Oral Infection

Updated: Oct 04, 2022
Author: Jeff Burgess, DDS, MSD; Chief Editor: Anil P Punjabi, MD, DDS 


Infection involving the oral cavity can be associated with significant morbidity. In addition, recent studies have suggested that some types of oral infection may potentially confound a number of systemic problems including cardiac disease, pregnancy, kidney disease, and diabetes.[1, 2]

The image below depicts candidiasis.

Candidiasis. White plaques are present on the bucc Candidiasis. White plaques are present on the buccal mucosa and the undersurface of the tongue and represent thrush. When wiped off, the plaques leave red erosive areas. Image courtesy of Matthew C Lambiase, DO.

Relevant anatomy

The oral cavity (see the image below) is oval shaped and is separated into the oral vestibule and the oral cavity proper. It is bound by the lips anteriorly, the cheeks laterally, the floor of the mouth inferiorly, the oropharynx posteriorly, and the palate superiorly. The oropharynx begins superiorly at the junction between the hard palate and the soft palate, and inferiorly behind the circumvallate papillae of the tongue. The bony base of the oral cavity is represented by the maxillary and mandibular bones.

Schematic representation of oral cavity and floor Schematic representation of oral cavity and floor of mouth. A: philtrum; B: upper labial frenulum; C: opening of Stensen's duct; D: labial commissure; E: hard palate; F: soft palate; G: intermaxillary commissure; H: base of tongue; I: lateral border of tongue, dorsal view; J: tip of tongue, dorsal view; K: tip of tongue, ventral view; L: lateral border of tongue, ventral view; M: ventral surface of tongue; N: lingual frenulum; O: floor of mouth; P: opening of Wharton's duct; Q: vestibular gingiva; R: vestibule. Teeth are numbered according to international classification.

The tongue is basically a mass of muscle that is almost completely covered by a mucous membrane. It occupies most of the oral cavity and oropharynx. It is known for its role in taste, but it also assists with mastication (chewing), deglutition (swallowing), articulation (speech), and oral cleaning. Five cranial nerves contribute to the complex innervation of this multifunctional organ.

For more information about the relevant anatomy, see Mouth Anatomy and Tongue Anatomy.


Microbiology of Oral Infection

Oral bacteria are diverse, but in the immunocompetent individual the interaction between the various complex competing microflora provides relative stability. The different structures and anatomy within the mouth afford various microenvironments that support different types of microbiologic organisms. In the first few years of life, the bacterial microbiota within the mouth is predominantly aerobic, but, as the teeth develop, favorable sites supporting pathogenic anaerobic bacteria emerge.

Biofilm, on teeth termed plaque, can build up in the mouth and reach substantial numbers. It has been estimated to reach up to 1011 microorganisms/mL in plaque that is not removed over several days. Apical periodontal infection has been associated with 200 bacterial species, and 500 bacterial species have been reported with marginal periodontitis.[3, 4] Evidence also exists that significant interaction of bacterial types within biofilm may either enhance or suppress metabolic activity that leads to dental infection.[5]

Factors that regulate the number of oral bacteria include general exposure, saliva, diet, bacterial retention, bacterial interaction, the complexity of the flora, native resistance, and hygiene. Change in the condition of any one of the above factors or combination thereof can result in oral hard or soft tissue infection.

For example, a diet rich in dietary carbohydrate such as refined sugar favors bacteria such as Streptococcus mutans, the organism that causes dental caries.[6] The consistency of the diet is also important in that courser foods eliminate particles that can sustain microorganisms. Specificity in terms of bacteria tissue adherence also appears to exist; for example, S mutans and Streptococcus sanguis typically adhere to hard surfaces, while Streptococcus salivarius is found primarily on the tongue.

A number of systemic diseases can reduce host defense mechanisms, leading to reductions in phagocytic activity, pulmonary clearance, and circulation, with these factors contributing to oral infection. They include malnutrition, alcoholism, diabetes, cystic fibrosis, renal failure, lymphoproliferative disorders, heart failure, and chronic lung disease.

Immunosuppressants and other medications used as cytotoxic chemotherapeutic agents, including steroids, can reduce host defense mechanisms leading to infection. Antibiotic medication can also alter the oral microbial environment leading to oral infection. For example, prolonged antibiotic therapy can reduce the normal bacterial flora, resulting in the selection of resistant flora and/or the emergence of competing fungal organisms. Other factors potentially confounding the possibility of oral infection include age, potential drug abuse, family and social environment, and the patient’s psychological status.

Oral infection can also be caused by viral and fungal organisms. Common viral infections include herpes simplex (primary and secondary recurrent herpes infection), varicella zoster (shingles), and coxsackievirus. The presence of the papilloma virus is considered an infection and has assumed importance in that it has been linked to the development of oral squamous cell carcinomas.[7]


Viral and Fungal Oral Infection

As mentioned previously, oral infection can also be caused by viral (eg, herpes simplex [primary and secondary recurrent herpes infection], varicella zoster [shingles], coxsackievirus) and fungal organisms. The presence of the papilloma virus (see image below) is considered an infection and has assumed importance in that it has been linked to the development of oral squamous cell carcinomas.[7]

Papillomas, which are of questionable viral origin Papillomas, which are of questionable viral origin, are frequent findings in the oral cavity, especially on the lateral/ventral tongue and soft palate.

