Abscess Stage
The abscess stage is the last stage of an infection. An abscess is an enclosed collection of liquefied tissue, or pus, that is the result of the body’s defensive reaction to foreign materials or organisms (Fig. 8.2). The abscess will form once the cellulitis stage begins to consolidate through the body’s immune system response through the use of appropriate antibiotics. Once an abscess is formed, the purulence that produced it will migrate by the path of least resistance. This may be either through the mucosa or skin or through the fascial pathways of the head and neck. An abscess that migrates through the deeper layers of the head and neck, through the lingual mandibular plate to the sublingual space for example, may block respiration (as in Ludwig’s angina) or enter the brain (as in cavernous sinus thrombosis or meningitis). This may be life threatening and require immediate surgical and medical attention. When an abscess spontaneously drains to an area outside the body, an orocutaneous fistula for example, it will continue until the source of the infection is treated.
Determination of infection stage.
One of the primary ways to distinguish among the various stages of infection is to palpate the area in question. The following should be noted:
Consistency of the swelling:
Routes of Infection
The principal routes for the spread of infection are through the following four mechanisms:
1. Vascular System: The vascular system of the head and neck allows for the spread of infection because pathogens may travel via the venous system, which drains into other tissues or organs (Fig. 8.3).
2. Thrombophlebitis: Infection may spread to the walls of the veins, which may also thrombose and create a condition referred to as thrombophlebitis. A lack of valves in the head and neck’s venous system allows retrograde flow of blood and may involve the cavernous sinus, pterygoid, and pharyngeal plexuses with infected thrombi.
3. Lymph Vessels: The lymph vessels are very prevalent in the head and neck (Fig. 8.4). They commonly drain the infected site and carry the infection to regional lymph nodes. The nodes become tender, enlarged, soft, and mobile on palpation. This is termed lymphadenitis.
4. Fascial Spaces: Once the infection is outside the bone, the loose areolar connective tissue produces a path of least resistance into the various surgical spaces of the head and neck, including the thoracic mediastinum (Fig. 8.5). The muscle attachments to the maxilla, mandible, and fascial compartments limit or direct the path of infection. Infections that may occur after surgeries involving reflection of muscle attachments may permit the infection to spread more easily into these surgical spaces. It is prudent to prophylactically cover patients with antibiotics when larger regions of soft tissues are reflected beyond the facial vestibule or mucobuccal fold, which violate the muscle attachments and invade the subcutaneous tissues.
Lymphatic Spread of Infection
The lymphatic system is a part of the greater lymphoid system and is a part of the body’s immune system. It is an accumulation of small vessels connected by lymph nodes that function as a fluid return system for the body. A filtrate of the blood plasma flows out of the capillaries into the surrounding tissues, where it becomes extracellular fluid and is eventually gathered by the lymphatic vessels. Through a continuous circulation process, the lymph nodes filter the extracellular fluids, while lymphocytes, produced within the lymph nodes, fight infectious organisms that are acquired throughout the system.
The head and neck region has a vast network of lymphatic drainage that aids in the fight of foreign microorganisms. There are approximately 600 lymph nodes in the body, but only the submandibular, axillary, or inguinal regions are palpable in the healthy patient. In the head and neck area the retropharyngeal, submental, submandibular and cervical lymph nodes are the most important to be evaluated in the diagnosis of infections. The retropharyngeal nodes are located behind the pharyngeal wall and drain to the upper deep cervical lymph nodes. The submental nodes are located under the chin, are small in number, and drain the anterior mandible and associated structures (mandibular incisors, the tip of the tongue, and the midline of the lower lip and chin), which then drain into the submandibular nodes or directly to the cervical nodes. The submandibular nodes are located around the submandibular gland, the areas of the maxillary teeth, maxillary sinus (except the maxillary third molars area), the mandibular canines, all mandibular posterior teeth, floor of the mouth, most of the tongue, the cheeks, the hard palate, and the anterior nasal cavity all drain to these nodes. As the submandibular lymph nodes drain a large and extensive area, they are usually the first to be noticed in the occurrence of oral infections. The cervical lymph nodes are divided into upper and lower divisions and are located deep in the neck. The upper deep cervical nodes are located on the lateral surface of the internal jugular vein and lie just beneath the anterior border of the sternomastoid muscle. They receive drainage from the submandibular and retropharyngeal nodes. The lower deep cervical nodes are also found on the lateral surface of the internal jugular vein and beneath the anterior border of the sternomastoid muscle (but lower, approximately 2 inches above the clavicle) and drain the upper deep cervical nodes and many of the nodes at the back of the neck. Both the upper and lower cervical lymph nodes are impractical to palpate.
