zr arse 287-25/30200/0 Copy © 198 by Walaa & Wilkin Co, Odontogenic infections DAVID W. Infections of the oral cavity are most commonly odontogenic in origin and include dentoalveolar as well as periodontal and deep fascial space infections. Such infections not only produce significant local symptoms but on rare occasions also result in life- threatening complications such as mediastinal or in- tracranial extension, retropharyngeal spread with air- way obstruction, pleuropulmonary suppuration and hematogenous dissemination. Current concepts in odontogenic infections of children and adolescents are reviewed in this article with special emphasis on their clinical presentation and management. MICROBIOLOGIC CONSIDERATIONS ‘The microbiota associated with odontogenic infec- tions are complex and generally reflect the combined influence of the indigenous oral flora and the unique microbiota of the underlying conditions. In the healthy oral cavity Streptococcus, Peptostreptococcus, Veillonella and diphtheroids account for more than 80% of the total cultivable flora, Quantitative studies indicate that obligate anaerobes occur in numbers as great as eight times those of facultative bacteria.* Facultative Gram-negative rods are uncommon in the healthy child but may be more prominent in seriously ill and hospitalized pationts.** In addition the oral cavity cannot be regarded as a single, uniform environment. Although representative species of microorganisms can be isolated from most areas of the mouth, certain sites tend to favor coloni- zation by specific organisms. For example Streptococ- cus salivarius and Veillonella spp. have a predilection for the tongue and buccal mucosa* and predominate before the eruption of teeth. In contrast Streptococcus sanguis, Streptococeus mutans as well as Actinomyces viseosus preferentially colonize the tooth surface while Fusobacterium, pigmented Bacteroides and an- aerobic spirochetes appear to be concentrated in the ssingival crevice.* Bacterial adherence and interagere- rom the Division of Infectious Disease, Departments of Medi cine (DWM, AWC) end Pediatrics (DWS), University of British Columbia, Vancouver General Hospital, and BC Children's Hosp. tal, Vancouver, Canna, “Adaress for reprints: Anchony W. Chow, M.D. Division of Tec i Disease, G. F. Strong Research Laboratories, Vancouver Gen ral Hospitel, 310 W. tot Avenue, Vancouver, BC, Canada, V5Z 1 Mo, MEGRAN, MD, DAVID W. SCHEIFELE, MD 267 VoL 3,Na.8 Print in 8c AND ANTHONY W. CHOW, MD gation, local environmental conditions such as oxygen tension and pH as well as other host factors” seem to govern these unique colonization patterns and in- fluence the composition of the oral flora. ‘The concept of microbial specificity of odontogenic infections has been appreciated only recently. In the case of dental caries an etiologic association with S, mutans has been firmly established.®* Similarly, in gingivitis and periodontitis a unique and specific bac- terial composition of the subgingival plaque has been identified. In the healthy periodontium the microflora is sparse, consisting mainly of Gram-positive orga- nisms such as S. sanguis and Actinomyces species. In the presence of gingivitis, however, the predominant subgingival flora shifts to a greater proportion of anaerobic Gram-nogative rods, and Bacteroides inter- ‘medius is the most common isolate." With estab- lished periodontitis the flora further increases in com- plexity with a preponderance of anaerobie Gram-neg- ative and motile organisms. Bacteroides gingivitis (for- rmerly Bacteroides asaccharolyticus) is then most com- monly isolated. ‘Thus, overall Bacteroides, Peptostreptococcus, Acti: omyees and Streptococcus are the most prevalent isolates in pyogenic orofacial infections arising from ‘odontogenic sources. Except in selected patients with serious underlying illnesses, Gram-negative bacilli and ‘Staphylococcus aureus aze not commonly associated with odontogenic infections." These data serve to underscore the importance of anaerobic transport and culture of specimens in the microbiologic diagnosis of these infections, ANATOMIC C Soft tissue infections of odontogenic origin tend to spread along planes of least resistance from the sup- porting structures of the affected tooth to various potential spaces in the vieinity. Accumulated pus therefore must perforate bone, generally at the site where it is thinnest and weakest, before extending into the periapical areas or deeper fascial spaces. In the young child the site of perforation is usually along the lateral aspect of the alveolar bone because the primary teeth are located superficially and anteriorly within the jaws, In contrast the permanent teeth are more deeply rooted, and thus the spread of infection NSIDERATIONS258 ovonrocENte