Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections

INTRODUCTION — Odontogenic infections, consisting primarily of dental caries and periodontal disease (gingivitis and periodontitis), are common and have local (eg, tooth loss) and, in some cases, systemic implications. In addition to producing pain and discomfort, odontogenic infections can extend beyond natural barriers and result in potentially life-threatening complications, such as infections of the deep fascial spaces of the head and neck. (See "Deep neck space infections in adults".)

Periodontal infection can also be associated with a number of systemic disorders. These include fever of unknown origin, bacteremic seeding of heart valves and prosthetic devices, preterm low birth weight children, and an increased risk for coronary heart disease and cerebrovascular events. (See 'Association with cardiovascular risk' below.)

A thorough understanding of the anatomic considerations, pathogenic mechanisms, and salient clinical features is essential for early recognition and effective management of these infections and their complications. The epidemiology, pathogenesis, and clinical manifestations of odontogenic infections will be reviewed here. The gingivitis and periodontitis syndromes that can occur and the complications, diagnosis, and treatment of these infections are discussed separately. (See "Overview of gingivitis and periodontitis in adults" and "Complications, diagnosis, and treatment of odontogenic infections".)

EPIDEMIOLOGY — Both dental caries and periodontal disease are prevalent in the United States and other countries, and odontogenic infections are a major source of disease burden globally [1-3].

●In the United States during 2011 to 2016, 1 in 4 adults aged 20 to 64 years and 1 in 6 adults 65 years or older had untreated tooth decay [1]. In the same survey, 2 percent of adults aged 20 to 64 years and 17 percent of those 65 years or older were edentulous (ie, had lost all of their natural teeth). Similarly, the prevalence of periodontitis in the United States, reported in the National Health and Nutrition Examination Survey (NHANES) during 2009 to 2014, was 42 percent among dentate adults 30 years or older; severe and non-severe periodontitis were reported in 4 and 25 percent among adults 30 to 44 years and in 9 and 51 percent of adults 65 years and older and 34 percent had non-severe periodontitis [2].

Earlier reports from NHANES suggested a substantial reduction in the prevalence rates of both dental caries and periodontal disease [4,5], primarily beginning in the mid-1970s and reaching a peak of 90 percent reduction in the mid-1990s [6]. These changes were attributed to the introduction and wide application of fluorides in drinking water and toothpaste, use of dentifrices, improved diet with sucrose substitutes, and general emphasis on oral health.

●The global burden of these conditions is considerable. Nearly half of the world population was found to suffer dental decay or periodontitis in the Global Burden of Disease Study in 2015 [3]. Untreated dental caries in permanent teeth affected 2.5 billion people worldwide (age-standardized prevalence rate of 34 percent). The rates for severe periodontitis and total tooth loss were 7 and 4 percent, respectively.

The highest incidence of odontogenic infections occurs between 21 and 30 years [7]. Males predominate over females at a ratio of 3 to 2 [8]. The main cause of tooth loss varies with age [9]. In the United States during 2015 to 2018, 12.9 percent of adults over the age of 65 were edentulous [9]. Dental caries is the most important cause before the age of 35 and periodontal disease after the age of 35. Both tooth decay and periodontal disease are important contributors to tooth loss after age 60. However, loss of teeth is no longer considered an inevitable and irreversible part of aging.

ANATOMIC CONSIDERATIONS — Humans have two sets of teeth: deciduous (milk or baby) teeth and permanent teeth. The 20 deciduous teeth erupt at approximately 6 months to 2 years of age and are shed between the ages of 6 and 12. These are gradually replaced by 32 permanent teeth, consisting in each half jaw of 2 incisors, 1 canine, 2 premolars, and, in adults, 3 molars.

Tooth structure — Each tooth has a visible crown that projects above the gingiva (gum), with one or more roots extending into the alveolar bone of the maxilla or mandible (figure 1). The crown and root meet at the neck of the tooth.

The tooth forms a peg and socket joint with the alveolar bone and is held in place by the periodontal membrane, which allows slight movement of the tooth. The hard tissues of the tooth are dentin, enamel, and cementum; the soft tissues are the pulp, the periodontal membrane, and the gingiva (figure 1).