Lymph Node Examination.
Ideally, in a lymph node examination, always examine both sides of the head simultaneously with the pads of the fingertips (most sensitive part of the hands) (Fig. 8.6). Use steady, gentle pressure to determine enlargement, inflammation, or pain with respect to the contralateral side. Evaluate for:
Fascial Spaces of the Face (see Fig. 8.5)
The fascial spaces of the face are subdivided into five spaces: the canine space, the buccal space, the masticatory space (further divided into the masseteric, pterygomandibular, and temporal spaces).
Canine Space.
The canine space is located between the levator anguli oris and the levator labii superioris muscles. Infection spreads to this space through the root apices of the maxillary teeth, usually the canine. Direct surgical access is achieved via incision through the maxillary vestibular mucosa above the mucogingival junction.
Buccal Space.
The buccal space is bounded anterior to the masticator space and lateral to the buccinator muscle with no true superior or inferior boundary and consists of adipose tissue (the buccal fat pad that fills the greater part of the space), the Stensen duct, the facial artery and vein, lymphatic vessels, minor salivary glands, and branches of cranial nerves VII and IX. When infection is involved in the buccal space, the space can serve as a conduit for spreading disease between the mouth and the parotid gland. Surgical access to the buccal space infections may be easily accomplished through the intraoral approach. More complicated infections, directed by location within the buccal space, may require a preauricular and/or submandibular approach.
Masticatory Spaces
Masseteric space (and submasseteric space).
The fascia that forms the borders of the masticator space is a well-defined fibrous tissue that surrounds the muscles of mastication and contains the internal maxillary artery and the inferior alveolar nerve. It is bounded anteriorly by the mandible, posteriorly by the parotid, medially by the lateral pharyngeal space, and superiorly by the temporal space. Infections in this space may be misdiagnosed as a parotid abscess or parotitis.18
The most pronounced clinical feature of infection in this space is trismus. Computed tomography (CT) scan or magnetic resonance imaging (MRI) may be an invaluable resource to distinguish abscess from cellulitis and the surgical course required for treatment.19
Intraoral surgical access to this space for simple, isolated abscesses is generally adequate to allow for drainage but with extension into adjacent spaces, an external approach may be required.
Pterygoidmandibular space.
The pterygoidmandibular space is bounded by the mandible laterally and by the medial pterygoid muscle medially and inferiorly. The posterior border is formed by parotid glandular tissue, which curves medially around the posterior mandibular ramus and anteriorly by the pterygomandibular raphe, the fibrous junction of the buccinator and superior constrictor muscles. Surgical access to this space may be achieved intraoral in the case of simple infections, but may require extraoral access when multiple adjacent spaces are involved.20
Temporal space.
The temporal fascia surrounds the temporalis muscle in a strong fibrous sheet that is divided into clearly distinguishable superficial and deep layers that originate from the same region with the muscle fibers of the two layers intermingled in the superior part of the muscle. Infections of odontogenic or implant treatment origin are rare in this space but may occur. If an abscess does develop in this space, intraoral incision and drainage is difficult and usually requires an extra oral approach. Communicating facial-zygomaticotemporal nerve branches piercing through the fascial and muscular planes of the temporal fascia in the superior part of the muscle are important landmarks to prevent temporal hollowing that may occur due to surgical access procedures.21
Sublingual Space.
The sublingual space is bounded between the mylohyoid muscle and the geniohyoid and genioglossus muscles. This space contains the lingual artery and nerve, the hypoglossal nerve, the glossopharyngeal nerve, Wharton’s duct, and the sublingual salivary gland, which drains into the oral cavity through several small excretory ducts in the floor of the mouth and a major duct known as Bartholin’s duct. Infectious spread to this space is through perforation of the lingual mandibular cortical plate (Fig. 8.7). Incision and drainage of abscesses in this area are generally adequately treated through a simple intraoral approach.
Submental Space.
The submental space is bounded anteriorly by the symphysis of the mandible, laterally by the anterior bellies of digastric muscles, superiorly by the mylohyoid muscle, and inferiorly by the superficial fascia of the platysma muscle. There are no vital structures that traverse the submental space. This space is usually involved in odontogenic infections from the anterior mandibular teeth as benign or malignant lesions in this area are rare. Surgical access for drainage of infection is generally through an extraoral incision below the chin (Fig. 8.8).
