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Odontogenic infectionDr. Ahmed M. Adawy Professor Emeritus, Dep. Oral & Maxillofacial Surg.Former Dean, Faculty of Dental MedicineAl-Azhar University

Orofacial infections may be odontogenic or non odontogenic in nature and the vast proportion of odontogenic infections are caused by the endogenous bacteria present in the oral cavity . Examples of odontogenic infections are periapical and periodontal infections. Most of non-odontogenic infections are associated with an underlying medical condition. Examples of non-odontogenic infections are that of the skin, tonsils, or maxillary sinuses. Occasionally, infections could develop following an anesthetic injection or a surgical procedure Odontogenic infection(1)

One of the most difficult problems to manage in dentistry is odontogenic infections. These infections may range from low-grade, well-localized infections that require only minimal treatment to severe life-threatening facial space infectionsOdontogenic infection

Odontogenic infectionThe predisposition of an infection is related to an interruption of the fine balance between the host, the micro-organism and the environment. This imbalance, in turn, may lead to the multiplication of micro-organisms followed by invasion of different structures. The severity of infection is related to the number and virulence of micro-organisms and resistance of the host

Odontogenic infectionOdontogenic infections are typically Polymicrobial. The most common species of bacteria isolated in odontogenic infections are the anaerobic gram-positive cocci Streptococcus milleri group and Peptostreptococcus, anaerobic gram-negative rods, such as Bacteroides (Prevotella) also play an important role. Aerobic bacteria has little effect (2)

Odontogenic infectionOdontogenic infections progress through 3 stages: inoculation, cellulitis and abscess . Sinus tract/fistula may be seen in neglected casesInoculationIs characterized by the entry of pathogenic microbes into the body without disease occurring. Aninfectioninvolves the proliferation of microbes resulting in triggering of the defense mechanism, a process manifesting as inflammation

(3)

Inflammation Inflammation is the series of changes which occurred in the living tissue in response to an irritant. The manifestation of inflammation is typical and is characterized by: rubor (redness), calor (hotness), tumor (swelling or edema), dolor (pain), and functio laesa (loss of function). This reaction is protective and aims at limiting or eliminating the irritant. Depending on the duration and severity, inflammation is distinguished as acute, subacute or chronic. Odontogenic infection

Cellulitis Is an acute diffuse painful indurated swelling of the soft tissues resulting from a diffuse spreading of purulent exudate along the fascial planes with or without suppurationAbscessA collection of pus in a cavity formed by disintegration of tissue as result of infection Odontogenic infection

Discharging SinusSome times abscess ruptures to produce a draining sinus tract. Usually, infection recur when the site of drainage closes. Sinus is thus a one side tract of a single compartment

Odontogenic infection

Fistulae A drainage pathway or abnormal communication between two epithelium-lined surfaces due to destruction of the intervening tissue. Fistula is thus an epithelialized tract opening in both side of two different compartmentsOdontogenic infection

Acute dentoalvealar abscessThe usual cause of odontogenic infections is necrosis of dental pulp, which is followed by bacterial invasion through the pulp chamber and into the deeper tissues. Necrosis of the pulp is the result of deep caries of a tooth, to which the pulp responds with a typical inflammatory reaction. Vasodilatation and edema cause pressure in the tooth and severe pain as the rigid walls of the tooth prevent swelling. If left untreated the pressure leads to strangulation of the blood supply to the tooth through the apex and consequent necrosis

The necrotic pulp then provides a perfect setting for bacterial invasion into the bone tissue. Pus is formed in the cancellous bone, and spreads in various directions by way of the tissues presenting the least resistance until a cortical plate is encountered Acute dentoalvealar abscess

Clinically, the condition has rapid onset. Radiographically, changes in bone density may not be noticeable (you have to wait for approximately 10 days to detect bone rarefaction). It is characterized by symptoms that are classified as local and systemic Local SymptomsPain The severity of the pain depends on the degree of inflammation. Initially,the pain is dull and continuous and worsens duringpercussion of the responsible tooth or when it comesinto contact with antagonist teeth. There is a sense of elongation of the responsible tooth and slight mobility

Acute dentoalvealar abscess

Local SymptomsEdemaEdema appears intraorally or extraorally and it usually has a buccal and more rarely palatal or lingual localization. This swelling presents before suppuration, particularly in areas with loose tissue, such as the sublingual region, lips, or eyelids. Usually the edema is soft with redness of the skin. During the final stages, the swelling fluctuates, especially at the mucosa of the oral cavity. This stage is considered the most suitable for incision and drainage of the abscess