The pulp filling the core of the tooth is composed of fibroblasts and connective tissue and is supplied by blood vessels and nerves entering the pulp cavity through the apical foramen. At the periphery of the pulp is a layer of odontoblasts. Odontoblastic processes extend through the dentin in small canals called dentinal tubules. The odontoblasts with their processes lay down dentin, which forms the bulk of the tooth. Dentin is similar to bone but is harder because of a greater calcium content.

The crown of the tooth is covered with enamel (figure 1), which is 99 percent inorganic and the hardest material in the body. The ultrastructure of enamel reveals units called enamel rods or prisms, which are embedded in a matrix. Both the rods and the interprismatic matrix are composed of apatite crystals.

Enamel is laid down by ameloblasts, which form a membrane called the enamel cuticle on the surface of the unerupted tooth. With eruption of the tooth, the cuticle is worn off and lost.

Similar to enamel coverage of dentin in the crown, cementum covers dentin in the root of the tooth from the neck to the apex. Cementum is structurally similar to bone, with cementocytes lying in lacunae and interconnected by canaliculi. Thick collagen bundles, known as Sharpey's fibers, run from the alveolar bone through the periodontal tissue into the cementum, and serve to anchor the tooth to the surrounding connective tissue.

The periodontium is the specialized tissue that surrounds and supports the tooth and consists of four components: (a) the gingiva that surrounds each tooth like a collar and extends down over the crest of the alveolar bone to connect to the tooth just above the neck, (b) the alveolar bone that anchors each tooth, (c) the cementum, a specialized calcified substance covering the root of the tooth, and (d) the periodontal ligament, a specialized connective tissue that supports the tooth in the alveolar bone by anchoring to the cementum (figure 1). The space formed between the tooth and the gingiva is called the gingival sulcus (crevice or recess).

Anatomic routes of infection — Odontogenic infections originate from plaque composed of bacteria that colonize the surfaces of the tooth. The type of infection varies with the site of the plaques:

●Plaques located on tooth surfaces above the gingival margin (supragingival plaque) lead to dental caries that may invade the pulp (pulpitis or endodontic infection), and eventually perforate the alveolar bone (periapical abscess).

●Plaques located on tooth surfaces beneath the gingival margin (subgingival plaque) lead to periodontal infections (eg, gingivitis, periodontitis, and periodontal abscess) that may eventually penetrate the fascial spaces of the face and mouth (orofacial space infections).

Soft tissue infections of odontogenic origin tend to spread along planes of least resistance from the supporting structures of the affected tooth to various potential spaces in the vicinity (figure 2). Accumulated pus 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 mandible, for example, the two points where the bone is weakest and where perforation tends to occur are on the lingual aspect in the region of the molar teeth, and anteriorly on the buccal aspect [10,11]. In the maxilla, the bone is weakest on the buccal aspect throughout, and is relatively thicker on the palatal aspect.

The local anatomic barriers of bone, muscle, and fascia predetermine the routes of spread, extent, and clinical manifestations of many orofacial infections of odontogenic origin:

●If pus perforates through either the maxillary or mandibular buccal plate inside the attachment of the buccinator muscle, infection will be intraoral; if the perforation is outside this muscle attachment, infection will be extraoral (figure 2). Thus, infection of the upper and lower molars, lower incisors, and lower canine teeth is often accompanied by extraoral manifestations.

●When a mandibular infection perforates lingually, it presents in the sublingual space if the apices of the involved teeth lie above the attachment of the mylohyoid muscle (eg, mandibular incisor, canines, premolars, and first molars), and in the submandibular space if below the attachment of the muscle (eg, the second and third molars) (figure 2).

There are a number of clinically important "fascial spaces" around the face and oral cavity that are often involved in odontogenic infections (figure 3). These are potential spaces between layers of fascia that communicate with one another to varying degrees. A thorough understanding of the "anatomic routes" of infection provides valuable information about the nature and extent of infection and also suggests the optimal surgical approach for drainage. Infections involving the deep fascial spaces of the neck are described elsewhere. (See "Deep neck space infections in adults".)

