INFECTION Introduction

Management of various types of infections constitute a significant part of the workload of a maxillofacial surgeon. In establishing the presence of an infection, there is interaction among three factors: host, environment and the micro-organism. In a state of homeostasis, a balance exists between the three. Disease occurs in case of an imbalance. The host defence mechanisms are the major factor in determining the outcome of an infection environment and microbes play only secondary roles. The occurrence of an infection basically results from an imbalance between the pathogenic potential of microbes and the host defence mechanism. The pathogenic potential of microbes has two main attributes virulence and quantity. Virulence refers to all the qualities of the pathogen that are harmful to the host, such as invasiveness, toxins, enzymes etc. The quantity of microbes refers to the number of organisms that initially infect the host.
Host factors:

Under normal circumstances, the host factors predominate over the microbe factors. The host defence mechanism has three major components local, humoral and cellular factors. Local defences include 1. Epithelial lining (skin surface) acts as a barrier apart from dehydrating the microbe by virtue of the surface dryness 2. Secretion and drainage system (skin and mucosal surfaces) removes micro-organisms by flushing and kills them by effecting a pH change or by the action of lysozymes. 3. Interference of normal microbial flora normal flora acts by interfering with microbial binding to the surface, by producing toxic by-products and by competing for nutrients. 4. Mucosal immune system immunocompetent cells are seen beneath the basement membrane. The humoral components of host defence include immunoglobulins and the complement system. The immunoglobulins (antibodies) react to the antigenic stimulation and the complement system consists of a group
Infections of orofacial region

of serum proteins that, by a series of reactions, produce and release byproducts whose functions are to a. initiate inflammatory reaction, b. regulate and enhance phagocytosis and c. attack bacterial cell membrane (opsonisation). The main cellular components of the defence system of the host are phagocytes and lymphocytes. Phagocytes are cells that are endowed with the ability to engulf particles, the examples being PMN cells (eosinophils and neutrophils), the monocytes of the blood and at the tissue level, macrophages. The lymphocytes may be B-cells or T-cells. B-cells are mainly responsible for the antibody dependant reactions, while T-cells are responsible for cell-mediated immunity by the production of lymphokines.
Microbial factors:

The oral mucous membranes are colonised by a stable, well-defined microbial flora. The microbiota of the mouth at birth is predominantly aerobic because of a lack of areas that favour colonisation of anaerobes. As the teeth erupt, sites become available for anaerobic conditions to develop, mainly in the gingival crevicular and interproximal areas, and anaerobic population increases. By their nature, the oral microbiota may be classified into grampositive cocci, gram-negative cocci, gram-positive rods and filaments, gram-negative rods and filaments, spirochaetes, fungi and yeasts, viruses and protozoa. The important among gram-positive cocci are the streptococci, peptostreptococci and staphylococci. Veilonella and Neisseria are the main species among gram-negative cocci. A majority of the microbes under the group gram-positive rods and filaments are actinomycetes and lactobacilli, relatively uncommon ones being Corynebacterium, propionibacteria, Rothia and Bacterionema. Among the gram negative rods and filaments are the species such as Bacteroides, Capnocytophaga, Eikenella, fusobacterium and Actinobacillus. Spirochaetes like Treponema, Borrelia and Leptospira commonly inhabit the gingival crevices and inter-proximal areas. The chief fungi inhabiting the oral cavity are Candida, Penicillium, Aspergillus, etc. Apart from these, viruses like Herpes simplex and cytomegalovirus, and protozoa like Entamoeba and Trichomonas are also common in the oral cavity.
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Initiation, multiplication and pathogenesis

Initiation
Many infections begin on the mucous membranes. To initiate an infection, the micro-organisms must be able to a) adhere to the mucosal surface and resist flushing by fluids, b) compete for space and nutrients with normal inhabitants, c) resist antagonistic factors produced by other microbes and host defences and d) penetrate the epithelium to invade deeper tissues. The adherence of microbes to the cell surface is apparently accounted for by the physico-chemical properties of specific surface sites or structures (e.g. surfaces of streptococci interact with glycoproteins on epithelial cells). Intermicrobial interrelationships play a part in initiation of infection by synergism in certain cases (e.g. non-haemolytic streptococci grows well if Staphylococcus aureus is present to provide hyaluronidase). As regards the microbe-tissue interactions, the host secretions contain enzymatic and antibacterial substances. Phagocytes may also be present. Bacteria probably survive these defences by a variety of mechanisms, including the presence of capsules and resistant cell wall components and possibly by local suppression of immune responses or reactions. The mechanisms involved in bacterial penetration are many. This may happen through a breach on the epithelial surface, through epithelial cells or between the cells. The initiation of fungal infections is very similar to those of bacteria. In viral infections, specific cell receptors are more critical.

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Multiplication
In order to multiply in the host tissues rapidly to establish an infection, the microbes require organic and inorganic nutrients and an optimum pH Another important pathogenic mechanism that contributes to the micro-organisms ability to invade a host is its capacity to interfere with host defences. The mechanisms include interference with humoral defences (e.g. lipopolysaccharides of gram-negative bacteria), interference with phagocytic activities (bacterial capsules interfere with humoral system and phagocytosis) and suppression of immune response (e.g. membrane components of Streptococcus A decrease antibody responses).