follows a more complex pattern in older children and adolescents, In the mandible, for example, perforation usually occurs on the lingual aspect when infection Fic, 1. Routes of spread of odontogenie orofacial infections song planes of least resistance. A, eorontl sation in region of fist ‘molar eet, mallaryantrom b, naga cavity, palatal pets sublingual space above mylohyoid muses), submandibular Golow mylohyoid muscle): intraoral presentation with infection spreading through the boceal plates inside the attachnnent of the Duceinator muscle; g,extraoral presentation to bucesl space with infection spreading through the buccal plates outside the attach rent ofthe Iuecinator moscl, B, lingual aspect of the mandible {apices of invelved tooth sbove the mylohyoid morele, with spread of infection to sublingual space; apices of invaved tooth below ‘the mylobyoid muscle, with spread of infection into submandibular space. Reproduced with permission from Chow eal" INFECTIONS. May, 1984 originates in the region of the molar teeth and on the buccal aspect when more anterior teeth are involved."” In the maxilla the bone is weakest on the buccal aspect throughout and relatively thicker on the palatal as- pect. If pus perforates through either the maxillary or mandibular buccal plate, it will present intraorally if inside the attachment of the buccinator muscle to the maxilla or mandible and extraorally if outside this muscle attachment (Fig. 1). Therefore infection of the upper and lower molars, lower incisors and the lower canine teeth often present with extraoral manifesta- tions, When a mandibular infection perforates lin- gually, it presents in the sublingual space if the apices of the involved teeth lie above the attachment of the mylohyoid muscle (for example mandibular incisor, canines, premolars and first molars) and in the sub- mandibular space if below the attachment of this muscle (for example second and third molars) (Fig. 1). Thus these local anatomic barriers of bone, muscle ‘and fascia predetermine the routes of spread, extent and clinical manifestations of many orofacial infec- tions of odontogenic origin. ‘The clinically important “fascial spaces” most often involved in odontogenic infections are illustrated in Figures 2 and 3, These are potential spaces between layers of fascia and they communicate with one an- other to varying degrees. A thorough understanding of the “anatomic routes” of infection not only provides valuable information about the nature and extent of infection but also suggests the optimal surgical ap- proach for drainage. DENTOALVEOLAR INFECTIONS Odontogenie infections originate in either the per- iodontium or the dental pulp. The latter site is most commonly involved, resulting in dentoalveolar infec- tions. Pulpal infection most frequently results from car- ious exposure, a process that usually begins in the pits and fissures of the occlusal surfaces of molars and B OUSy PALIN nso = Zig A getty MuscLe masseren [| p) MUSE ic, 2, Fascial spaces around the mouth and face, horizontal section a evel of oclusl surface of mandibular teeth B ronal view of the face, Rapadaced with permission from Chow eaVol. 3, No. 3 Arve lenge! baome Ptyenar Shera A Seroboid o. rhyrld olen De at Ad Porotd sland or Tonsil Loteral pharyngeal space Hyoid Internal carotid & B Intesnal juguler v io. 2, Relation of ates pharyngenl, ettopharyngeal and pre vertabral spaces tothe posterior and anterior layers of deep cervical fcia, croweacetion of neck at level of thyroid isthmus: 1, super 2, pretracheal space; 8, retropharyngeal space; 4, “danges" space, 6, prevertebral space. B, coronal section in tht supratyoid region ofthe neck. Reproduced with permission from Chow eta.” premolars. Food retention and subsequent plaque for- ‘mation occur less often in interproximal sites and the gingival margin except in infants who fall asleep with bottle of milk or juice. Demineralization and destruc tion of the enamel is followed by invasion of the pulp to produce either a localized or a generalized pulpitis. If drainage of the pulp is obstructed, rapid progression ‘with pulpal necrosis and proliferation of endodontic microorganisms occurs, leading to periapical abscess or invasion of alveolar bone. Periapical infection of a primary tooth often tracks laterally through the alveo- lar bone to present as a “gumboil” (Fig. 4). MEGRAN ET AL, 259 In early or reversible pulpitis the affected tooth is generally sensitive to percussion and to both heat and cold. The pain will stop abruptly, however, when the stimulus is withdrawn. During late or irreversible pul- pitis the tooth is also exquisitely painful to hot stimuli ‘but application of cold provides prompt relief. If drain- tage through the tooth is established early, chronic irritation from the necrotic