Primary viral infections involving the oral mucosa are covered elsewhere. However, a condition not typically described in the literature is intraoral recurrent herpes (see image below). This infectious process is the equivalent of the secondary recurrent lesion of herpes but occurs on the attached gingival tissue adjacent to the teeth, including the palate, rather than the lip. A prodromal phase often exists in which the tissue feels itchy or tingles. This dysesthesia is then followed by the development of multiple small punctuate ulcers that coalesce and are painful. The infection may last 10-14 days and reoccur in response to stress, fever, trauma, and hormonal alterations. No good evidence exists that sunlight activates the latent virus, as occurs with the secondary lip lesion.

Recurrent herpes is occasionally observed intraora Recurrent herpes is occasionally observed intraorally. Inside the oral cavity, recurrent herpes typically affects only keratinized tissues, such as the gingiva or the hard palate. Vesicles often break quickly, so the clinician may observe small clustered ulcers. Courtesy of Sheldon Mintz, DDS.

The most common oral mycotic infection is candidiasis, but other infections such as mucormycosis (phycomycosis), actinomycosis (see image below), aspergillosis, and pneumocystosis can occur under the right circumstances. Candida is an opportunistic organism and does not typically cause infection unless other host factors are compromised. Systemic conditions that can contribute to candidiasis include xerostomia, diabetes mellitus, and immune system suppression (eg, HIV infection or as a side effect of drying medications). Candidiasis can also result from poorly fitting prosthetic oral appliances and poor oral hygiene.

Image shows an oral fistula caused by actinomycosi Image shows an oral fistula caused by actinomycosis.

Candidiasis can occur in 3 forms: pseudomembranous, atrophic/erythematous, and chronic/hyperplastic. The first form, pseudomembranous, is characterized by multiple soft, white, slightly elevated plaques that can be wiped away, leaving an erythematous and bleeding surface (see image below). The second form is characterized by erythematous tissue that is sensitive to touch, and the third by confluent slightly raised white areas. Culturing for candida is useful in cases in which the diagnosis is unclear.[8]

Candidiasis. White plaques are present on the bucc Candidiasis. White plaques are present on the buccal mucosa and the undersurface of the tongue and represent thrush. When wiped off, the plaques leave red erosive areas. Image courtesy of Matthew C Lambiase, DO.

Caries and Periapical Infection

Caries are the most common odontogenic infection. Prevalence appears to vary depending on the region of the world surveyed.[9, 10] When dental infection is limited to the enamel and dentine of the tooth, it does not present a severe problem. A carious process that extends into the dental pulp chamber and the neural, vascular, and connective tissue contained within presents a more serious matter.

The bacteria that reach the pulp are mostly anaerobic and host resistance is limited by the constricted anatomy of the tooth pulpal chamber. Once the pulp has become involved, the inflammation and edema associated with the carious infection causes a vascular necrosis and the death of this tissue. This process then generally results in the infection spreading beyond the apex of the root (ie, the periapical region).


Osteomyelitis and Cellulitis

Once the infectious process has extended beyond the tooth, it may expand into the surrounding medullary bone and cause an osteomyelitis, or it may extend focally through the bone as a fistular tract draining into the oral cavity. The latter condition drains the infection, reduces general swelling, and results in a small soft tissue swelling and focal erythema at the site of the mucosal involvement.

However, a periapical infection may also evolve into a localized soft tissue abscess or a more diffuse and troublesome soft tissue cellulitis. The spread of infection into fascial spaces can be problematic for the patient and treating clinician. A cellulitis can involve incorporation of adjacent spaces and inferior (eg, neck and mediastinal region) and superior (eg, base of the skull, foramen ovale, and brain — cavernous sinus thrombosis) extension.

The relative risk of fascial space infection is related to the location of the space in relation to the anatomy of the head and neck. Low-risk anatomical areas include the region of the facial vestibule of the mandible, the body of the mandible, the buccal vestibule of the mandible, and the palate. Moderate risk areas include the mentalis space, submental space, sublingual space, submandibular space, buccal space, submasseteric space, superficial and deep temporal space, and the maxillary sinus. The highest-risk regions include the infratemporal and parotid spaces; the pterygomandibular, parapharyngeal, and peritonsillar spaces; and the cervical, infraorbital, periorbital region, and the base of the lower lip. Infection that has spread to these latter areas must be treated aggressively.