Mechanisms of pathogenesis
Generally, host tissue damage in infection is a result of direct action of microbial toxins or lytic substances, or an indirect result of host response by inflammation and anaphylaxis. Toxins can be produced by bacteria, fungi, protozoa and viruses. They can be exotoxins (those liberated by the pathogen) or endotoxins (a toxic surface component). Endotoxins are important mechanisms of pathogenesis by gram-negative bacteria, and cause leukopenia, haemorrhage, pyrexia and shock. This damage is more likely during extensive invasion of blood or during bacterial lysis. Toxicity by endotoxins is by direct damage on host membranes, causing inflammatory response and activation of complement pathway. Exotoxins are substances produced and excreted by bacteria during multiplication. They are potent in small amounts, specific in their site and mode of action, and may act away from the site of manufacture. Examples are toxins of Clostridium tetani and that of Group A Streptococci. These potent chemicals are the mechanisms of pathogenesis in a variety of serious infections.
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Pyogenic bacteria, in addition, may sometimes produce certain enzymes capable of damaging the host by lysing the cells or other tissue constituents. Collagenase is a common example. Immunopathologic reactions have been implicated in the pathogenesis of several bacterial infections. Cytotoxic reactions or Arthus type reactions are examples. Fungal infections occur mainly by the process of hypersensitivity though the fungi are also known to produce a variety of toxins. Viruses can damage the host cells by causing them to undergo rapid lysis or by causing changes that ultimately result in cell death by disruption of metabolism or initiation of an immunopathologic response.

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Infections of odontogenic origin

Pulpal infections
Most cases of pulpitis are primarily a result of dental caries in which bacterial invasion of pulp occurs from a cavity. Occasionally, there is bacterial invasion in the absence of caries, as in tooth fracture, or as a result of bacteraemia. Pulpitis may be classified as initial, acute and chronic. The initial pulpitis (focal reversible pulpitis/pulp hyperaemia) is an early mild transient phenomenon, localised chiefly to the pulpal ends of irritated dentinal tubules. The tooth is sensitive to thermal changes but the pain disappears when the stimulus is removed. Extensive acute inflammation is a frequent immediate sequel of focal reversible pulpitis. It is characterised by relatively severe pain elicited by thermal changes and persisting even after the stimulus is removed. The pain may be continuous and of a lancinating type, and its intensity may increase when the patient lies down. Chronic pulpitis may arise on occasion through quiescence of an acute pulpitis, but more often it occurs as it is from the onset. Pain is not a prominent feature of chronic pulpitis although the patient may feel a mild dull ache, more intermittent than continuous. The reaction to thermal change is dramatically reduced. Chronic hyperplastic pulpitis is an uncommon sequel of chronic open pulpitis Untreated pulpitis, either acute or chronic, will ultimately result in complete necrosis of the pulp tissue.

Acute alveolar abscess

(Dentoalveolar/periapical abscess)
This is the most common infection of odontogenic origin. It is an acute or chronic suppurative process of the dental periapical region. It is usually caused by carious involvement of a tooth traumatic injury irritation by mechanical means or chemical irritation (RCT) 6

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This abscess can develop directly as an acute apical periodontitis, but more commonly it originates in an area of chronic infection. In the initial stages, the pain is dull and continuous, but well localised to the offending tooth, which feels extruded from the socket. Initially, biting on the tooth to depress it may relieve pain, but later (when vascular stasis and thrombosis occur), percussion only produces more severe pain. Inflammation may cause the adjacent teeth to be uncomfortable, but not as painful. Pain may be referred to or radiate to other regions of the jaws or parts of face, never crossing the midline. When pus is forming in and beyond periapical tissues, systemic symptoms like pyrexia, malaise, lymphadenopathy etc. may be present. The radiographic changes of acute abscess may only be an apical widening of the periodontal ligament and a carious lesion. If it has been present for more than 10 days, other changes like loss of lamina dura or localised bone loss may be seen Treatment consists of removing the cause and draining the exudate.

Pericoronitis
Pericoronitis is an infection of the follicular soft tissues which surround the crown of a partially erupted tooth. Mandibular third molar is the most common offender, especially when an impaction prevents its eruption. The infection is caused by microbes from the mouth which gain entry to the follicular space surrounding the tooth crown. The follicle is normally sterile but when microbes from the mouth gain access to it through an opening, it gets infected. Inflammatory oedema then distends the soft tissues, forming a closed infected follicular space which cannot drain. The pus under pressure causes pain and trismus. Pericoronitis may be acute, subacute or chronic. In chronic cases, resorption of bone causing a distal pocketing of second molar may occur. Pericoronitis has a maximum incidence of occurrence between 17 and 25 years of age. The three chief symptoms are pain (and tenderness over the tooth), bad taste and trismus. In the acute stage, the patient may have a mild pyrexia, malaise, localised lymphadenopathy and a diffuse swelling. The gum flap (operculum) is acutely inflamed and is extremely tender. Sometimes pus exudes from under the flap and this may track
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forward on the buccal side, due to deflection by the attachment of buccinator, to form a soft tissue abscess, apparently associated with the 1 st or 2nd molar teeth. The extra-oral swelling is usually over the mandibular angle. The impacted tooth is seen in the radiograph, with eroded edges of surrounding bone, in case of a chronic infection. Treatment consists of a) eliminating trauma from opposing tooth extraction / grinding b) hot saline mouth gargles as hot as possible, for a period of 5 minutes every 2 hours c) analgesics primary relief of inflammation d) antibiotic therapy in case of systemic symptoms / presence of pus Penicillin / Metronidazole (both are equally effective) Given for 5 days (at least 3 days) e) local treatment anaesthetic gel / mouthwashes f) drainage incision of flap / using chemical cautery under the flap / operculectomy g) removal of the cause after pericoronitis has subsided.