pulp may result in periap- ieal granuloma or eyst formation. This condition is frequently asymptomatic but can be detected by dental radiographs. ‘The principles of treatment in dentoalveolar infee- tions include prompt elimination of infected pulp, deep periodontal scaling or extraction of the tooth. Dentoalveolar abscesses should be surgically drained. Antibiotic therapy is indicated if drainage cannot be adequately established or when infection has perfo- rated the cortex and spread into surrounding soft tissue. PERIODONTAL INFECTIONS In the early phase of periodontal disease infection is confined to the gingiva (gingivitis). Later the un derlying supporting structures (periodontal ligament, alveolar bone and cementum) are affected (periodon- titis), ultimately leading to complete destruction of the periodontium and permanent loss of teeth. In contrast to dentoalveolar infection and abscess, per: odontal infections tend to localize to intraoral soft tissues and seldom extend into deeper structures of the face or neck. Gingivitis. This is the most common periodontal disease during childhood with a peak incidence in adolescence. Almost all children have some evidence of gingivitis. Inflammation of the gingiva is initiated by local irritation and microbial invasion." In sim- ple gingivitis there is a bluish-red discoloration with ‘welling and thickening of the free gingival margin, Bleeding of the gums after eating or toothbrushing may be an early finding. There is usually no pain, but ‘mild fetor oris may be noticed. Successful treatment Fic, 4. "Gumbo in young cil260 ODONTOGENIC INFECTIONS consists of removal of dental plaque and maintainence of good oral hygiene. In acute necrotizing ulcerative gingivitis (Vincent's disease or trench mouth), the patient typically expe- riences sudden onset of pain in the gingiva which interferes with normal mastication. Necrosis of the interdental papilla results in a marginated, punched- out and eroded appearance of the gingiva. A superfi- 3, grayish pseudomembrane is formed and charac: teristic halitosis is present. Frequently there is asso ciated fever, malaise and regional lymphadenopathy. ‘Treatment includes local debridement and lavage with oxidizing agents, which usually brings relief from pain within 24 hours. Antibiotic therapy with penicillin or ‘metronidazole is indicated and is highly effective.”"" Pericoronitis. This is an acute localized infection associated with gum flaps (opercula) overlying a par- tially erupted or impacted wisdom tooth. Food debris and microorganisms become entrapped under the af- fected gingival tissues. The pericoronal tissues are erythematous and swollen but the underlying alveolar bone is not usually involved. If drainage is interrupted. infection extends along fascial planes, most often into the mastication space. Treatment of pericoronitis in- cludes gentle debridement and irrigation under the tissue flap. Antibiotics and drainage may be necessary if extension into soft tissue occurs. Excision of the operculum may also be considered. A similar, transient inflammation can also occur with the eruption of other teeth (“eruption gingivitis") Periodontitis. Although chronic gingivitis that be- ssins during childhood and adolescence generally pre- cedes the spread of infection to the periodontium, periodontitis in itself is usually a disease of adults. Manifested as painless gingival inflammation with pockets of periodontal pus, and ultimately leading to tooth loss, periodontitis is occasionally seen, however, in children with underlying systemic illnesses such as diabetes mellitus. Localized juvenile periodontitis is a particularly de- structive form of periodontitis seen in adolescents and is characterized by rapid and localized bone loss af- fecting the first molar and incisor teeth. Usually its ‘onset is insidious and occurs around the time of pu- berty. Females are more commonly affected than are males, dental plaque is often minimal and calculus is absent. Subgingival cultures have revealed predomi- nantly saccharolytic organisms such as Actinobacillus aactinomycetem-comitans and Capnoeytophaga spp. in contrast to B. gingivitis, which is seen in adult perio- dontitis."""" Impairment of neutrophil chemotaxis has been demonstrated in this condition.” The disease may remain localized or may progress to involve other teeth. The disease should be suspected when the first molars or incisors are found to be loose, especially ‘when gingival inflammation is absent or minimal, and ‘May, 1984 when similar disease is present in other family mem- bers. Recent experience suggests excellent therapeutic results with systemic totracyeline combined with local periodontal treatment involving root debridement and surgical resection of inflamed periodontal tissues