Spread of Oral Infection
Oral cavity consists of more than 500 bacterial taxa, several fungal species, few protozoal genera and many viruses as normal residents. Occurrence of infectious disease is determined by the interaction of the host, the organism and the environment. In a healthy state, there is a balance existing among these three factors. When the balance is lost disease occurs.
Odontogenic infection is one of the most common infections in humans. An oral infection can originate in the dental pulp and extend through the root canals of the tooth into the periapical tissues or it may originate in the superficial periodontal tissues and subsequently disperse through the spongy bone. Later it may perforate the outer cortical bone and spread in various tissue spaces or discharge onto a free mucous membrane or skin surface. It may become localized or extend diffusely. The spread of the disease depends upon a variety of factors and circumstances that may alter its course at any point. It is definitely dangerous if the infection escapes from the confines of the bone of the maxilla or the mandible.
The routes by which the infection can spread are: the lymphatic system, the blood stream or directly through the tissues. Factors affecting the ability of the infection to spread depend on the type and virulence of the organism, general health of the patient, the anatomical site of the initial infection, which decides the drainage of pus, and the effectiveness of the patient’s immune mechanism.
It is usually easy to determine whether an infection is present or not, based on local and systemic factors. Local changes include pain, swelling, restriction of movement, surface erythema, and pus formation. Systemic factors include toxic appearance, fever, lymphadenopathy, malaise, and increased white blood cell count.
Cellulitis is a diffuse inflammation of soft tissues which is not circumscribed or confined to one area, but which, in contrary to the abscess, tends to spread through tissue spaces and along fascial planes. This type of reaction occurs as a result of infection by microorganisms that produce significant amounts of streptokinase, hyaluronidase (the spreading factor of Duran-Reynolds) and fibrinolysins, which act to breakdown or dissolve hyaluronic acid, the universal intercellular cement substance, and fibrin. Streptococci are particularly potent producers of hyaluronidase and are therefore a common causative organism in cases of cellulitis. Streptococci in their growth phase consume local oxygen and metabolize nutrients to produce an acidic environment, which is conducive to the subsequent growth of anaerobic microbes. The anaerobes such as Prevotella and Porphyromonas species destroy collagen.
Cellulitis of the face and neck most commonly results from dental infection, either as sequela of an apical abscess or osteomyelitis, or following periodontal infection. The pericoronal infection or pericoronitis (q.v.) occurring around erupting or partially impacted third molars and resulting in cellulitis and trismus is an especially common clinical condition. Sometimes cellulitis of the face or neck will occur as a result of infection following a tooth extraction, injection, either with an infected needle or through an infected area, or following jaw fracture.
Injectable soft tissue fillers are used in plastic and reconstructive surgery, dermatology and cosmetic salons for facial augumentation and rejuvenation. Hyaluronic acid is normally used as fillers. Schütz P et al, have reported 22 cases of acute facial inflammation following infected facial tissue fillers. Of the 22 patients, three were diagnosed with facial cellulitis, four with periorbital abscess and 15 with a buccal space abscess.
The patient with cellulitis of the face or neck originating from a dental infection is usually moderately ill and has elevated temperature and leukocytosis. One feels painful swelling of the soft tissues involved that are firm and brawny. Much of the swelling is due to inflammatory edema. (Fig. 11-2). If the superficial tissue spaces are involved, the skin is inflamed, has an orange peel appearance and is even purplish sometimes. In the case of inflammatory spread of infection along deeper planes of cleavage, the overlying skin may be of normal color. In addition, regional lymphadenitis is usually present.
Infections arising in the maxilla perforate the outer cortical layer of bone above the buccinator attachment and cause swelling, initially of the upper half of the face. The diffuse spread; however, soon involves the entire facial area. Extension towards the eye is a potentially serious complication because of the cavernous sinus thrombosis through the veins of the inner canthus of the eye. When infection in the mandible perforates the outer cortical plate below the buccinator attachment, there is a diffuse swelling of the lower half of the face, which then sees a superior as well as cervical spread. Spread to the cervical tissue can cause respiratory discomfort.
As the typical facial cellulitis persists, the infection frequently tends to become localized, and a facial abscess may form. When this happens, the suppurative material present seeks to ‘point’ or discharge upon a free surface (Fig. 11-3). If early treatment is instituted, a resolution usually occurs without drainage through a break in the skin.
A microscopic section through an area of cellulitis shows only a diffuse exudation of polymorpho-nuclear leukocytes and occasional lymphocytes, with considerable serous fluid and fibrin, causing separation of connective tissue or muscle fibers (Fig. 11-4). Cellulitis presents only a nonspecific picture of diffuse acute inflammation.
