**6. Causes of infections**

#### **6.1. Pericoronitis**

submandibular space. As these spaces are partially separated by a thin sheet of mylohyoid muscle, infection in either space easily spreads into the other. It is generally believed that the midline enables free communication from either the sublingual or submandibular space.[3, 50]

Delineating the maxillary spread pattern is quite difficult, because limited data is available regarding its infections.[3] Nevertheless, it is plausible to consider that the observed difference in the spread profile between maxillary and mandibular infections may be due to differences in the distance between the original focal area in jaw bones and each of the spaces. For instance, maxillary infection was associated with temporalis muscle involvement more often than mandibular infection. Maxillary infection also spreads first to the masticatory space, but the temporalis and lateral pterygoid muscles are predominant targets for the infection. Involve‐ ment of the sublingual and submandibular spaces is rare. Otherwise, odontogenic infection arising in the mandible spreads first to the masticatory space. The masseter and medial pterygoid muscles in the masticatory space are most frequently involved. Thereafter, the infection spreads medially into the parapharyngeal space and posteriorly into the parotid space. Involvement of the sublingual and submandibular spaces seems to occur directly from

There are complex pathways which allow infection to spread along the facial and neck structures. Thus, it is important for dental practitioners to know more about the possibility of

**2.** The parotid and pharyngeal spaces are the secondary sites of spread from the masticatory

**3.** Mandibular infection spreads directly to the sublingual and submandibular spaces, and

**4.** Maxillary infection spreads to the deep facial and neck spaces in a different way from that

The pattern of maxillary infection spread differs from that of the mandible. Generally, the main maxillary spaces involved were found to be the buccal maxillary (19.05%) and canine (15.24%). [49] According to Yonetsu et al., the temporalis muscle was involved in 100% of the patients with maxillary infection. The involvement of the temporalis muscle in mandibular infections occurred only in 26% of the patients. The downward spread into the sublingual and subman‐ dibular spaces from maxillary infections did not occur. The lateral pterygoid and masseter muscles were frequently involved (86%) as in the cases of mandibular infection. Other spaces were also involved, but less frequently. The buccal space was involved in 57% of the patients

**The sequence of odontogenic infection spread** that most commonly occurs is:

**5.2. Fascial infections derived from maxillary odontogenic origins**

**1.** The masticatory space is the primary site of spread from mandibular infection.

the primary site of mandibular infection.[3]

346 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

of mandibular infection (Figure 2).

with maxillary infection[66] (Figure 2).

space.

a dental intervention to be a cause of severe infections.

Pericoronitis is an infection of the gingiva of a partially erupted tooth. The most frequent form of pericoronitis is caused by the partially erupted lower third molar, mainly due to the favorable niche that is created once the mucous cap covering the molar becomes retentive and deep enough to trap food particles and reduce the oxygen potential. These factors create the perfect microenvironment for the onset and subsequent development of a recurrent infectious, inflammatory condition caused by polymicrobial microorganisms, especially strict anaerobes. [19] Third molar pericoronitis may appear in either of its two acute variations, namely serous and suppurative, as well as in its chronic form; when either of the two acute forms previously mentioned stays untreated.

#### **6.2. Periapical lesions/Intra-oral abscess**

The most significant clinical condition of all bacterial infections of periapical origin is the socalled acute apical periodontitis.[16] It is usually the result of purulent pulpitis that spreads into the periapical space, therefore, it appears in the course of pulpal disease. In acute apical periodontitis there is an accumulation of pus inside the apical space of the tooth involved. This condition is commonly underestimated by dental practitioners in terms of its morbidity and mortality.[46] (Figure 3)

**Figure 3.** Clinical (A) and radiographic(B) aspects of a periapical lesion.

#### **6.3. Infection of sublingual, submental and submandibular spaces (Ludwig's Angina)**

Ludwig's angina is a rapidly spreading cellulitis that may produce upper airway obstruction, often leading to death. The most common source of Ludwig's angina is an odontogenic infection, from one or more grossly decayed, infected teeth, and is usually as a result of a native oral mixed aerobic-anaerobic flora. The patient with Ludwig's angina presents severe and obvious extra oral swellings including bilateral submandibular, submental, and sublingual spaces. Elevation and displacement of the tongue, trismus, drooling of saliva, airway obstruc‐ tion, sore throat, dysphagia and/or dyspnea are commonly present. With extensive use of drainage and antibiotics, most facial infections have satisfactory outcome before they have a chance to progress to Ludwig's angina.[1] (Figure 4)