MICROBIOLOGIC CONSIDERATIONS — The microbiota associated with odontogenic infections are complex and generally reflect the indigenous oral microbiota. Such infections are typically polymicrobial, and invasiveness is often influenced by synergistic interactions of multiple microbial species. Moreover, certain species or combinations may be more invasive or more resistant to therapy than others, and the components of these complex flora do not necessarily have equal pathogenic potential [12]. Accordingly, the numerically predominant cultivable microflora may not be the most pathogenic, and it may not be necessary to eradicate the complete microflora for effective therapy. More than 1000 distinct bacterial species have been identified. In most instances, the cultivable microflora probably represents less than 1 percent of the total existing bacterial population [13].

Indigenous oral flora and bacterial niches — In the healthy oral cavity, Streptococcus species, Peptostreptococcus, Veillonella, and diphtheroids account for more than 80 percent of the total cultivable flora [11].

However, 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, specific organisms tend to colonize certain sites, such as the tongue, tooth surface, gingival crevice, or saliva (table 1). As an example, quantitative studies indicate that in certain locations, obligate anaerobes are present in numbers as high as eight times those of facultative bacteria. Additionally:

●Streptococcus salivarius and Veillonella spp have a predilection for the tongue and buccal mucosa and predominate before the eruption of teeth [11].

●Streptococcus sanguinis (formerly S. sanguis), Streptococcus mutans, and Actinomyces viscosus preferentially colonize the tooth surface.

●Fusobacterium, pigmented Prevotella, and anaerobic spirochetes appear to be concentrated in the gingival crevice.

The cultivable microbiota in the saliva most closely resemble those on the dorsum of the tongue. Factors that appear to govern these localization patterns include selective adherence characteristics of certain bacteria for various cell types, local environmental conditions such as oxygen tension, oxidation-reduction potential (Eh) and pH, interbacterial coaggregation, and microbial inhibition [14]. Apart from anatomic considerations, numerous factors such as age, pregnancy, diet and nutrition, eruption of deciduous dentition, oral hygiene, smoking habits, the presence of dental caries or periodontal disease, antimicrobial therapy, hospitalization, and genetic or racial factors may all influence the composition of the oral flora [15].

Evolution from normal to pathogenic flora — The normal commensal microflora is closely adapted to its unique ecologic niche in the oral cavity within well-established structures known as biofilms. These highly organized microorganisms are encased in an extracellular matrix composed mainly of polysaccharides and exist in a relatively protected environment. Under normal "healthy" conditions, these commensal bacteria maintain an effective and nondestructive inflammatory barrier against potential pathogens [16]. Under pathologic conditions, however, this microbial homeostasis is disrupted, and the commensal microbiota shifts to a dysbiotic pathogenic form, which results in inflammation and tissue destruction [17,18]. In the past, it was believed that only certain microorganisms residing within dental plaques or biofilms are cariogenic or periodontopathic (ie, the "specific" plaque hypothesis of dental caries and periodontal disease). Modern studies utilizing culture-independent nucleic acid technologies suggest that dental caries or periodontitis is initiated by a synergistic dysbiotic microbial community propagated by the presence of "keystone pathogens" rather than single specific cariogenic or periodontopathic organisms (the "polymicrobial synergy and dysbiosis" hypothesis) [19,20].

The microbiota associated with different odontogenic infections probably reflects the acquisition of unique microflora during the development of a supragingival dental plaque and its progression to a subgingival dental plaque. Plaques or biofilms that accumulate above the gingival margin are composed mainly of gram-positive facultative and microaerophilic cocci and rods; plaques or biofilms that accumulate below the gingival margin are composed mainly of gram-negative anaerobic rods and motile forms, including spirochetes (figure 4) [21]. Microorganisms residing within the supragingival plaque are characterized by their ability to adhere to the tooth surface and by their saccharolytic activity. Microorganisms in the subgingival plaque are frequently asaccharolytic but proteolytic, and they need not be adherent.

Microbiology of odontogenic infections — Important differences in bacterial compositions have been noted for dental caries, gingivitis, and different forms of periodontitis in comparison with cultures from healthy tissues [22].

Dental caries — An etiologic association of S. mutans in dental caries has been firmly established [23]. S. mutans is the only organism consistently isolated from all decayed dental fissures and is the only organism consistently found in greater numbers in carious teeth than in noncarious teeth.