Cellulitis is treated by the administration of antibiotics including antianaerobics and also the removal of the cause of the infection. To avoid the further spread of infection or solidification of abscess, the patients should be advised not to massage the affected area with any medication. Although this condition is extremely serious, the resolution is usually prompt with adequate treatment, and untoward sequelae are uncommon.
Tissue spaces, or fascial spaces are potential spaces situated between planes of fascia that form natural pathways along which infection may spread producing a cellulitis, or within which infection may become localized with actual abscess formation. Knowledge of these fascial spaces, their boundaries, contents and relation to other structures is a necessity for the dentist because of the propensity for their involvement by spread of dental infection.
Shapiro defined the fascial space as potential tissue space, since none are actually spaces until pus has been formed. These potential spaces are compartments that contain structures such as salivary glands, fat or lymph nodes. Normally, these structures are surrounded by loose connective tissues, which can be easily stripped back by finger pressure, either during surgery in the patient, or by dissection in the cadaver to produce a cavity. In 1930 Grodinsky and Holyoke hypothesized that infections spread by hydrostatic pressure, with the flow of infected fluids guided by the resistance of certain tissue such as the fasciae, muscle, and bone.
Drainage by perforation of a bony plate occurs along lines of least resistance, so that, perforation of a thin cortex occurs before that of a thick cortex. The attachment of muscles may determine the route that an infection will take, channeling the infection into certain tissue spaces. The distribution and the interrelations of the many potential tissue spaces in the facial and cervical regions must be appreciated to understand the ease with which infection may spread throughout this area and even into distant areas.
From the maxillary central and lateral incisor the infection spreads to form labial, palatal abscess or vestibular abscess. Sometimes abscesses may form within the lip, which depends upon whether the pus penetrates above or below the muscle attachment.
Infections of the canine tooth may result in labial or vestibular abscess if the site of penetration of pus is below the muscle attachment. They form a canine space abscess if the site of penetration of the pus exists above the levator muscle of the upper lip.
Infections from molars form buccal or palatal abscess, if the site of penetration is below the buccinator muscle attachment and a buccal space abscess if the site of penetration of pus is above the muscle attachment.
From the mandibular incisor, the infection spreads to form a labial abscess if the pus penetrates above the muscle attachment, and forms a submental space abscess if it is below the muscle attachment.
If the pus from the first molar penetrates above the buccinator attachment, it forms a vestibular abscess on the buccal side, and below the muscle attachment results in a buccal space abscess. A sublingual abscess may be formed if the pus penetrates through the lingual side.
In second molars there are four possibilities, namely a vestibular or buccal space abscess if the pus penetrates through the buccal side and sublingual or a submandibular abscess if it penetrates through the lingual side. Infections from the third molars form submandibular or pterygomandibular or submasseteric abscesses.
The canine space is the region between the anterior surface of the maxilla and the overlying levator muscles of the upper lip. Infection of this space manifests as swelling with obliteration of the nasolabial fold and sometimes pus may drain through the inner canthus of the eye.
The buccal space is bounded medially by the buccinator muscle and its covering buccopharyngeal fascia; laterally by the skin and subcutaneous tissues; anteriorly by the posterior border of the zygomaticus major muscle above; the depressor anguli oris muscle below; and posteriorly by the anterior edge of the masseter muscle. Superiorly, the space is bounded by the zygomatic arch (Fig. 11.5A), and inferiorly by the lower border of the mandible.
Figure 11-5 Infections involving spaces.
(A) Buccal space. (B) Submasseteric space. (C) Submandibular space. (D) Submental space (Courtesy of Dr RS Nealakandan, Meenakshi Ammal Dental College, Chennai).
Clinically, the buccal space infection is dome shaped, and periorbital edema develops due to impaired venous and lymphatic drainage. Swelling begins at the lower border of the mandible and extends upward to the level of the zygomatic arch. Trismus is usually not present.
The infratemporal space is bounded anteriorly by the maxillary tuberosity; posteriorly by the lateral pterygoid muscle, the condyle and temporal muscle; laterally by the tendon of the temporal muscle and the coronoid process; and medially by the lateral pterygoid plate and inferior belly of the lateral pterygoid muscle. The infratemporal space contains the pterygoid plexus, the internal maxillary artery, the mandibular nerve, mylohyoid nerve, lingual nerve, buccinator nerve and chorda tympani nerves, and the external pterygoid muscle.
Infection in this space is often difficult to diagnose. Clinically an infratemporal abscess usually produces swelling extraorally over the region of the sigmoid notch and intraorally in the tuberosity region. The entire cheek may also be swollen if the buccal space is involved. The patient may exhibit trismus and sometimes swelling of the eyelids, especially if the postzygomatic fossa is involved. The involvement of the pharynx may cause dysphagia and severe pain or a feeling of pressure in the area of the infection.