Periodontal abscess
This lesion usually arises silently as a result of infection in a periodontal pocket. Where drainage is impaired, the symptoms will include pain and tenderness in addition to a localised swelling which presents near the gingival margin and pus is readily released on probing. The affected tooth is often tender and mobile. Radiographs show thickening of periodontal ligament and variable amounts of bone loss, mainly at the alveolar crest region. Initial treatment includes drainage of the exudate through the gingival sulcus and relief of pain by relieving the tooth out of occlusion. Periodontal therapy is to be decided by the general condition of the dentition and supporting bone. When the tooth is to be preserved, the vitality should be assessed especially in cases of deep pockets. With marked bone loss and mobility, tooth extraction becomes necessary.

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Soft tissue abscess

Infections arising from dental causes (mentioned above) may spread in two different ways within the soft tissues. (a) from bone through periosteum to form an abscess in the soft tissue. This is localised and surrounded by oedema, and tend to point towards skin or mucosal surface. (b) the organisms may multiply to form an acute, rapidly spreading cellulitis. (Apart from these, the infection may involve medullary bone to cause various forms of osteomyelitis.) The location of formation of a soft tissue abscess of odontogenic origin is determined by muscle attachments, especially that of buccinator in the case of mandible. Other sources of soft tissue abscess include abrasions/trauma, ulcers of mucosa, abscess at injection site, bactermia, lymph node infections etc. Staphylococcus aureus is the usual offender the symptoms vary with the severity of infection. Treatment is incision and drainage of pus, antibiotics as necessary and removal of the initiating cause.

Focal sepsis
The spread of dental infection through the vascular and lymphatic channels has led to the concept of focal sepsis (William Hunter-1899). A patient with gross oral sepsis can have repeated bactermias caused by mastication or dental treatment, which drives the micro-organisms from the periodontal tissues to the blood stream. The bactermia is maximal in the first few minutes, lasts up to an hour and usually is low-grade i.e. 1020 organisms per ml of blood. Occasionally, it may be responsible for infection or induced hypersensitivity reactions at a remote site. For a diagnosis of focal sepsis, the previous medical history, the present state of health and the oral condition must be taken into account. Examination of oral cavity must include oral mucosa, testing vitality and assessing the periodontal condition of teeth. Dead teeth and periodontal disease increase the risk of bactermia. Oral sepsis has been related to

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many conditions like rheumatoid arthritis, valvular heart disease, endocarditis and renal, ocular, gastro-intestinal, skin, neurological and pulmonary diseases. There is firm evidence that bactermia from oral sepsis may lead to subacute bacterial endocarditis, particularly when damaged heart valves are present following attacks of rheumatic fever or in those with congenital heart disease. In the case of valvular heart disease, it is mandatory to eliminate all oral/dental foci of sepsis. The most important measures are to eliminate periodontal disease and to remove non-vital teeth. The use of antibiotic prophylaxis is a little controversial, but the general consensus is that it is mandatory in suspected individuals. The prophylactic regimen listed in the 1997 Committee report of AHA and adopted by ADA in July 1998 is as follows: 1. Amoxycillin 2grams one hour before the procedure (pdiatric dosage 50 mg/kg body wt) 2. For penicillin-allergic cases Clindamycin 600 mg one hour before the procedure (pdiatric dosage 20 mg/kg body wt) Cephalexin 2 grams one hour before the procedure (pdiatric dosage 50 mg/kg body wt) Azithromycin 500 mg one hour before the procedure (pdiatric dosage 15 mg/kg body wt) If oral administration is not possible, a) Ampicillin 2 grams I/M or I/V 30 minutes before the procedure (pdiatric dosage 50 mg/kg body wt) b) For penicillin-allergic cases Clindamycin 600 mg I/M 30 minutes before or I/V immediately before the procedure (pdiatric dosage 20 mg/kg body wt) Cephazolin 1 gram I/M 30 minutes before or I/V immediately before the procedure (pdiatric dosage 25 mg/kg body wt) (No post-operative doses; if excessive bleeding occurs, an extra antibiotic dose is given 2 hours later)

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Facial cellulitis
Cellulitis is a diffuse inflammation of the soft tissues which is not circumscribed or confined to one area, but which tends to spread through tissue spaces and along facial planes. This type of infection occurs as a result of infection by microbes producing significant amounts of hyaluronidase and fibrinolysins, which acts to break down hyaluronic acid (the universal cementing substance) and fibrin. A patient with cellulitis of face or neck is usually moderately ill, and has an elevated temperature and leukocytosis. There is a painful swelling of the involved soft tissues which is firm and brawny. The swelling is limited by anatomical restrictions. As the swelling persists, the infection tends to localise and a facial abscess may form. Regional lymphadenopathy is a common sign. Cellulitis is treated by administration of antibiotics and removal of the cause of the infection. One of the major complications of facial cellulitis is compression by the swelling of the airway and the alimentary tract, causing dyspnoea and dysphagia. Another major complication is media stinitis.