Acute dentoalvealar abscess

Systemic SymptomsThe systemic symptoms usually observed are: fever, chills, malaise with pain in muscles and joints, insomnia, nausea, and vomiting. Laboratory tests usually show leukocytosis, an increased erythrocyte sedimentation rate, and a raised C-reactive protein (CRP) levelTreatment Extraction of the tooth (or removal of the necrotic pulp by an endodontic procedure) results in resolution of the infection

Acute dentoalvealar abscess

Spread of odontogenic infectionRoutes of Spread of Odontogenic Infection:a. By direct continuity via the tissueb. Via the lymphatics into the regional lymph nodes and subsequently into the blood streamc. Haematogenous spread leading to thrombophlebitis, bacteremia or septicemia. Thrombus may propagate along the veins, entering the cranial cavity via emissary veins to produce cavernous sinus thrombosis

Whether the pus spreads buccally, palatally or lingually depends mainly on the position of the tooth in the dental arch, the thickness of the bone, and the distance it must travelDirect spread

The length of the root and the relationship between the apex and the proximal and distal attachments of various muscles also play a significant role in the spread of pus

Direct spread

Sometimes, infection may spreads towards the fascial spaces, forming serious abscesses called fascial space infection. The fascial spaces are potential areas and do not exist in healthy individuals. Bone, muscle, fascia, neurovascular bundles, and skin can all act as barriers to the spread of infection. It should be remembered however, that no tissue barrier or boundary is so restrictive to universally prevent spread of infection into contiguous anatomical spaces Fascial space infection

Facial spaces have been classified as either primary or secondary spaces infection Primary maxillary spaces Canine Buccal InfratemporalPrimary mandibular spaces Submental Buccal Submandibular Sublingual

(4)Fascial space infection

Secondary fascial spacesMassetericPterygomandibularSuperficial and deep temporalLateral pharyngealRetropharyngealPrevertebral Fascial space infection

Primary maxillary spaces Upper lip Infection at the base of the upper lip typically originates from the upper anterior teeth. It spreads to the orbicularis oris muscle, from the labial sulcus between the levator labii superioris muscle and the levator angularis oris muscle

Canine spaceSpread of infection to the canine fossa usually originates from maxillary canine or upper premolar teeth, often presenting above the buccinator muscle attachment. These swellings usually obliterate the nasolabial fold and may extend to the lower eyelid

Buccal spaceThe attachment of the buccinator muscle to the base of the alveolar process can control the spread of infection in the region of the mandibular and maxillary molars. An infection spreads intraorally, superficial to the buccinator muscle, in front of the anterior border of the masseter muscle. Thus, the clinical manifestations of infection in this space are characterized by swelling confined to the cheek

PalateThe palate is usually involved in infections originating from the maxillary lateral incisor or the palatal roots of the posterior teeth. The infection spreads from the apices of these teeth, perforating the palatal alveolar bone, and pus accumulates below the palatal mucoperiosteum

Infratemporal spaceExtension of infection from maxillary molars can pass into the infratemporal space. The space is located behind the zygomatic bone posterior to the maxilla and medial to the insertion of the medial pterygoid muscle. The infratemporal space is bounded superiorly by the greater wing of the sphenoid and is in close proximity to the inferior orbital fissure, with a possible risk of spread of infection to the orbit. Infection may ascend into the cavernous sinus (through venous plexus in the ovale and spinosum foramen)

Infratemporal space

Infratemporal space

The submental space lies between the two anterior bellies of the digastric muscle. Anteriorly and laterally this space is bounded by the body of the mandible. It is contained, superficially, by the platysma muscle and, deeply and superiorly, by the mylohyoid muscle. Infection of this space usually arises from mandibular anterior teeth, where the infection perforates the lingual cortex; swelling of the submental region is a characteristic clinical feature. The skin over the swelling is stretched and hardened, and the patient experiences considerable pain and difficulty with swallowing

Primary mandibular spaces Submental

Submental space

Submandibular spaceThe submandibular space is located below the mylohyoid muscle, medial to the ramus and the body of the mandible. It is bounded anteriorly by the attachments of the anterior belly of the digastric muscle and posteriorly by the posterior belly of digastric muscle and the stylomandibular ligament. Infection from the posterior mandibular teeth may pass lingually, below the attachment of the mylohyoid muscle, into this space. Clinically, swelling of the submandibular region tends to obliterate the angle of the mandible, causing pain and redness of the skin overlying this region. Dysphagia is also usually a marked symptom

Submandibular space

Sublingual spaceInfection spreads into this space as the result of perforation of the lingual cortex, above the attachment of the mylohyoid muscle. This space is bounded superiorly by the mucous membranes and inferiorly by the mylohyoid muscle. The genioglossus and geniohyoid muscles form the medial boundary. Laterally, this space is bounded by the lingual surface of the mandible. Infection in this space will raise the floor of the mouth and displace the tongue, medially and posteriorly. Such tongue displacement may compromise the airway and immediate intervention may be required. Dysphagia and difficulty with speech are also common