Periodontal abscess. This may be foeal or diffuse and presents as a red, uctuant swelling of the gingiva which is extremely tender to palpation. These ab- ‘cesses always communicate with a periodontal pocket from which pus can be readily expressed after probing. ‘Treatment is surgical and aimed at drainage of locu- lated pus. DEEP FASCIAL SPACE INFECTIONS Odontogenie infections may extend to the potential fascial spaces of the lower head and upper neck. Table ‘Leompares the clinical features of these “space infec- tions.” Masticator spaces. ‘These consist of the masse- teri, pterygoid and temporal spaces, which commu- nicate with each other as well as with the buceal, submandibular and lateral pharyngeal spaces (Fig 2. Infection originates most frequently in the molar tecth, particularly the third molars (wisdom teeth). Clinically the hallmark of masticator space infection is trismus and pain in the area of the body or ramus of the mandible. Swelling may not be a prominent finding, especially in the masseteric compartment, since infection exists deep to large muscle masses that obscure or prevent clinically apparent swelling. If infection extends internally it can involve an area close to the lateral pharyngeal wall, resulting in dys- phagia Infection of the deep temporal space usually origi- nates from involvement of the posterior maxillary molars. Little swelling is observed early, but as the infection progresses the cheeks, eyelids and whole side of the face may become involved. Direct extension into the orbit may also occur. Infections of the mas- ticator spaces tend to localize and treatment includes antibiotics and surgical drainage Buccal, canine and parotid spaces. As noted previously the relation of the root apices of the man- dibular or maxillary bicuspid and molar teeth to the origins of the buccinator muscle determines whether infection will exit intraorally into the buecal vestibule or extraorally into the buccal space (Fig. 1). Infection of the buccal space is readily diagnosed because of marked cheek swelling with minimal trismus and sys- temic symptoms. There is a great tendency to resolu- tion with antibiotic therapy alone. Involvement of the maxillary incisors and canines ray result in a eanine space infection which presents as dramatic swelling ofthe upper lip, canine fossa and frequently the periorbital tissues. Pain is usually mod- erate and systemic signs are minimal. On occasion aVol, 3, No.3 MBORAN ED A 261 TABLE 1 Comparative tures of odntgeie dep fei pase infections of he od end neck ae Gini Fearne efosdn Fay Timm Sling yaaa Byanen Noten hie) Pres Ponies May aot Im ett Ah a Powe maxilary molar Preset None aceon ats). Almont bent icra Mintost Minna! Checmortec). Ateneo See ee incom Melerte Nove" Uperipenine fsa Abert Abwont Maser space Tense” None Ripe o marted) Absent Aen Soph ied nendiular cnt Minimal Smandiuer™ Abect Abo mas Minis incsor Prevent Minimal Flor ofmouth (tomer) Pettit Prot Tmrcroment ""ylvement fine bseret Laer phagneeat ri Masicator pats Tnlenso Prominent Al of ow Pree Occasion Poser NisictarSee Mat Mn” Bebenms os. Pt Se er Retwpharynges] Lateratpharyngel sco Prevent MinialPostesorpharyx nds Prewst ——Pretnt ‘un daage) Distant vie pate i) Pretaceal Retephuegedopect Prevent None gpoparynx Pent severe Anterior esophagas purulent maxillary sinusitis may result due to direct extension of infection into the adjoining antrum. ‘Treatment consists of antibiotics and drainage, which ‘ean be accomplished intraorally. Odontogenic parotid space infection generally rep- resents secondary spread from a masseterie space in- fection in the area of the ramus of the mandible (Fig. 2), Swelling of the angle of the jaw is marked but trismus is absent. Intense pain, fover and chills are common. Closely related to the posterior aspect of the lateral pharyngeal space, such infections have the potential to extend directly into the “danger” and visceral spaces and thence to the posterior medias- tinum (Fig, 3), Treatment consists of antibiotics and judicious drainage ‘Submandibular and sublingual spaces. These two spaces are separated by the mylohyoid muscle (Fig. 1), and the submandibular space is further di- vided into the submaxillary and submental spaces. Infection in these spaces usually arises from the sec- ‘ond and third mandibular molar teeth since their root apices lie inferior to the mylohyoid muscle. Typically there is ewelling but little trismus and the condition rust be distinguished from submandibular sialadeni- tis and lymphadenitis of other causes. Therapy in- cludes antibiotics, dental extraction and extraoral sur- gical drainage. Infections of the sublingual space generally arise from mandibular incisors since their root apices lie above the mylohyoid muscle, Brawny, erythematous, tender swelling of the floor of the mouth is noted, beginning close to the mandible and spreading medi ally, Elevation of the tongue may occur in late stages. Surgical drainage of the sublingual space should be performed intraorally by an incision through the mu- cosa parallel to Wharton's duct bilaterally. A subman- dibular approach can be used if the submandibular space is also to be drained. "The term “Ludwig's angina” has been loosely ap- plied to a heterogeneous array of infections involving the sublingual, submaxillary and submandibular spaces.