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Infections of specific tissue spaces

Tissue spaces or fascial spaces are potential spaces situated between planes of fascia, bone and muscles, which form natural pathways along which infection may spread. Scott in 1952 classified tissue spaces into 1. Superficial compartment Buccal space 2. Floor of the mouth (a) sublingual space (b) submandibular space (c) submental space 3. Masticator space (a) (Superficial) temporal space (b) Deep temporal space (c) Submasseteric space (d) Superficial pterygoid space 4. Parapharyngeal space Deep pterygoid space 5. Parotid compartment 6. Paratonsillar space

1. The superficial fascial compartment

This has as its inferior margin the lower border of the mandible, and as its superior margin the inferior border of the zygomatic arch, zygoma, and inferior orbital margin. Posteriorly, it extends to the posterior border of the vertical ramus of the mandible, where it meets the fascial covering of the parotid gland. Anteriorly, it follows the anterior bony aperture of the nasal cavity and extends from anterior nasal spine to the symphysis. Its superficial boundary is facial skin and deep boundary is buccinator and masseter muscles and external aspects of maxilla and mandible. The muscles of facial expression, buccal pad of fat, branches of facial nerve, blood vessels and lymph nodes are contained in this space.

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Buccal space

This is a part of the superficial space, superficial to the buccinator and buccopharyngeal fascia, behind the labial musculature. It contains the buccal fat pad, Stensens duct and the facial artery. Molar infections exiting superiorly to the maxillary origin of the muscle or inferiorly to the mandibular origin, enter this space.

2. The floor of the mouth

This is contained within the inner aspect of mandible with the mucosa of the floor of the mouth situated anteriorly and the skin covering the chin below. The mylohyoid muscle subdivides the floor of the mouth into the superior sublingual space and the inferior submandibular and submental spaces, the latter situated between the anterior bellies of digastric muscles. The submandibular and sublingual spaces communicate at the posterior edge of mylohyoid muscle.
Submandibular space

The submandibular space is separated from the overlying sublingual space by the mylohyoid musculature. It encloses the submandibular salivary gland and lymph nodes. Infections of this space usually originated from mandibular second and third molars and produce a swelling near the angle of the jaw. It is one of the most commonly involved in infections. There are also communications to other spaces in the floor of the mouth, lateral pharyngeal space, cranial fossa or even the media stinum.
Sublingual space

The sublingual space is bound superiorly by mucosa of the floor of the mouth, inferiorly by the mylohyoid muscle, anteriorly and laterally by the body of the mandible and posteriorly by the hyoid bone. Infection may arise from mandibular teeth by perforation of lingual cortical plate or by extension from submandibular space. Infections may produce an obvious swelling in the floor of the mouth, and may cause both dyspnoea and dysphagia.
Submental space

The submental space is situated between mylohyoid muscle and platysma, and is laterally bounded by the digastric muscles. If infection
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from the lower incisors exits labially through the mandibular bone, inferior to the muscle attachments, the submental space becomes involved. Infection in this space presents as an anterior swelling in the submental area and its spread is similar to that in submandibular and sublingual spaces.
Ludwigs angina

Ludwigs angina is a severe cellulitis beginning usually in the submandibular space secondarily involving the sublingual and submental spaces as well. The disease is not considered to be true Ludwigs angina under all spaces in the floor of the mouth are involved bilaterally. The chief sources of infection odontogenic, trauma and osteomyelitis. Mandibular 2nd and 3rd molars are the offenders in 80% of cases. The patient with Ludwigs angina presents with a rapidly developing board-like swelling of the floor of the mouth and consequent elevation of the tongue. There is brawny induration, tissues dont pit on pressure, and manifests a lifeless appearance. Sharp limitations are noticed to the extent of swelling. As the disease continues and involving the neck, edema of the glottis may occur presenting a life threatening condition. Infection may also spread to parapharyngeal spaces. Treatment consists of massive antibiotics and supportive therapy. In very severe cases edema of glottis may necessitate tracheostomy. Surgical intervention is aimed at reviving tissue tension and establishing drainage, in most case pus is not obtained. A bilateral through and through incision is given in the submandibular region extending from the skin piercing platysma and mylohyoid to the base of the tongue. The wound is probed for pus pockets. No sutures are given.

3. The masticator space

This contains the vertical ramus of the mandible and its surrounding masseter and medial pterygoid muscles, together with a portion of temporalis. The facial sheaths surrounding these muscles are formed by the splitting of the anterior layer of the deep cervical fascia.
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This occurs at the anterior, posterior and inferior margins of the ascending ramus to form a well-defined space.
Temporal and infratemporal spaces

Superiorly, there is a recess around the temporalis muscle known as the temporal or zygomaticotemporal space which is limited superficially by a thick sheet of temporal fascia which arises from zygomatic arch. Deep to the temporalis, the space is limited by the temporal bone; the muscle creating two subdivisions termed superficial and deep temporal spaces. The infratemporal space is bounded anteriorly by the maxillary tuberosity, posteriorly by the lateral pterygoid space, laterally by the tendon of temporalis and coronoid process and medially by lateral pterygoid plate and deep head of medial pterygoid muscle. This space contains the pterygoid plexus, the internal maxillary artery and the mandibular, mylohyoid, lingual, buccal and chordae tympani nerves. Infection in this space may cause trismus, sometimes swelling of eyelids, involvement of pharynx causing dysphagia, and severe pain or feeling of pressure in the area of infection. The lower part of masticator space is subdivided into submasseteric space and superficial pterygoid space (pterygomandibular space) by the ramus of mandible.
Submasseteric space

The submasseteric space is situated between the masseter muscle and the lateral surface of the ramus. The masseter attaches to the ramus at three sites deep part on the lateral surface of coronoid process, middle part on lateral surface of ramus and superficial part near angle of mandible. The submasseteric space is parallel to the attachment of middle part and is a narrow region between deep and middle parts. Posterior limit of this space is parotid gland. Anterior limit is retromolar fossa. Infections of this space usually occur from a mandibular third molar. The patient may suffer from severe trismus and pain, and there may be a facial swelling.
Pterygomandibular (Superficial pterygoid) space

Bounded laterally by the inner surface of the ascending ramus, medially by the medial pterygoid muscle and superiorly by the lateral
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pterygoid muscle, infection of the pterygomandibular space may arise through extension from pericoronitis of a mandibular third molar. Severe trismus results from infection of this space and extreme radiating pain is common. There is no clinical facial swelling evident although swelling of lateral posterior region of the soft palate may occur.