**Figure 4.** Clinical presentation of Ludwig's angina.

### **6.4. Cervical cellutis**

**Figure 3.** Clinical (A) and radiographic(B) aspects of a periapical lesion.

348 A Textbook of Advanced Oral and Maxillofacial Surgery Volume 2

chance to progress to Ludwig's angina.[1] (Figure 4)

**Figure 4.** Clinical presentation of Ludwig's angina.

**6.3. Infection of sublingual, submental and submandibular spaces (Ludwig's Angina)**

Ludwig's angina is a rapidly spreading cellulitis that may produce upper airway obstruction, often leading to death. The most common source of Ludwig's angina is an odontogenic infection, from one or more grossly decayed, infected teeth, and is usually as a result of a native oral mixed aerobic-anaerobic flora. The patient with Ludwig's angina presents severe and obvious extra oral swellings including bilateral submandibular, submental, and sublingual spaces. Elevation and displacement of the tongue, trismus, drooling of saliva, airway obstruc‐ tion, sore throat, dysphagia and/or dyspnea are commonly present. With extensive use of drainage and antibiotics, most facial infections have satisfactory outcome before they have a Cervical cellulitis is most commonly from odontogenic origin and despite modern antibiotic therapy, cases with an initial delay in diagnosis and treatment may still result in this lifethreatening situation.[17, 58-60] Odontogenic infections are usually locally confined, selflimiting processes. However, under certain circumstances, like anatomical variations or suppression of the immune system of some patients, these infections may pass through the bony, muscular, and mucosal barriers and spread into contiguous and distant spaces, resulting in severe fulminating infections in the body cavities.[60]

When cervical cellulitis involves the parapharyngeal, retropharyngeal, and viscerovascular spaces, the purulent process has easy access to the mediastinum, pericardium, and thorax, thereby increasing mortality rates.[13, 17, 58-60] Because of the fulminant nature of descending cervical cellulitis with mediastinal complications, prompt recognition followed by broadspectrum antibiotic therapy, immediate surgical intervention, and intensive medical support are required.[13, 61]

The second and third mandibular molars are the teeth most frequently implicated in the cause of odontogenic deep neck infections.[17, 58, 60, 61] Because their roots lie below the mylohyoid muscle, medial perforation of a periapical abscess has immediate access to the submandibular space. Then, a collection of pus in the neck spreads along the cervical fascial planes, resulting in complications.[13]

### **6.5. Descending Necrotizing Mediastinitis (DNM)**

Acute purulent mediastinitis occasionally develops as a complication of odontogenic infection, in which case it is denominated descending necrotizing mediastinitis.[17] This is a serious infection involving the connective tissue that fills the interpleural spaces and surrounds the median thoracic organs. It is one of the most dreaded and the most lethal form of mediastinitis, which occurs as a complication of oropharyngeal abscesses or as a complication of cervical trauma, with severe cervical infection spreading along the fascial planes into the mediastinum. As infection spreads along deep cervical fascial planes into the mediastinum, widespread cellulitis, necrosis, abscess formation, and sepsis may concomitantly occur. The delay of diagnosis and late or incomplete drainage of the mediastinum are the main causes for high mortality rates associated with this condition.[4]

Even with the use of computed tomography scanning or magnetic resonance examination, aggressive drainage, and modern antibiotic treatment, the mortality rate of descending necrotizing mediastinitis remains high. Surgical management, particularly the optimal form of mediastinal drainage, remains controversial with support ranging from cervical drainage alone to cervical drainage and routine thoracotomy.

#### **6.6. Necrotizing fasciitis**

Abscesses of the peritonsillar region are among the most common deep abscesses of the head and neck. Although rare, complications resulting from this disease may be life threatening. One of the most dangerous complications is necrotizing fasciitis, which is a rare soft tissue infection characterized by progressive destruction of fascia and adipose tissue that may not involve the skin.[62, 63] Necrotizing fasciitis is characterized by its fulminating, devastating, and rapid-progressing course.[64] Diabetes mellitus, burns and malnutrition are common predisposing factors. Initially, cervical necrotizing fasciitis is predominantly characterized by a "simple" infection in the upper aerodigestive tract like pharyngitis or even tonsillitis. Typically, the general condition gets worse within a very short period of time with cardiovas‐ cular decompensation due to a toxic shock-like condition. Cervical necrotizing fasciitis initially involves the superficial muscular system and superficial fascial planes of the head and neck or it may result from a deep soft tissue infection, such as odontogenic infections or even pharyngitis, which spreads along the deep fascial planes.

If the disease is not recognized in time the infection can rapidly involve the great vessels or mediastinum, producing systemic toxicity and sepsis.[65, 66] The basis of successful treatment comprises aggressive surgical debridement and drainage of the involved necrotic fascia and tissue along with intensive broad-spectrum intravenous antibiotic coverage.[63]