Submandibular Space.
The submandibular space extends from the hyoid bone to the mucosa of the floor of the mouth, and is bound anteriorly and laterally by the mandible and inferiorly by the superficial layer of the deep cervical fascia. The mylohyoid muscle separates it superiorly from the sublingual space, which communicates with it freely around the posterior border of the mylohyoid. The mylohyoid muscle also plays a key role in determining the direction of spread of oral infections. As it attaches to the mandible at an angle, infections that perforate the mandible on the lingual side above the mylohyoid line will involve the sublingual space below.
Surgical access for abscess drainage may be either intraoral or extraoral, but is generally more suited for the extraoral approach. When infection has spread to the bilateral submandibular spaces, it represents one of the components (along with submental and bilateral sublingual space involvement) of Ludwig’s angina (Fig. 8.9). Surgical drainage in these situations is almost always through multiple extraoral incisions.
Lateral Pharyngeal Space.
The lateral pharyngeal space is an inverted cone with its base at the base of skull and apex at the hyoid bone and is bounded posteriorly by the prevertebral fascia, anteriorly by the raphe of the buccinator and superior constrictors muscles, and laterally by the mandible and parotid fascia. Infections present with pain, fever, neck swelling below the angle of the mandible and trismus (Fig. 8.10). Rotation of the neck away from the side of swelling causes severe pain from tension on the ipsilateral sternocleidomastoid muscle.
Spread of oral infection to this space may produce an ominous sign. Airway impingement due to medial bulging of the pharyngeal wall and supraglottic edema may occasionally occur, which may require the procurement of a stable airway by either tracheotomy or intubation. The treatment of lateral pharyngeal space infections requires surgical drainage through either a transoral or extraoral approach.22 While an intraoral approach may reach the anterior compartment, extraoral access through a submandibular approach will allow for adequate access.
Significant Complications of Infections
Head And Neck
Osteomyelitis
Osteomyelitis is an inflammatory condition of the bone that originates as an infection of the medullary space and eventually extends into the cortical bone and periosteum. The bone infection becomes active in the calcified portion of the bone and will produce pus in the medullary cavity and beneath the periosteum, which compromises the blood supply. This initiates ischemia of the bone, which results in necrosis. Osteomyelitis of the jaws has two main classifications, acute and chronic, based on the duration of the disease. Chronic osteomyelitis has classically been defined as a condition that has lasted over 1 month.23 While there are many subclassifications, acute and chronic osteomyelitis are generally subclassified as suppurative or nonsuppurative and usually is different in the etiology, microbiology, pathogenesis, and treatment in comparison to long bone osteomyelitis.24
Osteomyelitis has been associated with dental implants, usually starting as a periimplant radiolucency with eventual osteolytic changes. Case reports have also shown that implants placed in association with retained tooth roots have caused osteomyelitis infections.25Left untreated, osteomyelitis may become refractory with bacteria induced peri-implantitis that may lead to deep bone invasion of bacteria, and the spread of infection into deeper tissues. 26
Accurate diagnosis of mandibular osteomyelitis is based on clinical, radiographic, histologic, and microbiologic findings followed by surgical debridement of the infected area and a long-term antibiotic regimen (Figs. 8.11 to 8.13). Radiographic changes show a poorly defined, radiolucent bone loss with intermixed radiopaque areas, which show the classic signs of sequestrum. Conventional radiography of mandibular osteomyelitis has a higher specificity than its sensitivity, which makes early detection difficult. Radiographic signs of mandibular osteomyelitis are generally not apparent until they extend at least 1 cm in bone and compromise 30% to 50% of bone mineral content and may not be radiographically apparent in adults for up to two weeks.27 Typical early bony changes seen on conventional radiography may include: periosteal thickening, lytic lesions, endosteal scalloping, loss of trabecular architecture, and new bone apposition.28 This gives the classic “moth-eaten” appearance that is diagnostic for osteomyelitis.