4. Parapharyngeal space
This has two main parts the lateral pharyngeal space and the retropharyngeal space. The deep pterygoid space is also considered to be an upper recess of the parapharyngeal space. The lateral pharyngeal space is bounded anteriorly by the buccopharyngeal aponeurosis and the pterygoid muscles, posteriorly by the prevertebral fascia and medially by the lateral wall of pharynx. Infection of this space may impinge on the pharynx, causing dysphagia or even dyspnoea. Trismus is usually present. The source of infection may be a second or third molar, and may be direct extension from the tooth or from submandibular space. This space communicated with the media stinum by the prevertebral fascia, so that infection may reach that area by direct extension. The retropharyngeal space is bounded anteriorly by the wall of the pharynx, posteriorly by the prevertebral fascia and laterally by the lateral pharyngeal space and carotid sheath. Infection here may result from medial extension of infection in the lateral pharyngeal space, and may displace the buccopharyngeal fascia forward, the abscess impinging on the pharynx. The infection may spread down to the media stinum since the prevertebral fascia extends down to that area.

5. Parotid space
The parotid gland is completely enclosed in a compartment of the superficial layer of deep cervical fascia. This space also contains associated structures like the facial nerve, auriculotemporal nerve, posterior facial vein, external carotid artery and its terminal branches. The gland itself is situated outside the masseter, with the deep part extending across the ramus of the mandible to lie medial to it. Because of the tenacious, unyielding nature of the parotid fascia, the infections of parotid space are extremely painful and tender. Infection in
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this space is usually an extension of the infection in the lateral pharyngeal space or by retrograde spread through parotid duct. It typically points medially or inferiorly to open into the oral cavity or to the neck. Since the fascia is thin at the deep part, the pus may break into the lateral pharyngeal space.

6. Paratonsillar space
This contains the tonsil and lies between the superior constrictor laterally and the mucous membrane covering the anterior and posterior pillars of fauces medially. Superiorly it extends to the soft palate. Peritonsillar abscess (quinsy) is usually caused by penetration from the depth of a tonsillar crypt or the supratonsillar fossa, but may occur occasionally by complication of third molar infection. There may be acute pain on one side of throat radiating to the ear. Dysphagia and mild trismus are common features. The fully developed abscess causes a tense swelling in the anterior pillar of fauces, and a bulge in the soft palate on the affected side. Systemic symptoms may also be present. Treatment of quinsy involves incision and antibiotics.

7. Other potential spaces

Apart from those mentioned in the Scotts classification, certain other potential spaces exist in the head and neck area, to which odontogenic infections may spread.
Buccal space

This is bounded anteromedially by the buccinator muscle, posteromedially by masseter and laterally by deep fascia covering parotid gland. It is limited below by the deep fascia of mandible. The buccinator muscle acts as an effective barrier to the spread of infection, especially in an early stage. Pus from periapical infection of molar teeth, which emerges from the bone above the origin of buccinator in upper jaw or below its origin in mandible, will spread to the outer side of buccinator and give rise to a local buccal space abscess. Drainage is effected by a horizontal incision low down inside the cheek.

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Space of the body of the mandible

This is enclosed by a layer of fascia derived from the outer layer of deep cervical fascia, which attaches to the inferior border of the mandible and then splits to enclose the body of the mandible. Superiorly it is continuous with the alveolar mucoperiosteum. Infections in the space may be dental or vascular in origin or may arise from other spaces, and usually result in abscess of labial or buccal vestibule of lower teeth.
The upper lip

Infections at the base of the upper lip usually occur as a result of an abscess of upper canines or incisors. The pus forms on the oral side of orbicularis oris muscle and tends to point in the vestibule. Treated by incision in vestibule or extraction of teeth.
The canine fossa

A periapical abscess which discharges buccally from an upper canine or first premolar may lead to an accumulation of pus in the canine fossa, deep to the muscles of facial expression moving the upper lip. If the infection perforates the labial bone above the attachment of levator anguli oris, it localises deep to levator labii superioris. If pus accumulates in canine fossa the nasolabial fold is obliterated by the swelling and there may be a drooping of angle of the mouth. Oedema of lower eyelid also may occur. Treated by incision and drainage at the vestibule with extraction of the tooth
Subperiosteal abscess of palate.

The mucoperiosteum of palate has mucosal and periosteal layers bound together strongly. No actual space exists between mucoperiosteum and bone but the periosteum may be stripped by accumulating pus. As the apex of lateral incisor is close to palatal bony surface, this is the most common source of a palatal abscess. The abscess may track
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posteriorly even to the area of soft palate but almost never across the midline. Pus beneath the palatal mucosa produces a circumscribed fluctuent swelling usually confined to one side of palate, with little tendency to discharge spontaneously. Incision of a palatal abscess should be carried out in anteroposteriorly to avoid dividing the greater palatine vessels.