* However, for therapeutic and prognostic pur- poses, this diagnosis should be restricted to the classic description: (1) the infection is always bilateral; (2) both the submandibular and sublingual spaces are involved; (3) a rapidly spreading, indurated cellulitis is present without abscess formation or lymphatic involvement; and (4) the infection begins in the floor of the mouth. A dental source of infection has been found in 50 to 90% of reported cases and the second and third mandibular molars are most commonly in- volved. Clinically patients present with a brawny, boardlike swelling in the submandibular spaces that does not pit on pressure (Fig. 5). The mouth is usually held open and the floor is elevated, pushing the tongue to the roof of the mouth. Eating and swallowing are difficult and respiration may be impaired by obstruc- tion from the tongue, Rapid progression can result in edema of the neck and glottis and may precipitate asphyxiation. Fever and systemic toxicity are usually present and may be severe. Treatment requires high doses of parenteral antibiotics, airway monitoring, ‘arly intubation or tracheostomy when required, soft tissue decompression and surgical drainage. Lateral pharyngeal space. Also known as the pharyngomaxillary space, this area in the lateral neck262 ODONTOGENIC INFECTIONS Fig. 5. Luca's angina that oginsted ofthe mandibulat incisor, «periapical abscess is shaped like an inverted cone, with its base at the skull and its apex at the hyoid bone (Fig. 3). Of note, its medial wall is continuous with the carotid sheath, Involvement can occur in pharyngitis, tonsilitis, par- otitis and otitis as well as odontogenic infections. If the anterior compartment is infected the patient will exhibit fever, chills, marked pain, trismus and swelling below the angle of the jaw. Dysphagia and medial displacement of the lateral pharyngeal wall may also occur. Posterior compartment infection is character ized by septicemia with little pain or trismus, Swelling is often missed because itis usually internal and deep, behind the palatopharyngeal arch. Complications, particularly if the posterior compartment is involved, include respiratory obstruction from edema of the larynx, internal jugular vein thrombosis and erosion of the internal carotid artery. Since laryngeal edema may progress suddenly, close observation is necessary, and prophylactic tracheostomy may be required, High dose antibiotics and surgical drainage comprise ther- apy. It is usually prudent to wait for the infection to localize before drainage is attempted, unless respi tory obstruction or hemorrhage necessitates early sur- gical intervention, May, 1984 Retropharyngeal, “danger” and pretracheal spaces. The retropharyngeal space comprises the pos- terior part of the visceral compartment in which the esophagus, trachea and thyroid gland are enclosed by the middle layer of deep cervical fascia (Fig. 8). Lying behind the hypopharynx and esophagus, it extends into the superior mediastinum. Posterior to this com- partment lies the “danger” space which descends di- rectly into the posterior mediastinum to the level of the diaphragm. Infection of the retropharyngeal space may result from contiguous infection of the lateral pharyngeal space or via lymphatic spread from more distant sites in the nasopharynx to involve the retro- pharyngeal nodes. Retropharyngeal abscess is most ‘commonly encountered in infants and young children since the retropharyngeal Iymph nodes tend to atro- phy after 4 years of age." The onset of disease is often insidious, but dysphagia, dyspnea and nuchal rigidity develop and high fever and chills may also be present. Bulging of the posterior pharyngeal wall is observed and may be located more to one side than the other, especially early in the course of infection. Lateral soft tissue radiographs of the neck generally reveal marked widening of the retropharyngeal space. Potentially life-threatening, infection. of this space requires prompt surgical drainage. Complications include hem- orrhage, spontaneous rupture into the airway with asphyxiation, laryngeal spasm, bronchial exosion and thrombosis of the jugular vein, ‘The pretracheal space comprises the anterior por- tion of the visceral compartment and