Sublingual space

Secondary fascial spacesSubmasseteric space

The most common source of infection in the submasseteric space is from lower third molar pericoronitis. This space is bound laterally by the masseter muscle and medially by the outer surface of the ramus of the mandible. It is in direct communication with the lateral pharyngeal space posteriorly. The temporalis muscle divides the superior part of this space into two portions, the superficial temporal space and the deep temporal space. Severe trismus due to spasm of the masseter muscle is a characteristic feature of involvement of this fascial space

Submasseteric space

Temporalspace

Massetricspace

Pterygomandibular space

Infection in this space is manifested by trismus, due to the involvement of the pterygoid muscles. This space is bounded medially by the medial pterygoid muscle and laterally by the medial surface of the mandible, anteriorly by the pterygomandibular raphe, and posteriorly by the deep lobe of the parotid gland. The lateral pterygoid muscle forms the roof of this space

Pterygomandibular space

Pterygomandibularspace

Lateral pharyngeal spaceThis space is located on the lateral side of the neck, bounded medially by the superior constrictor muscle of the pharynx and posterolaterally by the parotid space. The lateral pharyngeal space contains the carotid sheath, glossopharyngeal nerve, accessory nerve, and the hypoglossal nerve, as well as the sympathetic trunk. Thus, spread of infection into this space carries a significant danger of spreading into a descending neck infection and involvement of the mediastinum. Clinically, stiffness of the neck, swelling of the lateral wall of the pharynx, medial displacement of the tonsils, dysphagia, and trismus are among the characteristic clinical features of involvement of this space

Lateral pharyngeal space

Retropharyngeal space

This space is located between the posterior wall of the pharynx and the prevertebral fascia. This space is in direct communication with the base of the skull, superiorly, and the mediastinum, inferiorly. It has the same characteristic clinical features as infection of the lateral pharyngeal space and carries a significant complication risk of a descending neck infection

Evaluation of patients with dentofacial infectionsPatients with dentofacial infections may present with various signs and symptoms, ranging from less important to extremely serious. Quick assessment of the patients situation is essential as the first step of therapy. If the patient shows central nervous system changes, airway compromise, or toxification, then immediate hospitalization, aggressive medical treatment, and surgical intervention may be necessary. Basic principles of patient evaluation must be followed. A complete patient history, physical examination, laboratory investigation, radiological investigation, and accurate and appropriate interpretation of findings must be made. Following these basic principles provides the best chance of accurate diagnosis and treatment(5)

Principles of Treating Infection 1- Proper knowledge of anatomy, anatomical landmarks and vital structures of the face and neck is necessary to predict pathways of spread of infections and to drain these spaces 2- Remove the cause (i.e. extract the tooth, open & extirpate the pulp)3- Incision & Drainage (never let the sun set on undrained pus)4- Antibiotics

Incision & DrainageFor intraoral abscess, stab incision is done through the mucosa down deep to the underlying bone. Incisions for extra-oral abscesses should be placed in a skin crease to leave the least evident scar. Once the skin incision is made, blunt evacuation of pus might be done using a curved haemostat. The abscess cavity should be kept open to allow continuous drainage. Corrugated rubber, ribbon gauze, or tubular plastic drain might be used

Incision & Drainage of Submandibular abscessIncision and drainage helps to get rid of toxic purulent material, to decompress edematous tissues, to allow better perfusion of blood, which contains antibiotic and defense elements, and to increase oxygenation of the infected area

Antibiotic therapy in orofacial infectionsAntibiotics is generally indicated when the swelling is diffuse and spreading, and especially if fever is present and infection spreads to the fascial spaces, regardless of whether there is an indication of the presence of pus. Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a culture sample. Odontogenic infections are polymicrobial.Historically, penicillins have been used to treat odontogenic infections.

With the ever-increasing bacterial resistance to penicillin-based antibiotics with dental pathogens and concurrent clinical failures with penicillins, other agents have become increasingly attractive. Amoxicillin/clavulanate,clindamycin, and metronidazole are useful alternatives in combating the anaerobic bacteria involved in dentoalveolar infection . Clindamycin has more recently become a drug of choice for the management of odontogenic infections because of the bacterial susceptibility to this drug, great oral absorption, low emergence of bacterial resistance and good antibiotic levels in bone. Antibiotic therapy in orofacial infections(6)

Criteria for hospitalization 1. Rapidly progressive cellulitis2. Dyspnea(shortness of breath ordifficult breathing)3. Dysphagia(difficulty in swallowing)4. Spread to deep facial spaces5. Fever of more than 38 C6. Intense trismus (inter-incisal distance less than 10 mm)7. Failure of initial treatment8. Severe involvement of general health status 9. Immunocompromised patients (diabetes, alcoholism or drug addiction, malnutrition, treatment with corticoids,.)(7)