Given the difficulty of detecting early stage osteomyelitis with conventional radiography, CT scanning and MRI are considered standard of care in the diagnosis of osteomyelitis because they are sensitive and specific. CT provides excellent delineation of even the most subtle osseous changes such as abnormal thickening of the affected cortical bone with sclerotic changes, encroachment of the medullary cavity, and chronic draining fistulas. Although CT may show these changes earlier than do conventional radiographs, CT is less desirable than MRI because of decreased soft tissue contrast as well as exposure to ionizing radiation. A T1-weighted short inversion time recovery (STIR) MRI has been shown to be able to detect bony changes indicating osteomyelitis as early as the subacute phase.29
Histologically, suppurative osteomyelitis is characterized by intense microorganism-provoked marrow inflammation and marrow vessel thrombosis with retention of viable osteoclasts and periosteum, which creates an environment conducive to continual bacterial proliferation.30 In the past, Staphylococcus aureus was thought to be the main causative organism of osteomyelitis. However, given the unique environment of the oral cavity, there tends to be a mixed infection with hemolytic streptococci and a predominance of oral anaerobes (e.g., Peptostreptococcus, Fusobacterium, and Bacteroides). Additionally, various other organisms, such as Actinomyces spp and Treponema pallidum, cause other types of osteomyelitis.31
Treatment of osteomyelitis usually involves removal of the suspected source, antibiotic therapy, medical treatment, and surgical intervention. Topazian has established the principles of treatment for osteomyelitis to include: (1) evaluation and correction of host defense deficiencies; (2) Gram staining, culture, and sensitivity; (3) radiographic imaging; (4) administration of stain-guided empirical antibiotics; (5) removal of mobile teeth/implants and sequestra; (6) administration of stain-guided antibiotics; (7) possible placement of irrigating drains; (8) and sequestrectomy, debridement, decortication, resection, and reconstruction.1 The complete resolution of the infection should be the main focus of management in patients with chronic osteomyelitis of the mandible, and aggressive surgical management is more likely to result in an ideal outcome.
Medication-Related Osteonecrosis of the Jaws (MRONJ)
In 2003 simultaneous and independent reports were published by Marx32 and Ruggiero33describing nonhealing exposed bone cases in the oral-facial region in patients treated with oral and intravenous bisphosphonate drugs. Shortly thereafter the manufacturers of intravenous bisphosphonates pamidronate (Aredia) and zoledronic acid (Zometa) notified health care professionals concerning the risk of developing osteonecrosis of the jaws in patients using these medications.34
Most recently, the American Association of Oral and Maxillofacial Surgeons (AAOMS) recommended changing the terminology of this condition. Previously termed bisphosphonate-related osteonecrosis of the jaw (BRONJ), the condition is now referred to as medication-related osteonecrosis of the jaws (MRONJ). This was related to the fact there is a growing number of osteonecrosis cases involving the maxilla and mandible associated with other intravenous antiresorptive, antiangiogenic, and monoclonal antibody medications, such as Denosumab (Prolia, Xgeva), which is a fully human monoclonal antibody used for the treatment of osteoporosis, treatment-induced bone loss, bone metastases, and giant cell tumor of bone.
AAOMS has recently initiated guidelines on the signs and symptoms of MRONJ in comparison with other nonhealing issues.35 Treatment guidelines have also been established which relate to various stages of the condition (Table 8.3). (The preoperative management of patients on bisphosphonates and antiresorptive medications is discussed in Chapter 2). Current or previous treatment with antiresorptive or antiangiogenic agents:
• Exposed bone or bone that can be probed through an intraoral or extraoral fistula(e) in the maxillofacial region that has persisted for more than 8 weeks; and
• No history of radiation therapy to the jaws or obvious metastatic disease to the jaws.