completely sur- rounds the trachea. Most commonly infections reach ‘this space through perforations of the anterior esoph- geal wall, but on occasion they develop through con- tiguous extension from a retropharyngeal space infec- tion, ‘The clinical presentation is characterized by severe dyspnea, but hoarseness may be the first com- plaint. Swallowing is difficult and regurgitation of fluids through the nose may occur. Prompt surgical drainage is critically important because of the risk of ‘extension into the mediastinum. COMPLICATIONS OF ODONTOGENIC INFECTIONS Complications of odontogenic infections can occur either by hematogenous spread or by direct extension, ‘Transient bacteremia is common during or after var- ious dental procedures, especially extraction of in- fected teeth,” and its relationship to bacterial endo- carditis and infections of cardiovascular prostheses is well-documented.’ Prophylactic antibiotic treatment during dental procedures, although frequently used, remains a controversial issue, especially in the absence of preexisting valvular heart disease. Complications caused by direct extension are discussed below. ‘Suppurative jugular thrombophlebitis and ca- rotid artery erosion. ‘These uncommon complica-Vol. 3, No. 3 tions of odontogenic infection usually arise from the lateral pharyngeal space. Once extension has occurred infection tends to spread up and down this vascular sheath. ‘The onset of suppurative jugular thrombo- phlebitis is acute, with shaking chills, spiking fevers and profound prostration. Tenderness and induration along the sternocleidomastoid muscle and swelling of| the lateral pharyngeal wall with neck rigidity are usually present, However, findings may be subtle. Septic pulmonary emboli and metastatie abscesses to the brain and other organs are not infrequent. ‘The usual recommended treatment consists of external drainage of the lateral pharyngeal space and ligation of the internal jugular vein. Important warning signals which may herald major hemorrhage due to erosion of the carotid artery in- clude multiple episodes of minor bleeding from the oral cavity or ear and ecchymoses of oral and cervical tissue, With the onset of major hemorrhage, manage- ‘ment consists of maintenance of the airway, restora- tion of blood volume and emergency ligation of the artery. Septic cavernous sinus thrombosis. ‘This dreaded complication of orofacial infections is also rare in the postantibiotic era. Infection of the maxil- lary teeth was the most common dental cause, Clinical features suggestive of this complication include: (1) early signs of venous obstruction in the retina, con- Junctiva and eyelids; (2) paresis of the third, fourth ‘and sixth cranial nerves; (3) abscess formation in neighboring soft tissue; (4) evidence of blood stream invasion; and (5) presence of meningeal irritation, ‘Treatment requires early recognition, high dose intra- venous antibiotics and surgical decompression of the underlying predisposing. infection, Maxillary sinusitis, In many individuals the roots of the maxillary molars lie in close proximity to the ‘maxillary antrum. At times congenital bony defects occur, with the roots adjacent to the sinus membrane. In these cases sinusitis can result from direct exten- sion of an odontogenic infection or from perforation of the sinus floor during extraction of a maxillary tooth.!” The clinical presentation of secondary sinus involvement is similar to that of primary disease, Osteomyelitis of the jaws. The mandible is much more susceptible to osteomyelitis than is the maxilla, mainly because the cortical plates of the former are thin and its vascular supply is relatively poor. Despite this osteomyelitis secondary to odontogenic infection is uncommon. When it does occur there is usually a predisposing condition such as compound fracture, diabetes mellitus or steroid therapy. Pus accumulating beneath the periosteum elevates it from the cortex and may lead to mucosal or cutaneous abscesses and fistulae. Severe mandibular pain is a common symp- tom. Periapical infection of primary teeth seldom ex- tends to involve the subjacent developing tooth buds. MEGRAN ET AL. 263, Chronic sclerosing osteomyelitis is a clinical variant characterized by # localized, hard, nontender swelling over the mandible. Actinomycosis is a common cause of this form of osteomyelitis of the jaws. ‘Treatment of osteomyelitis of the jaws is compli- cated by the presence of teeth and persistent exposure to the oral environment. Antibiotic therapy needs to bbe prolonged, often for weeks to months, Adjuvant surgical therapy may be required and hyperbaric ox- ‘ygen should be considered, particularly forthe chronic sclerosing variety.2** ‘THERAPEUTIC CONSIDERATIONS Dental caries and periodontitis. For both the prevention