Complications.
Apart from the obvious complications of spread of infection through tissue spaces and systemic toxemia, two obvious complications of odontogenic infections from the upper teeth are maxillary sinusitis and cavernous sinus thrombosis.

Maxillary sinusitis
An acute or chronic inflammation of the maxillary sinus is often due to the direct extension of dental infection, but originates also from other infectious diseases. Acute sinusitis may result from an acute exacerbation of an acute or chronic inflammatory periapical lesion or by extraction of a maxillary bicuspid or molar, and perforation of the sinus. Patients with acute maxillary sinusitis suffer moderate pain and tenderness as well as swelling overlying the sinus. Pain may be referred to teeth or ear. These may be discharge of pus through the nose. Treatment of the condition includes removal of the infecting locus and antibiotic therapy. Chronic sinusitis may develop as an acute lesion subsides, or may develop as it is. Clinical symptoms are generally lacking. Vague pain or stuffy sensation may be present. Treatment consists of removal of the cause and the removal of the affected lining.

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Cavernous sinus thrombosis.

Intracranial complications of dental infection may include subdural empyema, brain abscess, leptomeningitis etc but the most common one is cavernous sinus thrombosis. This is a serious condition consisting in the formation of a thrombus in the cavernous sinus or its communicating branches. There are many routes by which infection from teeth or face may reach the cavernous sinus. Infection from the face and lip are carried via the facial and angular veins, while dental infections are carried by the pterygoid plexus. The former is very rapid with a short fulminating course because of the large open system of veins leading directly to the cavernous sinus, while the latter has a much slower course because of many small twisting passages. Diagnostic features of cavernous sinus thrombosis include 1. Signs of blood stream infection, evidenced by fever chills, rapid pulse etc. 2. Evidence of venous obstruction exophthalmos, oedema of eyelids, photophobia, and multiple retinal haemorrhages. 3. Paralysis of cranial nerves III, IV and VI. 4. Abscess formation in neighbouring soft tissues. 5. Evidence of meningeal irritation. 6. A known site of infection The disease was once almost invariably fatal, death occurring by meningitis or brain abscess. The advent of antibiotics has decreased the mortality rate. Cavernous sinus thrombosis will require energetic antibiotic therapy and heparinisation to prevent extension of the thrombus. A neurosurgical consultation is necessary as a matter of urgency.

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Management of infections
Diagnosis
The first stage in the management of any infection, acute or chronic, is to make an accurate diagnosis. In most cases, the patient with infection presents with the classic signs and symptoms of pain and swelling, surface erythema, pus formation and limitation of motion. Systemically, features like fever, lymphadenopathy, malaise, a toxic appearance and leukocytosis may be found. Once it is determined that an infection has indeed taken place, the treatment is planned. The principles of treatment are first to control the infection, second to support the patient and third to remove the cause of the infection.

Control of infection
The infection may be controlled by administering antibiotics and where pus is formed, by establishing drainage. Where the airway is impaired, incision of the oedematous tissues to relieve pressure and a tracheostomy may be indicated. The principles of antibiotic therapy are discussed later.

Drainage of pus
Anaesthesia a general anaesthetic is the best choice, provided the anaesthetist considers the patient fit. It is essential to position the patient with the head lowered and neck extended so that pus and debris cannot be inhaled. If general anaesthesia cannot be administered due to respiratory distress or obstructions, the possible solutions are(a) use of local analgesia ethyl chloride spray (b) blind nasopharyngeal intubation followed by GA (c) nasopharyngeal intubation using fibre-optic laryngoscope
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(d) elective tracheostomy under LA followed by GA Where the patient is unfit for GA, a local anaesthetic is administered, preferably with sedation such as diazepam, using a sufficiently low dose for consciousness to be retained.
Soft tissue infections

Where the infection is superficial, the most fluctuent point is located. The incision must be made close to this site, giving consideration to the anatomy of the area and the cosmetic result. It should be made on or parallel to a skin crease and in one stroke. Access should be sufficient to admit a fingertip to break down any loculations in the abscess cavity. A pair of curved Spencer-Wells artery forceps or sinus forceps may be used to deepen the wound. A swab for bacteriophage examination may be taken at this point. A drain of corrugated rubber or nylon is inserted as deeply as possible into the wound and held in place by a suture through the skin. The drain should be left in situ for 2-4 days until the discharge has ceased. Where resolution is delayed, wider investigations such as blood and urine tests should be performed to identify disorders like blood dyscrasias, diabetes or renal diseases. Finally when infection has been controlled, the cause must be removed.
Vestibular region

Abscess in the buccal sulcus should be drained by making a horizontal incision in the reflected non-attached mucosa opposite the tooth or teeth, which are the cause of infection. A drain is seldom necessary. In the lower premolar region, the mental nerve must be avoided.
Palatal region

Incision is made in antero-posterior direction to avoid sectioning of greater palatine vessels. A short length of ribbon gauze drain is tucked
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loosely into the abscess cavity and sutured to one edge of wound for 24 hours.
Superficial facial compartment

This space is drained through extra oral incisions. Injury to vital anatomic structures like the facial artery, facial nerve, mental nerve, parotid duct etc should be avoided. Where the abscess cavity is close to the mandible, it may be better to institute a through and through drainage.
The floor of the mouth