Gingivitis and periodontitis — In gingivitis and periodontitis, a unique and specific bacterial composition of the subgingival plaque has been identified [24]:

●In the presence of gingivitis, the predominant subgingival flora shifts to a greater proportion of anaerobic gram-negative rods, and Prevotella intermedia (formerly Bacteroides intermedius), Capnocytophaga spp, Finegoldia magna, and Peptostreptococcus spp are most commonly isolated.

●In adults with "established" periodontitis, the flora further increases in complexity, with a preponderance of anaerobic gram-negative and motile organisms and spirochetes. Porphyromonas gingivalis (formerly Bacteroides gingivalis), P. intermedia, Aggregatibacter actinomycetemcomitans, Tannerella forsythensis (formerly Bacteroides forsythus), and Treponema denticola are most commonly isolated.

●In "early-onset" periodontitis, a clinical variant seen primarily in adolescents, the subgingival plaque consists mainly of saccharolytic organisms, with A. actinomycetemcomitans and Capnocytophaga spp as the most common identifiable species. P. gingivalis is rarely found in this condition.

Suppurative odontogenic infection — In suppurative odontogenic infections such as periapical abscesses or deep fascial space infections, polymicrobial flora are usually present; the predominant isolates are Fusobacterium nucleatum, pigmented Bacteroides spp, Peptostreptococcus spp, Actinomyces spp, and Streptococcus spp [25].

Conventional cultures may fail to detect some potential pathogens in suppurative odontogenic infections. In a study of 50 odontogenic abscess specimens, Streptococcus spp (43 percent), Staphylococcus spp (21 percent), and Prevotella spp (21 percent) were the predominant organisms identified by conventional culture whereas Prevotella spp (40 percent), Streptococcus spp (31 percent), and Fusobacterium spp (22 percent) were the predominant organisms identified by 16S RNA gene analysis [26]. Furthermore, conventional culture could not identify any pathogens in 10 percent of the specimens.

The microbiota of odontogenic abscesses is highly diverse, with strict anaerobes playing an important pathogenic role. In a 16S RNA gene analysis study that compared the microbiome of odontogenic abscess with that of saliva in 50 patients, anaerobic bacteria were dominant in abscesses (98 versus 53 percent) while facultative anaerobes and aerobes were dominant in saliva (2 versus 47 percent) [27]. Prevotella spp, Fusobacterium spp, and Porphyromonas spp were more prevalent in abscess samples and Streptococcus spp less common while Veillonella spp, Rothia spp, and Neisseria spp were more prevalent in saliva.

Except in patients with serious underlying illnesses, facultative gram-negative bacilli and Staphylococcus aureus are uncommonly isolated in North America. However, in other parts of the world, such as Southeast Asia, a high incidence of S. aureus and facultative gram-negative bacilli has been reported in odontogenic deep neck space infections [28,29]. The reason for this geographic disparity is unclear.

PATHOGENESIS AND PREDISPOSING FACTORS — As mentioned in the preceding section, plaque formation plays a central role in both dental caries and periodontal infection and the type of infection varies with the site of the plaque.

Dental caries — Dental caries refers to the localized destruction of dental hard tissues by supragingival plaque bacteria, particularly S. mutans and Streptococcus sobrinus that are both acidogenic (acid-producing) and aciduric (able to grow at low pH) [30]. The ingestion of carbohydrates, especially monosaccharides and disaccharides is also important [31]. Studies of decayed fissures have identified high levels of these mutans streptococci, as have studies comparing the microflora of carious and non-carious teeth [32]. These streptococci are transmissible between humans, and infants are often infected by salivary contact with their mothers [33]. S. mutans readily colonize the tooth surface shortly after eruption. However, they do not become cariogenic until exposed to dietary sucrose, which can be rapidly sequestered and utilized by plaque-associated organisms, including S. mutans and other acidogenic and aciduric organisms [30].

The following mechanisms contribute to this process [30]:

●Plaque bacteria that ferment dietary sucrose produce acids that lower the pH on the tooth surface, promoting demineralization and eventually, tooth decay.

●Plaque bacteria, such as S. mutans, can also utilize sucrose to produce extracellular polysaccharides, known as glucans, which constitute biofilms that enable mutans streptococci to avidly stick to the tooth surface, thereby causing decay in the underlying structures [34].

Thus, both acidogenicity (ability to produce acid) and aciduricity (ability to grow at low pH) are important attributes for S. mutans and others to survive and flourish within a cariogenic plaque and cause tooth decay.