of caries and the treatment of periodonti- tis, the goal is control of the supragingival and subgin- gival plaques. With the emerging concept of microbial specificity in these infections, the prospect of specific antimicrobial therapy appears increasingly promis- ing. In localized juvenile periodontitis, for ex: ample, systemic tetracycline in conjunction with local periodontal treatment has yielded excellent results Unfortunately administration of tetracycline to chil- dren under 5 years of age can cause staining of the permanent dentition and is not generally recom~ mended. Apart from tetracycline therapy in localized juvenile periodontitis, however, current efforts specif- ically to suppress plaque-associated pathogenic bac- teria with systemic antibiotics have not been very successful in humans. ‘This may be due to inadequate concentrations of antibiotis in the specific target sites within the plaque. Although penicillin, vancomycin and tetracycline all appear to have cariostatic effects in animal models, only topical application of vaneo- mycin has been shown to reduce dental caries to some degree in humans.” Topical chlorhexidine appears more effective in reducing S, mutans populations from tooth surfaces® but has a bitter taste and stains the enamel. Other important. approaches to preventing caries and periodontitis include improved oral. hy- iene, diet modification with sucrose substitutes and active immunization against caries by use of vaccines prepared from S, mutans. Suppurative odontogenic infeetions. The most important therapeutic modality for pyogenic odonto- genic infections is surgical drainage and removal of necrotic tissue, Potentially involved fascial spaces should be carefully examined and incision and drain- age performed at the optimal time, Premature incision into ¢ poorly localized cellulitis can disrupt the normal physiologic barriers and cause further extension of infection, Antibiotic therapy is important in halting local spread of infection and preventing hematogenous dis- semination. Penicillin remains the antibiotic of choice for treatment of orofacial odontogenic infections de- spite recent reports of a relative increase in resistance264 of certain oral anaerobes, particularly Bacteroides me- laninogenicus.®*® Penicillin has an enviable record in the treatment of these infections and is both safe and cost-effective, Nevertheless treatment failure with penicillin in orofacial infections due to beta-lacta- ‘mase-producing Bacteroides strains has been re- ported. Thus in seriously ill patients and in patients who have had an unfavorable or delayed response to penicillin, alternative therapy with clindamycin ap- pears justified. Clindamycin has remained active against nearly all penicilin-resistant, and sensitive, major anaerobic isolates associated with odontogenic infections. ‘The cephalosporins, particularly cephalothin and cefazolin, remain highly active against oral anaer- ‘obes™ and are excellent alternative agents. Cefoxitin, carbenicilin, ticarillin, moxalactam and cefotaxime all have enhanced activity against aerobic Gram-neg- ative bacteria as well as beta-lactamase producing oral anaerobes and are suitable candidates for treatment of mixed orofacial infections in severely ill or immu- nocompromised patients. Both erythromycin and tet- raeycline are not considered preferred choices because of their suboptimal antimicrobial. activity in vitro against certain anaerobes. Amoxicillin ampicillin and doxyeycline (for children over 5 years of age) may be ‘used for oral therapy in less serious infections. Met- ronidazole is effective in acute necrotizing ulcerative tingivitis. It has excellent tissue penetration, but ‘should not be used alone in mixed infections since its activity against anaerobic Gram-positive bacteria is variable, and it haa no activity against aerobic or facultative bacteria." ‘CONCLUSION Odontogenic infections and their complications ‘vary in their clinical presentation and manifestations Awareness of the mierobiology of the oral flora in the normal and diseased state, as well as a thorough understanding of the anatomy of the head and neck, are essential to the recognition and management. of these problems. Further advances in the study of the ‘oral microbiota and their complex interactions should enhance the knowledge of the pathophysiology of or- ‘facial infections. Potential preventive measures and their widespread application promise to reduce the impact of odontogenic infections in the future. REFERENCES 1. Gordon DF, Sturman M, Loetche Wik Improved ioation of fuuerbic bacteria from the gingival erevin are of man. App Microbiol 21048, 1271 2, Valenti WM, "rel RB, Bentley DW: Factors prodipoting to bropharyngtal colonization with Gram-negative bain 1 ge. 0 Bal J Med 298:1108, 1978. 