In this region, superficial abscesses pointing on the skin may be drained by an external approach. The important structures to be protected are the submandibular duct, genial tubercle area and lingual nerve. But trismus is unlikely to be so severe that intraoral drainage cannot be performed. In a patient with Ludwigs angina, energetic treatment should be started without delay. The patient must be admitted in hospital and high dosages of antibiotic instituted. Surgical decompression is usually necessary to safeguard the airway. Progress is assessed by monitoring remission of dysphagia and dyspnea. The administration of GA is hazardous. It is safest to use LA. Bilateral submandibular arrowhead incisions or through-and-through incisions may be used. Before the operation, the need for elective tracheostomy should be considered.
The masticator space

The tissue spaces in this region may be drained through an intra oral incision along the anterior border of the ascending ramus. a closed pair of Spencer-Wells artery forceps should be inserted lateral to the ramus when

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draining submasseteric space abscess, or along medial aspect of ramus when pterygomandibular space is involved. In superficial pterygoid infections or massive infections of submasseteric space, an extra-oral drainage may be required. In the case of latter, care must be taken not to injure the branches of the facial nerve or the large arteries. Drainage of the temporal space may be obtained through an intraoral incision under he zygomatic arch, or extra-orally in the temple area. When the temple area presents a boggy, ballooned appearance, the temporal fascia underneath has necrosed. The dead fascia should be removed either by irrigating through the I&D openings and blindly exploring the temporal regions with a haemostat, or by extending the opening 2 to 3 cm to facilitate direct excision of the necrotic fascia.
Parapharyngeal space

Intra-oral incision along the anterior border of the ramus is used to drain pus in this space also. The closed blades of forceps are entered through the incision deep to medial pterygoid muscle. If the abscess has tracked down the neck, extra-oral incision 1 cm below and behind the angle of mandible or at the posterior border of sternomastoid may be required. In the case of retropharyngeal space infection, the incision is at the posterior wall of pharynx, should be vertical and placed 1 cm from the midline. Two serious vascular complications of parapharyngeal space infection are thrombophlebitis of internal jugular vein and erosion aneurysm.
The parotid compartment

Intra-oral or extra-oral incisions may be used. Infections deep to the parotid gland are drained using through-and-through incisions. The extraInfections of orofacial region

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oral approach is by going through the skin of the temple between temporal and zygomatic branches of the facial nerve.
Paratonsillar space

Infection of this space readily enters the soft palate which may be incised with guarded blade and drained via its inferior surface. Curved artery forceps is inserted and directed towards the tonsillar fossa, where there is often a well-defined abscess cavity.

Support of the patient

The patient should be admitted for treatment if i. Compression of airway or dysphagia due to infection are suspected, ii. iii. The patient is very unwell, The patient is unable to manage at home, There must be careful monitoring of fluid intake and output. Intravenous fluids, nourishment, analgesics and sedatives may be given as necessary. The use of hot packs and ice-packs are not advocated.

Removal of the cause

This is done after the reduction of acute phase to prevent the recurrence of infection. Careful examination to determine the cause is important.

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Principles of antibiotic therapy

I) Whether to use antibiotics
When the clinician is confronted with a patient with a possible infection, the preceding factors must be weighed carefully. Minor infections in patients with intact host defences may not require antibiotic therapy. Even some moderately severe infections can be treated without antibiotics if proper drainage can be achieved. Antibiotics are required in minor infections in patients with depressed host defences, and in cases which do not lend themselves to surgical drainage (e.g. endodontic therapy with no drainage achieved through root canal).

II)

Choosing the appropriate antibiotic

The following guidelines are useful in selecting the proper

antibiotic.

1. Identification of the causative organism.

This may be determined either in laboratory where the organism can be isolated from pus, blood or tissue, or empirically based upon knowledge of pathogenesis and clinical presentation of specific infections. Antibiotic therapy can thus be initial (empirical) or definitive. Initial empirical therapy may be instituted with some reliability when the focus of the infection is known; aetiopathogenesis is known and organisms that commonly lead to such infection is common knowledge. Most dental infections can be treated in this way because 80% of the causative organisms are streptococcus and some are caused by staphylococcus, Neisseria and anaerobes. In these cases, laboratory identification is necessary only if the organism is found to be resistant to therapy. Post-operative wound infections and infections of wounds from trauma present a different story. Precise laboratory determination must be accomplished for a definite treatment.

2. Determination of antibiotic sensitivity

When the disease is not responding to initial antibiotic therapy, or in case of post-operative infections, the causative organism must be
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identified and antibiotic sensitivity must be determined. This is well exemplified by the emergence of penicillinase producing strains of staphylococcus species which resisted treatment with penicillin G, which was the drug of choice for many decades. Antibiotic sensitivity may be determined by disc diffusion technique or tube dilution technique. In serious infection or when toxic antibiotics are used, the latter is more helpful since it also gives the plasma level necessary to kill the organism.

3. Use of a specific narrow spectrum antibiotic

Upon receipt of culture and sensitivity report, there may be a choice of 4 to 5 antibiotics. Selection should be done in such a way that the antibiotic with the narrowest spectrum should be used. This reduces the risk of resistant strains and super-infections, since the normal flora is preserved.

4. Use of the least toxic antibiotic

The second principle is to select the least toxic drug. Some antibiotics can kill or injure human cells. Other factors being equal, use of less toxic antibiotic is advisable. The clinician should continuously be alert for signs of toxicity.

5. Patients drug history

Previous allergic reactions and previous toxic reactions should be noted. Potential interactions with other drugs should also be considered.