TABLE 8.3
Staging and Treatment Strategies for MRONJ
| MRONJ Staginga | Treatment Strategiesb |
| At risk category: No apparent necrotic bone in patients who have been treated with either oral or IV bisphosphonates | |
| Stage 0: No clinical evidence of necrotic bone, but nonspecific clinical findings, radiographic changes, and symptoms | |
| Stage 1: Exposed and necrotic bone, or fistulae that probes to bone, in patients who are asymptomatic and have no evidence of infection | |
| Stage 2: Exposed and necrotic bone, or fistulae that probes to bone, associated with infection as evidenced by pain and erythema in the region of the exposed bone with or without purulent drainage | |
| Stage 3: Exposed and necrotic bone or a fistula that probes to bone in patients with pain, infection, and one or more of the following—exposed and necrotic bone extending beyond the region of the alveolar bone (i.e., inferior bone and ramus in the mandible, maxillary sinus and zygoma in the maxilla) resulting in pathologic fracture, extraoral fistula, oral antral/oral nasal communication, or osteolysis extending to the inferior border of the mandible of sinus floor |
Although the true pathophysiology of MRONJ is not yet fully understood, decreased bone turnover (altered bone remodeling or over suppression of bone resorption) and infection are thought to be central to the pathogenesis of MRONJ.36
Histologically, MRONJ is characterized by marrow spaces with empty Howship lacunae and an absence of osteoclasts and viable periosteum. This suggests a noninflammatory drug toxicity to bone by osteoclastic death leading to oversuppression of bone renewal. Many additional hypotheses have been proposed such as angiogenesis inhibition, constant microtrauma, suppression of innate or acquired immunity, vitamin D deficiency, soft tissue toxicity to bisphosphonates, and inflammation (Fig. 8.14).37–40
Bisphosphonates prevent the renewal of old and injured bone because they make it brittle and prone to fracture, have a half-life in bone of 11 years due to irreversible binding to bone, and (when administered intravenously) accumulate in bone 142.8 times faster than oral bisphosphates.41 Additionally, osteoclastic resorption of bisphosphonate-loaded bone results in osteoclast death in which the cell bursts and releases retained bisphosphonate molecules inside the cell that redistribute in the local bone or bone marrow in a redosing effect.
Recently, the presence of biofilm has emerged to explain the etiology of many chronic infections, and this may be a contributing factor in the development and proliferation of MRONJ. Biofilm is an aggregation of bacterial colonies and other microorganisms such as yeast, fungi, and protozoa that have established a microenvironment from the secretion a mucilaginous protective coating in which they are encased that may be extremely difficult to treat with medications alone.
Sedghizadeh et al looked at biofilm composition on specimens from individuals who had sequestrectomy of bone for MRONJ.42 They found that bone specimens from affected sites in all patients revealed large areas occluded with biofilms comprising mainly bacteria and occasionally yeast (Candida spp). The specimens included a large number of bacterial morphotypes and included species from the genus Fusobacterium, Bacillus, Actinomyces, Staphylococcus, and Streptococcus. Bacterial colonization of the denuded bone in MRONJ has suggested that bisphosphonates may increase bacterial adhesion and biofilm formation. Kos et al discovered an up to a seven-fold increase in bacterial colonization on pamidronate-coated hydroxyapatite disc compared to controls.43 They postulated that the nitrogen group on pamidronate may act as a steric factor that facilitates anchoring of bacteria to the hydroxyapatite surface or may attract bacteria by direct electrostatic interaction. These studies lay credence to the high probability that increased bacterial adhesion in the presence of bisphosphonates may promote MRONJ and osteomyelitis development.
Individuals taking oral bisphosphonate therapy for short durations of time, less than 3 years, do not appear to have significantly higher rates of implant failure or infection.44 However, for patients taking long-term oral bisphosphonate therapy (exceeding 3 years) with concomitant prednisone treatment, there may be a significant increase in the incidence of both implant failure and infection. This phenomenon may be location specific because implants placed in the posterior mandible or maxilla in patients with a history of long-term oral bisphosphonate have a greatly increased risk of MRONJ development.45 Individuals who have received at least three or more doses of any intravenous antiresorptive medication (e.g., Reclast) may be considered an absolute contraindication to dental implant therapy with an almost guaranteed development of MRONJ.46
Cavernous Sinus Thrombosis
Cavernous sinus thrombosis is a very rare but extremely dangerous major complication of head and neck infections. Although the advent of antibiotics has decreased the incidence of the condition, a clinician should be able to recognize its signs and immediately refer the patient to the proper specialists.
The cavernous sinuses are trabeculated sinuses located at the base of the skull that drain venous blood from valveless facial veins. Infections may be delivered to this location from sources of infection in the vicinity of this vein, most likely those located in the midface. Initial symptoms are progressively severe headache or facial pain, usually unilateral and localized to retroorbital and frontal regions with high fever. Eventually, paralysis of the ocular movements in the eye on lateral gaze is a classic sign of this condition. This is termed ophthalmoplegia because it is due to compression of the sixth cranial nerve (lateral ocular gaze) from the pressure of purulence in the confined space of the sinus. Proptosis (anterior bulging of the eye) and eyelid edema also develop and may occur bilaterally. As the condition progresses, facial sensation may diminish confusion, and seizures, and a decreased level of consciousness may develop. Treatment involves removal of the infection source as well as administration for weeks of intravenous antibiotics and fluids because surgery is considered difficult and problematic (Fig. 8.15).
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