Teeth have at least three intrinsic mechanisms that protect against carious decay:

●A constant flow of saliva, which is at a neutral pH, bathes the tooth, buffers and washes away bacterial acids, and supplies calcium and phosphate to remineralize and repair damaged tooth surfaces. In addition, saliva and its various constituents, such as lactoferrin, lysozyme, lactoperoxidase, beta-lysin, and immunoglobulins, possess important antimicrobial activity against plaque-associated bacteria.

●The cleansing action of the tongue and buccal membranes, which remove food particles from the proximity of the tooth.

●The acquisition by the tooth of an acellular, structureless, and bacteria-free coating known as the acquired pellicle, which is of salivary origin and acts as a surface barrier to most dietary and bacterial acids [30].

The oral cavity also has an innate immune response that is characterized by secretion of various antimicrobial peptides (defensins) by oral epithelial tissues in response to bacterial stimuli or inflammation [35,36]. Commensal and pathogenic bacteria utilize different pathways in defensin induction, and epithelial cells from different body sites appear to have common signaling mechanisms to distinguish commensal from pathogenic bacteria [37].

A final protective modality is tooth brushing and flossing to physically remove food particles and bacterial plaques adherent to the tooth surface. With poor dental hygiene, the acquired pellicle becomes colonized with bacteria and is replaced by supragingival and subgingival bacterial plaques that ultimately progress to dental caries and periodontitis.

Older individuals form dental plaques more rapidly, although patients of all ages are susceptible to the development of plaque if daily oral care is withheld [38]. Gingival recession, which is both more common and more severe with advancing age [39,40], increases the susceptibility to root caries.

Periodontal disease — Periodontal disease is mainly caused by microorganisms within the subgingival dental plaque, which penetrate the gingival epithelium, elicit an inflammatory host response, and ultimately result in destruction of the periodontium (figure 1) [22,41]. This tissue destruction results in apical migration of gingival tissues (gingival recession), loss of periodontal attachment, and an increase in the depth of the gingival crevice (periodontal pockets). Animal and human studies have shown that periodontal disease is caused by tissue destruction due to inflammation induced by a predominantly anaerobic periodontopathic subgingival plaque flora [42,43]. Specific virulence factors by selective periodontopathic bacteria, such as lipopolysaccharide and proteolytic enzymes, play a role. However, host factors, such as an exaggerated inflammatory response and genetic predisposition, as well as environmental factors, such as smoking and malnutrition, may be even more important [22]. In contrast to its role in dental caries, dietary carbohydrate intake does not appear to have a significant role in the pathogenesis of periodontal disease.

Predisposing factors for periodontal disease include:

●Inadequate oral hygiene and advancing age, which are the two major risk factors

●Hormonal effects, with exacerbation of disease activity during puberty, menstruation, and pregnancy

●Certain underlying diseases, such as diabetes mellitus, various genetic disorders that impair neutrophil function, and rheumatoid arthritis [44-47]

Bone loss is a serious complication of periodontal disease. The mechanism by which this might occur was evaluated in a study in which peripheral blood lymphocytes from patients with periodontitis were transplanted into immunodeficient mice [48]. Aggregatibacter actinomycetemcomitans stimulated the human CD4+ cells to express osteoprotegerin ligand, which is an osteoclast activator.

CLINICAL MANIFESTATIONS

General — Odontogenic infections may originate from any of the following: the dentoalveolar structures, the periodontium, or the pericoronal tissues (figure 5). Mandibular molars and premolars are most commonly affected [7]. Toothache with or without trismus is the most common clinical presentation [8]. In addition to local symptoms, these infections can also be associated with a number of systemic disorders such as fever of unknown origin, bacteremic seeding of heart valves and prosthetic devices, preterm birth of low birth weight children, and an increased risk for coronary heart disease and cerebrovascular events [49-51].

Dentoalveolar infections — Dentoalveolar infections include dental caries, pulpitis, and periapical abscess.

Dental caries — Caries occur at either the coronal or root surfaces of the affected tooth (figure 5). The prevalence of coronal caries among dentate persons in the United States increases rapidly with age up to the mid-forties and remains stable thereafter; in contrast, the prevalence of root caries continues to increase dramatically with advancing age [52,53]. Coronal caries are more likely to present as recurrent lesions around existing restorations; they are more difficult to detect clinically than new carious lesions.