The inferior portion of the infratemporal space is called the pterygomandibular space and it lies between the internal pterygoid muscle and the ramus of the mandible. The postzygomatic space extending anteromedially from the infratemporal space and is considered a part of it.
Infection in the pterygomandibular space may arise through extension from a pericoronitis of a mandibular third molar and has occurred in cases of injection of local anesthetic solution into this space. Severe trismus results from infection in this location, and extreme radiating pain is common. There is no evidence of clinical facial swelling, although swelling of the lateral posterior portion of the soft palate may occur. Injection of the maxillary tuberosity with an infected needle or solution has also caused infection of the infratemporal fossa. The pterygomandibular space abscess must be distinguished from the peritonsillar abscess. In the latter there is no dental involvement and less trismus.
The lateral pharyngeal space, one of the parapharyngeal spaces, is bounded anteriorly by the buccopharyngeal aponeurosis, the parotid gland and the pterygoid muscles, posteriorly by the prevertebral fascia, laterally by the carotid sheath and medially by the lateral wall of the pharynx (Fig. 11-6).
Infection of this space with abscess formation may impinge on the pharynx, causing difficulty in swallowing and even in breathing. The pain also may be referred to the ear. Trismus is usually present. An anesthetic may be required to confirm the diagnosis. The tonsillar pillars and tonsil are displaced medially, and so is the uvula. This infection must be differentiated from a peritonsillar abscess. In the latter condition trismus is less severe or absent, and the tonsil, instead of being normal, is enlarged and inflamed.
Lateral pharyngeal space infections have the potential to spread upward through various foramina at the base of the skull and cause cavernous sinus thrombosis, meningitis, and brain abscess. They can also spread posteriorly into the retropharyngeal space or invade the carotid sheath. The lateral pharyngeal space communicates with the mediastinum by the prevertebral fascia, so that the infection may reach this area by direct extension.
Infection here may result from medial extension of infection in the lateral pharyngeal space, and an abscess may form, displacing or pressing the buccopharyngeal fascia forward and impinging on the pharynx.
Patients with a retropharyngeal space infection will have pain, dysphagia, dyspnea, and nuchal rigidity. Bulging of the posterior pharyngeal wall is seen, which is often more prominent on one side because of adherence of the median raphe of the prevertebral fascia.
Downward extension of a retropharyngeal space infection will result in mediastinitis. In addition to the possibility of mediastinitis, it may cause thrombosis of the internal jugular vein and erosion of the internal carotid artery, resulting in fatal hemorrhage.
Since the prevertebral fascia extends inferiorly to the posterior mediastinum, it is possible for the infection in this retropharyngeal space to spread down to the mediastinum. Radiographs of lateral soft tissue can be helpful in establishing a diagnosis by permitting visualization of the widened retropharyngeal space. A computed tomography can also be used.
The parotid space contains the parotid gland and all associated structures, including the facial nerve, the auriculotemporal nerve, the posterior facial vein, and the external carotid, internal maxillary, and superficial temporal arteries.
Infection in the parotid space reaches the gland from the lateral pharyngeal space or by retrograde extension along the parotid duct, typically points medially or inferiorly and opens into the neck or oral cavity. Primary infections of the parotid space break into the lateral pharyngeal space readily because the fascia is thin over the deep portion of the parotid space. Spreading of the infection superiorly to the temporal fossa may also occur. A parotid space infection can be distinguished from a submasseteric space infection since there is lack of trismus, the elevatsion of the lobule of the ear, and the possible escape of pus from the parotid duct when the gland is milked.
The space of the body of the mandible is enclosed by a layer of fascia derived from the outer layer of the deep cervical fascia, which attaches to the inferior border of the mandible and then splits to enclose the body of the mandible. Superiorly, it becomes continuous with the alveolar mucoperiosteum and muscles of facial expression, which have their attachment on the mandible. The space contains the mandible, anterior to the ramus as well as the covering periosteum, fascia, muscle attachments, blood vessels, nerves, teeth, and periodontal structures. Shapiro pointed out that infections in this space may be dental, periodontal or vascular in origin, or may arise from fractures or by direct extension from infection in the masticator or lateral pharyngeal spaces.
Infections originating from incisors, cuspid or bicuspid teeth can involve the space of the body of the mandible; there is an induration or fluctuation of the labial sulcus if the outer cortical plate is involved. The infection is restricted to the floor of the mouth when the inner cortical plate is involved.
An infection originating from the molar teeth and involving the outer cortical plate results in a swelling in the oral vestibule if the infection perforates the bone above the external oblique line and the buccinator attachment. If perforation is below this line, the infection may point on the skin and lingual spread from infected bicuspid or molar teeth is into the floor of the mouth, when perforation of the bone is above the level of attachment of the mylohyoid muscle. The infection extends into the submandibular space or medially and posteriorly into the lateral pharyngeal space below the mylohyoid.