8, Rosenthal 8, Pager IB Relevance of Gram-negative rosin the normal pharyngeal flora. Arm Intern Med 8:95, 1975 4. Hardie J: Microbial flor of the oral evity. Orel Microbiology dnd Injetious Disease. ated by GS Schuster. Baltimore, Wi {tama & Wilns, 1088, 162 ODONTOGENIC INFECTIONS 5 6 0, n, 2B 1 22. May, 1984 Sener GS, Buaets GW: Th miro of oe and ae ‘inca lfm Management of Infect of te Ora on Merit! Reon ed by RG Topas, Mi Goldberg Pde, Wi Sounder C181, p89 Hire JM Bowden GH Te nol soba fora of he Mouth "Ths Normal Mlb Prof Mon Bed by FA $inge 4G Car New Yor, Academic prs 19, 2 ‘edie DANS aes GN Issn and etn co int feng he fm of the oth. Te rel Meri Fry of aie ty PA Skinner, 40 Coe. New Nor Aeanie Pre ip ama Sade HD Biol, punolg tod exsiogeisiy of Spc mtn Moi ee WE, a0 Sch lean” Cre onsite nec ‘ceed hy GS Scone: alinoe, Wile © Wit fs it pS? Fret MR Prodontl dite, Or! Micrbisayand If: fas Disses by Schur. alenore Wits Winn,» 280 Van Plot Heldeman WH: Mroil aloof perio: Sonal unc jC oro at ast ‘Moore WBC” Holdman LV, Sort RM, a: Dacasilgy tfeapetinbl ing a oan ed una nfe!inmee Sec ate Binlei Gorkach 8 Anserbi nections of the bead and eck Otel Clin Noh Am 850, 8 ‘renter RN ames Ry Marr Rly a Merb and sna apes of ints eo and mata ‘pod Oa Sure 8 10 [Slteg ME, Toparin Ro Otonognc nections ad dep ‘cals non of dnt og Managem! of Ce tia oft Oral nt Mosifoa Regn Hey" ‘cnt Geng Phan, WH Sumer Co 3, pre Bho AW, Roe SM, Bey FA Ori edt inte tions. An Int Med a, a 7. Chow AW: Infections ofthe oral cavity, neck and head. Prin- ciples and Pratce of Infectious Diseases. Second Edition. Belted by GL Mandel, RG Doughas, JG Bennett New York John Wiley and Sons, In, in pres, 1984 “Massler M: Epidemiology of gingivitis in cilden. J. Am Dent Asso 45:319,1952 Seevansky 8, Tanner ACR, Hatljce AD, et.al: Provent status ‘of studies on the microbial etiology of periodontal diseases, Hlost-Parasite Interactions in Periontal Ducts. Bited by BJ Genco, SE Mergenhagen. Weshington, DC, American So ciety for Mirobilogy, 1082, p 1 ‘Shinn DLS, Squires 8, MeFadzcan JA: The treatment of Vin zns dasa with metronidazole. Dent Prac 15:27, 1905 . Stephen KW, MeLatehie MF, Mason DK, tal: Tveatment of acute ulorative gingivitis (Vineont's type), Bri Dent J 12:38, ie [Newman MG: Anaerobic orl and dental infection, Rev Infact Dis oS107, 1854 Lindhe J: "Treatment of leslie jvenile periodontitis, Host- ° Slots J, Mashim D, Levine MG, et a: Periodontal therapy in humans. |. Microbiological and cinial effects of asngle course of penidntalecaling and rot plas taeyeline therapy Peridento 9049-509, 198 Barkin RM, Bonis SL, Eighammer RM, etal Ladwig angina in children J Pediatr 87565, 1975 Shuith JE Retrophsryngeal bwcees with reference to abmor- null large percentage of eult ease. Ann Ota 4400, 1906 Caford Jd, Sconyers JR, Moriarty JD, e al: Bactoreaia after tooth extractions studied withthe ad of prereduced anaerobic ally sterilized culture medi. Ap! Mierobio 27:27, 1974 ‘Topazian RO: Osteomyelitis ofthe jan Mangement of Infc- tims of the Oral and Maullofacat Region, Edited by RG ‘Topaaitn, MH Goldberg. Philadelphia, WB Saunders, 1881, p 2 ‘Sanders: Curent concepts in the management of exteome- Iti ofthe mandible J Oral Med 340, 1978,Vol. 3, No. 3 30, Loo H, Kornman K: Strategies inthe use of antibacterial agents ‘nperiodonta disease. Hos?-ParasitaInteractians in Peredontal Diseases. Edited by FU Geneo, SE Merpenhagen, Washington, DDG, American Society for Microbiology, 1982, p 376 81, MeGihee JR, Michalek SM: Innmunobology’ of dental cares: ‘Microbial aspects and local immunity. anna Rev Mierobick 35395, 181 292, Mormay PR, Rosenblatt JB: Peniilin recistance end pencil nade production in linia slats of Bacteroides melaninage- us Antimicrob Agents Chemother 11:80, 1977 38, Bason RS, Rosenblatt JE, Lae DT, et a: Recont experience (MEGRAN ET AL, 265 with antimicrobial ascepiiity of aerobic bacteria: Incas Ing resistance to pencilin. Mayo Clin Proe67:787, 1982 '34, Heimat A von Konow L, Nord CR: loation of f-lactamnase producing Bocteroideswruis associated with clinical falures ‘wth pencilin treatment of human orofacial infections. Arch (ral Biol 25:68, 1980 85, Busch DR, Kureehi LA, Sutter VL, et al: Susceptibility of respiratory tract anaerobes to orally administered peniilins fn cephalosporins. Antimireb Agents Chemother 10713, 1876 136, Hood FC: The place of metronidazole in Ue treatment of acute orofacial infection. Antimicrob Agents Chemaher 15:71, 1978 Harpa amouretta (Roding), Indo-Pacific tle love erp.” Sina fog harp abel Die 14,1982, this is one of only two found in Hawaion wate. ‘The technique sed to predoce these roentgenograph- photograph ia expe in Pediatr Infect, Steven D. Crow, MD. Copyright © Seashell Architetare, 197, Box 682, Richardson, TX 75680