The earliest findings are the presence of pits and fissures on the affected tooth surface, which gradually becomes stained due to demineralization of enamel and dentin. Further destruction eventually leads to collapse of the overlying enamel. Since there are no cells or vascular elements in enamel or dentin except for the secondary odontoblasts lying on the pulpal surface, the diseased area is incapable of healing and replacement.

The typical clinical presentation of a new carious lesion is a soft to rubbery textured and discolored defect on the tooth surface. Rapidly progressive caries tend to be soft and can be painful due to involvement of the pulp.

Most coronal caries develop slowly, since the infection must spread through highly calcified enamel and dentin. As a result, the lesions are more likely to be longstanding, hard, and asymptomatic. The carious process progresses silently until the infection has invaded deeply enough into the pulp to cause pulpal reaction, and eventually the crown is destroyed.

Root caries occur on the tooth surface where gingival recession has occurred, and are characterized by discrete, well-defined, soft, and discolored defects on the root surface or at the junction of the crown and the root. Root caries can be more difficult to diagnose than coronal caries, since they tend to occur in the interproximal tooth surfaces, which are relatively inaccessible to brushing and are particularly prone to decay from retained food debris.

Pulpitis and periapical abscess — Infection of the pulp (pulpitis) can occur in one of three ways:

●Through a defect in the enamel and dentin that results from extension of a carious lesion, traumatic fracture, or a dental procedure

●Through the apical foramen or lateral canals (eg, from a periodontal pocket or an adjacent tooth with a periapical abscess)

●Through hematogenous seeding of the pulp that has been irritated mechanically

Once infected, the acute inflammatory reaction causes a rapid build-up of pressure inside this rigid and unyielding space, compressing the blood vessels that enter the pulp cavity through the apical foramen, and causing ischemia and necrosis of the pulp tissue (figure 5). Pus may egress out of a cavity in the crown if one exists; it may extrude apically into the surrounding periodontal tissue, resulting in acute periapical periodontitis; or it may erode out of the apical foramen, resulting in periapical or alveolar abscess. The accumulation of pus causes loss of bone and periodontal tissue, and may extend to involve other teeth.

The early and dominant symptom of acute pulpitis is a severe toothache that can be elicited by thermal changes, especially cold drinks. The involved tooth also may be sensitive to palpation and percussion. As the disease progresses, the pain becomes severe and continuous, with increased intensity in the recumbent position.

In a more indolent form of the condition, called chronic pulpitis, the inflammation is low grade with partial drainage of the infected material. Symptoms are characterized by a mild and dull intermittent pain that is not affected by thermal changes.

A more serious complication, lateral extension of the abscesses into planes of least resistance, results in deep fascial space involvement. (See "Deep neck space infections in adults".)

Periodontal infections — Periodontal disease includes gingivitis and periodontitis. The main complication of periodontal disease is tooth loss, although local and systemic spread of infection can occur, leading to periodontal abscess and possibly orofacial space infections. The different syndromes are discussed in detail elsewhere. (See "Overview of gingivitis and periodontitis in adults".)

Gingivitis — The most common periodontal disease in childhood, gingivitis, has a peak incidence in adolescence. The manifestations, which can range from mild to severe, include swelling, bluish purple discoloration of the gingiva, and a tendency to bleed after eating or brushing. There is usually no pain, but a mild fetor oris (halitosis) may be noticed.

The inciting dental plaque may be difficult to observe until it has reached a certain thickness and becomes discolored or is calcified (calculus or tartar). Calculus is prevalent among all age groups, ranging from 74 to over 90 percent [54]. The frequency of subgingival calculus, but not the percentage of involved sites, increases directly with age, probably related to the preponderance of gingival recession and root caries in older individuals.

Acute necrotizing ulcerative gingivitis, also known as Vincent's angina or trench mouth, is relatively rare in the post-antibiotic era. The patient typically experiences a sudden onset of pain in the gingiva, and the tissue appears eroded with superficial grayish pseudomembranes. Other manifestations include halitosis, altered taste sensation, fever, malaise, and lymphadenopathy.

Periodontitis — The presentation of periodontitis differs between adults and children or adolescents.