Ludwig's Angina Ludwig's Angina is a massive indurated brawny cellulites, occurs bilaterally in the submandibular, sublingual & submental spaces. Infection is propagated by lymphatic spread or directly through submandibular space. Cellulitis is then rapidly spread to involve bilaterally the parapharyngeal and pterygoid spaces

Clinically, the condition is characterized by:1. Painful bilateral swelling of floor of mouth and elevation of tongue.2. Bilateral firm, brawny painful, diffuse swelling of upper part of neck3. Difficulty in swallowing and breathing4. Rapid pulse, high fever, fast respiration5. LeucocytosisPatient should be hospitalized. Conservative treatment includes intravenous antibiotic therapy and close airway observation . Pus is evacuated, when indicated, by through & through drainage

Ludwig's Angina(8)

Cavernous sinus thrombosis

Infections may spread via hematogenous route to the cavernous sinus occurs from:1- Anteriorly: a) Superior labial venous plexus to b) Anterior facial vein, then via c) Superior or inferior ophthalmic vein into the cavernous sinus2- Posteriorly: from retromandibular vein to the ptrygo- mandibular venous plexus, the emissary vein passing through foramen ovale, spinosum, to cavernous sinus3- Superior petrosal sinus (inside the ear)

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Anteriorpathwayophtalmic v.infraorb. v.deep facial v.Posteriorpathwaypterygoid plx. oval orspinosum for.

Dangerous triangle of the faceNever squeeze infection boil in the dangerous area

OsteomylitisOsteomylitis is defined as an inflammation of the bone marrow with a tendency to progression to involve adjacent cortical plates and often periosteal tissues. The incidence of osteomyelitis is much higher in the mandible due to the dense cortical bone that prevents the penetration of periosteal blood supply, and the inferior alveolar artery is the only supply to the mandible. It is much less common in the maxilla due to the excellent blood supply from number of different arteries. In addition the maxillary bone is much less dense than the mandible (10)

Classification of Osteomylitis1- Acute suppurative2- Subacute3- Chronic suppurative4- Rarely, a sclerotic nonpurulent form of osteomylitis occurs; this is termed Garrs sclerosing osteomylitis. Other related disorders are chronic recurrent multifocal osteomylitis; tuberculous osteomylitis Acute and chronic osteomylitis is distinguished by the development of dead bone sequestra. Sequestra is an island of dead bone that have not been resorbed

Radiographic FeaturesThe appearance of moth-eaten bone or sequestrum of bone, is the classic feature of chronic osteomylitis

Surgical Options

Classic treatment is sequestrectomy and saucerization. The aim is to dbride the necrotic bony sequestra in the infected area and improves blood flow Decortication involves removal of the dense, often chronically infected and poorly vascularized bony cortex till reaching good bleeding bone, and placement of the vascular periosteum adjacent to the medullary bone to allow increased blood flow and healing in the affected area

1. Dahln G. Microbiology and treatment of dental abscesses and periodontal-endodontic lesions. Periodontol 2000.28:206;2002.2. Kuriyama T, et al. Bacteriologic features and antimicrobial susceptibility in isolates from orofacial odontogenic infections. Oral Surg Oral Med Oral Pathol Oral Radiol Endod 90: 600, 2000.3. Miliro M, Ghali GE, Larsen PE, Waite P, editors. Petersons principles of oral and maxillofacial surgery. 2nd ed. Hamilton (ON): BC Decker; 2004. 4. Flynn T. . Contemporary oral and maxillofacial surgery. In Hupp JR, Ellis E III, Tucker MR. Editors 5th ed. St-Louis: Mosby; pp317-336, 2008. 5. Malik N. A. Textbook of Oral and Maxillofacial Surgery. . 2nd ed. Jaype Brothers Medical Publishers (P) Ltd. India pp. 587-636, 2008. 6. Kuriyama T, et al. Antimicrobia susceptibility of 800 anaerobic isolates from patients with dentoalveolar infection to 13 oral antibiotics. Oral Microbiology Immunology 22: 285, 2007. 7. Martnez BA. Et al. Consensus statement on antimicrobial treatment of odontogenic bacterial infection. Av. Odontoestomatol . 21: 321, 2005.

References:

8. Larawin, vJ. et al. Head and neck space infections, Otolaryngology-Head and Neck Surgery, 135: 889, 2006. 9. Desa V, Green R. Cavernous sinus thrombosis: current therapy. J Oral Maxillofac Surg 70: 2085, 2012. 10. Topazian RG, Goldberg MH, Hupp JR. Oral and maxillofacial Infections 4th ed. Philadelphia: W.B. Saunders. pp.214235,2002.

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