment pain, and include:
■ phenolic compounds (e.g., camphorated monochlorophenol, cresatin)
■ aldehydes (e.g., formocresol and glutaraldehyde)
■ calcium hydroxide
■ some antibiotics.
These compounds are potent antibacterial agents under laboratory test conditions in vitro, but their efficacy in clinical use is unpredictable. Blood and serum seeping into the canal system are thought to inactivate these agents over time. Some of the aldehyde derivatives have been proposed to neutralize canal tissue remnants and to render them inert.
Calcium hydroxide Ca(OH)2: the drug of choice for temporarily sealing the canal; the solution is highly alkaline but not toxic even affecting tough bacteria such as Enterococcus faecalis. It also inactivates bacterial endotoxins, dissolves necrotic tissue remnants and bacteria and their by-products. The antibacterial effect of Ca(OH)2 is owing to its alkaline pH. Extrusion of the material into the periapical tissues can cause tissue necrosis and pain.
Corticosteroids: anti-inflammatory agents with no antimicrobial activity, advocated as intracanal medicaments to reduce postoperative pain.
Chlorhexidine gel: a 2% chlorhexidine gel is used as an intracanal medicament. It can be used alone in gel form or mixed with calcium hydroxide. The gel has sustained antimicrobial activity for up to 21 days. When used in combination with Ca(OH)2, its antimicrobial activity is greater than the combination of Ca(OH)2 and saline.
• Dental caries is the main cause of pulpal and periapical infections; other routes include periodontal pocket and, rarely, anachoresis (i.e., haematogenous seeding).
• Dentoalveolar infections are usually polymicrobial in nature and endogenous in origin, with a predominance of strict anaerobes.
• Ideally, an aspirated sample of pus should be collected for microbiological examination of a dentoalveolar abscess in the head and neck region.
• Drainage of pus is the mainstay of treatment of dentoalveolar and periodontal abscesses; elimination of the infective focus and antibiotic therapy should be considered on an individual basis.
Ludwig’s angina is a spreading, bilateral infection of the sublingual and submandibular spaces; it is a life-threatening infection.
Prompt intervention and maintenance of the airway are of critical importance in the management of Ludwig’s angina; high-dose, empirical, systemic antibiotic therapy is also essential.
Periodontal abscess: an acute or chronic destructive process in the periodontium, resulting in localized collection of pus communicating with the oral cavity through the gingival sulcus and/or other periodontal sites (and not arising from the tooth pulp).
• Periodontal abscess is an endogenous, polymicrobial infection with a predominantly anaerobic, periodontopathic flora.
• Alveolar osteitis (dry socket) is possibly a polymicrobial opportunistic infection with a predominance of anaerobic flora; the exact aetiology is unclear.
• Suppurative osteomyelitis of the jaws is uncommon; it is mostly seen in immunocompromised patients. Usually a polymicrobial infection, it requires both medical and surgical intervention.
• Cervicofacial actinomycosis: an endogenous granulomatous disease, usually presenting at the angle of the mandible and related to trauma or a history of tooth extraction, mainly caused by Actinomyces israelii; ‘sulphur granules’ may be present in pus.
• Actinomycoses are managed by surgical drainage and long-term antibiotics, preferably penicillin.
• Commensal skin flora such as Staphylococcus aureus, Staphylococcus epidermidis and C. acnes may be isolated from infected facial lacerations.
• Endodontic infections are usually endogenous in nature, caused by infestation of the pulp and the root canals by oral commensal microbiota.
• Most flora of primary endodontic infections are anaerobic in nature.
• Enterococcus faecalis is a common pathogen mainly seen in secondary endodontic infection and its virulence is due to its ability to survive in a high pH and high salt milieu as well as its resistance to antibiotics.
• Infected root canals cannot be ‘sterilized’; the mainstay of therapy is to reduce the bacterial burden compatible with treatment.
Review questions (answers on p. 367)
Please indicate which answers are true, and which are false.
34.1 Which of the following statements on dentoalveolar abscess are true?
A. it is often precipitated by bacteria from the systemic route (anachoresis)
B. it has a polymicrobial aetiology
C. it is frequently implicated as a cause of brain abscess
D. it often resolves without antibiotics after adequate drainage
E. it is a localized collection of pus with an epithelial lining
34.2 Which of the following statements on Ludwig's angina are true?
A. the majority of cases are due to submandibular sialadenitis
B. it may warrant an urgent tracheostomy
C. often the patient is toxic
D. it needs to be treated with high-dose, parenteral metronidazole and penicillin
E. a copious amount of pus is yielded on surgical drainage
34.3 Microorganisms that are frequently implicated in the pathogenesis of periodontal abscess include:
A. Treponema pallidum
B. haemolytic streptococci
E. Porphyromonas spp.
34.4 Which of the following statements on actinomycosis are true?
A. abdominal lesions are more prevalent than cervicofacial lesions
B. Aggregatibacter actinomycetemcomitans is an associated co-pathogen
C. lesions contain sulphur
D. it is caused by a slow-growing, filamentous Gram-positive organism
E. a 1-week course of penicillin is adequate
Brook, I. (2005). Microbiology of acute and chronic maxillary sinusitis associated with an odontogenic origin. The Laryngoscope, 115, 823-825.
Brook, I., Frazier, I. H., & Gher, M. E. (1996). Microbiology of periapical abscess and associated maxillary sinusitis. Journal of Periodontology, 67, 608-610.
Ingle, J. I., Backland, L. K., & Baumgartner, J. C. (2008). Endodontics (6th ed.). Hamilton: BC Decker Inc.
Lewis, M. A. O., MacFarlane, T. W., & McGowan, D. A. (1990). A microbiological and clinical review of the acute dentoalveolar abscess. The British Journal of Oral & Maxillofacial Surgery, 28, 359-366.
Marsh, P. D., & Martin, M. V. (2009). Oral microbiology (5th ed.). London: Churchill Livingstone.
Siqueira, J. F., & Rôças, I. N. (2004). Polymerase chain reaction based analysis of microorganisms associated with failed endodontic treatment. Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics, 97, 85-94.
Siqueira, J. F., & Rôças, I. N. (2009). Diversity of endodontic microbiota revisited. Journal of Dental Research, 88, 969-981.
Waltimo, T. M., Sen, B. H., Meurman, J. H., et al. (2003). Yeast in apical periodontitis. Critical Reviews in Oral Biology and Medicine, 14, 128-137.