●Periodontitis in the adult tends to be a chronic process, characterized by gingival inflammation and accompanied by loss of supportive connective tissues including alveolar bone, resulting in loss of attachment of the periodontal ligament to the cementum (figure 5) . The prevalence of severe periodontitis (defined as 3 to 7 mm of loss of attachment) rises sharply with advancing age. (See 'Epidemiology' above.)

The destructive process is slow, probably due to years of dental neglect and chronic gingivitis. Plaque and calculi are abundant both supragingivally and subgingivally, and frank pus may be present in the periodontal pockets. Rapidly progressive periodontitis is a variant in adults in whom the process of tissue loss is accelerated.

●In early-onset periodontitis, more common during childhood or adolescence, there is a more rapid vertical bone loss often localized to the molars, although other teeth may be involved. Plaque is usually minimal, and calculi are not seen. The etiology of this rare condition is unknown, although neutrophil dysfunction has been reported in some of these otherwise healthy patients [55].

Periodontal abscess — Periodontal abscess may be focal or diffuse and presents as a red, fluctuant swelling of the gingiva, which is extremely tender to palpation. The abscesses always communicate with a periodontal pocket from which pus can be readily expressed after probing.

Pericoronitis — Pericoronitis is an acute localized infection caused by food particles and microorganisms trapped under the gum flaps (figure 5). The infection involves the wisdom teeth in adolescents and adults, and occurs during the eruption of the permanent teeth in children. The major symptoms include pain and limitation of movement on opening the jaw, discomfort on mastication and swallowing, and facial swelling.

The pericoronal tissues are erythematous and swollen, and digital pressure can often express an exudate from under the infected flap. The masticator spaces are often involved, which can produce trismus. Localized painful lymphadenopathy may be noted, and the breath is usually foul.

Association with cardiovascular risk — Chronic poor oral health and tooth loss may be associated with modest increases in coronary and cerebrovascular disease; this effect appears to persist after adjustment for known cardiovascular disease risk factors [56-58]. The magnitude of this effect was illustrated in a study of 1203 men followed for a median of 24 years in which radiographic bone loss was used as a marker of chronic periodontitis [59]. Among men less than 60 years of age but not in older men, the risk of coronary heart disease was increased (hazard ratio 2.12) comparing those with the highest versus the lowest category of radiographic bone loss.

The mechanisms by which chronic periodontitis predisposes to coronary heart disease are not well understood, but an adverse effect of systemic inflammation on endothelial function may play a role [60,61]. In addition to local infection, other factors may contribute to systemic inflammation including intermittent bacteremia and release of bacterial endotoxins of oral origin into the bloodstream, an effect that can be induced by gentle chewing [62].

The effect of treating severe periodontitis on endothelial dysfunction was evaluated in a randomized trial in which 120 patients with severe periodontitis were assigned to either community-based periodontal care or intensive periodontal treatment [63]. The oral benefits of intensive therapy were associated with a significant improvement in endothelial function at six months. It is not known if intensive therapy would improve endothelial function in the long term or whether such interventions prevent the progression of cardiovascular disease or improve cardiovascular outcomes [58,64].

SUMMARY

●Epidemiology – Odontogenic infections, consisting primarily of dental caries and periodontal disease (gingivitis and periodontitis), are common and have local (eg, tooth loss) and, in some cases, systemic implications. In addition to producing pain and discomfort, odontogenic infections can extend beyond natural barriers and result in potentially life-threatening complications, such as infections of the deep fascial spaces of the head and neck. The main cause of tooth loss varies with age. Dental caries is most important before the age of 35 and periodontal disease after the age of 35. Both tooth decay and periodontal disease are important contributors to tooth loss after age 60. (See 'Introduction' above and 'Epidemiology' above.)

●Anatomic considerations – Each tooth has a visible crown that projects above the gingiva (gum), with one or more roots extending into the alveolar bone of the maxilla or mandible (figure 1). The crown and root meet at the neck of the tooth. The tooth forms a peg and socket joint with the alveolar bone and is held in place by the periodontal membrane, which allows slight movement of the tooth. The hard tissues of the tooth are dentin, enamel, and cementum; the soft tissues are the pulp, the periodontal membrane, and the gingiva (figure 1). (See 'Anatomic considerations' above.)