6. Use of bactericidal drugs

This is especially true in case of patients with depressed host defences, since the dwindled numbers of microbes make the job easier for the phagocytes to complete the treatment.

7. Cost of the antibiotic

Certain newer, highly effective antibiotics and other factors being equal, the cost to the patient should be considered. The use of brands with a proven history of success should be encouraged, since in some cases, cheaper drugs with similar labels may be less effective.

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III)

Principles of antibiotic administration

This involves considerations of dosage, route of administration and

combination therapy.

1. Proper dose
The goal of any drug therapy should be to prescribe or administer sufficient amounts to achieve the desired therapeutic effect, but not enough to cause injury to the patient. Optimum dosage may be determined by laboratory studies. When the disc diffusion method is employed, the amount of antibacterial activity in the zone surrounding the disc (after a standard dose of the antibiotic) is comparable to that present in the normal patients plasma. Further, the minimum inhibitory concentration (MIC) of the antibiotic can be determined. The MIC of the usual antibiotics for most common bacteria has been established. For therapeutic purposes, the peak concentration of the antibiotic at the site of infection should be 3 to 4 times the MIC. Dosage greater than this generally does not improve the therapeutic results, and increases the likelihood of toxicity.

2. Proper time interval

The frequency of dosing the drug is of equal importance as the dosage itself. Each antibiotic has an established plasma half-life (T), during which one half of the absorbed dose is excreted. The T has been established for various antibiotics. The usual dosage interval for the therapeutic dosage of antibiotics is four times the T. Because most antibiotics are eliminated via the kidneys, the patient with pre-existing renal disease and subsequent decreased clearance require longer interval between doses. An alternative technique is to decrease the dose and maintain the same time interval.

3. Proper route of administration

In some infections, only parenteral administration produces the necessary serum level of the antibiotic. Although convenient, the oral route usually results in the most variable absorption. Most oral antibiotics
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require a fasting state 30 minutes before or 2 hours after a meal for maximum absorption. When long-term parenteral administration is necessary, repeated intramuscular injections are poorly accepted by the patients, and the use of intravenous route should be considered. By switching from the parenteral to the oral route on the 2 nd or 3rd day of antibiotic therapy, recurrence of the infection is more likely. However, after the 5th day of parenteral administration, the blood levels achievable with oral administration usually are sufficient.

4. Combination antibiotic therapy

The usual result of a combination drug therapy is a broad-spectrum exposure that leads to depression of the normal host flora and increased opportunity for resistant bacteria to emerge. For routine infections, the disadvantages of combination therapy outweigh the advantages. There are, however, certain specific indications for combination antibiotic therapy. They are i. Need to broaden the antibacterial spectrum in the patient with life-threatening sepsis of unknown cause ii. Need to increase the antibacterial effect against a specific organism iii. For prevention of rapid emergence of resistant bacteria iv. Empiric therapy for severe odontogenic infections.

IV) Monitoring the patient

The main aspects requiring monitoring are

1. Response to treatment
Patients rarely have a noticeable response to antibiotic therapy for the first 24 to 48 hours unless surgery to accomplish drainage is also performed. Most commonly, the response begins by the second day. In an uncomplicated odontogenic infection, one would expect marked resolution to occur by the fourth day. An additional 3 days should be allowed for complete eradication of offending bacteria.

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If there is no improvement or the condition deteriorates, the causes of failure in treatment of infections are i. ii. iii. iv. v. Failure to drain abscess Obstruction of a duct Presence of foreign body Presence of open portals like catheters Poor host response, underlying systemic conditions like diabetes mellitus vi. Failure of antibiotic to reach the site of infection, as in osteomyelitis vii. Poor patient compliance in taking prescribed amount of drug at proper time interval. viii. Inadequate dose ix. Wrong bacteriologic diagnosis.

2. Development of adverse reactions

Adverse reactions occur very frequently with the use of antibiotics. The reactions encountered include hypersensitivity reactions, toxic reactions and side effects like gastro-intestinal disturbances.

3. Super infections and recurrent infections.

During the treatment of an infection with antibiotics, the normal host bacteria that are susceptible to the drugs are eliminated or drastically reduced in number. Then the pathogenic bacteria resistant to the antibiotic may cause a secondary infection, or super-infection. A common secondary infection is the overgrowth of Candida in the oral cavity or vagina. An occasional infectious situation may be masked, or put into a remission state by the antibiotic therapy, only to recur when the therapy is stopped. The patient should be observed for several weeks after the stoppage of therapy. Some infections, such as actinomycosis and osteomyelitis, require a more careful and longer follow-up.

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Conclusion
The incidence, morbidity and mortality of odontogenic infections have drastically diminished by the advent of antibiotic therapy. But the potential lethality still persists. Doctors, especially surgeons must constantly be alert to the potential seriousness of infections. In serious cases, maintenance of airway, intense antibiotic treatment and supportive therapy, and surgical intervention are imperative.

References
1. Management of infections of the oral and maxillofacial regions. Topazian and Goldberg. 3rd edition. 1994 2. A Textbook of Oral Pathology. Shafer, Hine and Levy. 1993. 3. Surgery of the Mouth and the Jaws. JR Moore (ed) 1987 4. Killey and Kays Outline of Oral Surgery. Part I. Seward, Harris and McGowan. 1987. 5. Asia-Pacific Dental News. Oct-Dec 1997. 6. Basic Principles of Oral and Maxillofacial Surgery. Vol. I. (eds.) Peterson, Marciani, Indresano. 1997.

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