●Microbiology – In the healthy periodontium, the microflora is sparse and consists mainly of gram-positive organisms, such as Streptococcus sanguinis and Actinomyces spp. In the presence of gingivitis, the predominant subgingival flora shifts to a greater proportion of anaerobic gram-negative bacilli, with Prevotella intermedia as the predominant isolate. (See 'Indigenous oral flora and bacterial niches' above and 'Evolution from normal to pathogenic flora' above.)

●Pathogenesis

•Odontogenic infections originate from plaque composed of bacteria that colonize the surfaces of the tooth. The type of infection varies with the site of the plaques:

-Plaques located on tooth surfaces above the gingival margin (supragingival plaque) lead to dental caries that may invade the pulp (pulpitis or endodontic infection), and eventually perforate the alveolar bone (periapical abscess).

-Plaques located on tooth surfaces beneath the gingival margin (subgingival plaque) lead to periodontal infections (eg, gingivitis, periodontitis, and periodontal abscess) that may eventually penetrate the fascial spaces of the face and mouth (orofacial space infections). (See 'Anatomic routes of infection' above.)

•Dental caries are caused by microorganisms within the supragingival plaque, which include gram-positive facultative and microaerophilic cocci and rods. The mutans group of streptococci, particularly S. mutans and S. sobrinus, are the primary organisms associated with dental caries. The ingestion of carbohydrates, especially monosaccharides and disaccharides is also important. (See 'Dental caries' above.)

•Periodontal disease is caused by tissue destruction due to inflammation induced by a predominantly anaerobic periodontopathic subgingival plaque flora. In well-established periodontitis, the flora further increases in complexity with a preponderance of anaerobic gram-negative bacilli and motile organisms. Aggregatibacter (Actinobacillus) actinomycetemcomitans (a HACEK infection), Porphyromonas gingivalis, Prevotella intermedia, Treponema denticola, and Tannerella forsythensis (formerly, Bacteroides forsythus) are the predominant isolates. (See 'Periodontal disease' above.)

•Soft tissue infections of odontogenic origin tend to spread along planes of least resistance from the supporting structures of the affected tooth to various potential spaces in the vicinity (figure 2). The local anatomic barriers of bone, muscle, and fascia predetermine the routes of spread, extent, and clinical manifestations of many orofacial infections of odontogenic origin (figure 3). (See 'Anatomic routes of infection' above.)

●Dentoalveolar infections – Dentoalveolar infections include dental caries, pulpitis, and periapical abscess. Caries occur at either the coronal or root surfaces of the affected tooth (figure 1).

•Dental caries – The typical clinical presentation of a new carious lesion is a soft to rubbery textured and discolored defect on the tooth surface. (See 'Dentoalveolar infections' above.)

•Pulpitis – The early and dominant symptom of acute pulpitis is a severe toothache that can be elicited by thermal changes, especially cold drinks. The involved tooth also may be sensitive to palpation and percussion. As the disease progresses, the pain becomes severe and continuous, with increased intensity in the recumbent position. (See 'Pulpitis and periapical abscess' above.)

●Periodontal disease – Periodontal disease includes gingivitis and periodontitis. The main complication of periodontal disease is tooth loss, although local and systemic spread of infection can occur, leading to periodontal abscess and possibly orofacial space infections. (See 'Periodontal infections' above.)

•Gingivitis – The manifestations of gingivitis, which can range from mild to severe, include swelling, bluish purple discoloration of the gingiva, and a tendency to bleed after eating or brushing. There is usually no pain, but a mild fetor oris (halitosis) may be noticed. (See 'Gingivitis' above.)

•Periodontitis – Chronic adult periodontitis, which is characterized by gingival inflammation with accompanying loss of supportive connective tissues including alveolar bone, results in loss of attachment of the periodontal ligament to the cementum. The destructive process is slow, probably due to years of dental neglect and chronic gingivitis. Plaque and calculi are abundant both supragingivally and subgingivally, and frank pus may be present in the periodontal pockets. (See 'Periodontitis' above.)

●Association with cardiovascular risk – Chronic poor oral health and tooth loss may be associated with modest increases in coronary and cerebrovascular disease; this effect appears to persist after adjustment for known cardiovascular disease risk factors. (See 'Association with cardiovascular risk' above.)