Signs and symptoms for the various space infections vary. For example, infection of the sublingual space itself is not evident by external examination. However, the patient feels like the tongue has been pushed up, and difficulty swallowing can exist. In contrast, Ludwig angina, which represents a more extensive involvement, not only of the sublingual space but space below the mandible, severely displaces the tongue upwards and backwards. Extensive swelling of the anterior neck extending down to the clavicles may become evident. With extension of the infection, the patient is febrile and breathing is often labored. Obstruction of the throat due to edema of the glottis causes further deterioration.

Other commonly observed general signs of cellulitis include jaw-opening limitation (eg, trismus), and distension of the involved region (eg, the lip, cheek), and bulging of muscle (eg, the temporalis). In cases of parotid space infection, suppuration from the parotid duct may be present. Typically, pain is described as throbbing and severe tenderness to palpation exists. Pain worsens often quickly over time and is not controlled by nonprescription medication.

Osteomyelitis can follow chronic odontogenic infection not involving cellulites. The incidence of the disease has decreased with the advent of antibiotics, caries prevention, and restorative dentistry. However, chronic diseases, immune deficiency, and vascular abnormality may predispose an individual to the infection.

The course of osteomyelitis can include suppuration with abscess or fistula formation and jaw bone sequestration. Acute osteomyelitis is associated with the classical features of infection including fever, leukocytosis, lymphadenopathy, pain, and soft tissue swelling. If the condition involves the lower jaw there may be lip dysesthesia or paresthesia. Chronic osteomyelitis may also involve purulent discharge, tooth loss, or pathologic fracture. The condition typically involves symptom remission and recrudescence.[11] Note that osteomyelitis can result from local or metastatic neoplasm as well as jaw bone fracture.

Diffuse sclerosing osteomyelitis is a variation of osteomyelitis, but it involves fairly focal areas of chronic infection that can cause periosteal and cortical bulging in adults (typically) without frank sequestration of the cortex. However, internal sequestration occurs. Low-grade persistent pain exists. Condensing osteitis is the name of the condition involving bone sclerosis associated with long-standing pulpitis or pulpal necrosis without demonstrative infection. Infection associated with removal of a tooth is termed alveolar osteitis or dry socket. Another newly defined condition involving infection of implants from adjacent dental infection is termed retrograde periimplantitis.


Periodontal Disease

The most common oral mucosal infection is periodontal disease. This condition is considered a major public health problem in many countries.[12] Periodontitis has been associated with the proliferation of the bacteria Actinobacillus actinomycetemcomitans,Porphyromonas gingivalis, and Prevotella intermedia. Infection involves the supporting structures of the teeth and causes progressive loss of gingival attachment with absorption of supporting alveolar bone. This results in periodontal pocket formation, which can lead to further disease including tooth loss. When a deep periodontal pocket closes along the superior interface with a tooth trapping bacteria, this condition can lead to abscess.

Several forms of periodontal infection are described. They include aggressive periodontitis, which occurs in otherwise healthy individuals but causes rapid bone loss; chronic periodontitis characterized by gingival pocket formation and bone loss occurring over a prolonged period of time; periodontitis as a manifestation of systemic disease; and necrotizing periodontal disease, which involves severe necrosis of the gingival tissue. This condition is most often associated with the presence of systemic conditions such as HIV infection, malnutrition, and immunosuppression.

Known contributory factors to periodontal infection include age, plaque and calculus, smoking, diabetes mellitus, general health status, and social economic level. Low bone density of osteoporosis appears to be a shared risk factor for periodontitis rather than a causal factor.[13]  A study by Teeuw et al on 313 dental patients found that suspected new diabetes was found in 18.1% of patients diagnosed with severe periodontitis (78 patients) compared to 9.9% and 8.5% in patients with mild or moderate periodontitis and the control group.[2]

Periodontitis is preceded by infection and inflammation of the attached gingival adjacent to teeth. This is termed gingivitis. Both gingivitis as well as periodontitis may be asymptomatic unless a frank abscess exists. Symptoms of gingivitis and periodontitis include foul breath and gingival tenderness with palpation; signs can include gingival bleeding, tooth mobility, and gingival erythema and swelling. See images below.

Moderate chronic gingivitis. Note that the papilla Moderate chronic gingivitis. Note that the papillae are edematous and blunted. They may bleed with brushing. Note areas of edema overlying some of the root areas. Pallor is seen in these areas. Image courtesy of Robert J. Lindberg, DMD.
Severe periodontal disease. Loss of the gingival t Severe periodontal disease. Loss of the gingival tissue is seen, making the teeth appear long. Even more effacement of the papillae is present. Heaped up ridges are observed in the areas overlying the roots. Image courtesy of Robert J. Lindberg, DMD.

Minor Salivary Gland Infection

Infection involving the intraoral minor salivary glands is relatively rare. However, minor gland infection can follow sialolithiasis. This condition begins with the formation of a small calculi or stone that blocks the duct of the minor gland. A secondary infection may then ensue. Sialadenitis can also follow viral infection and can be associated with neoplastic activity. The condition typically causes erythema and swelling of the minor gland duct. Minor glands are located throughout the mouth but most frequently in the cheek, lip, and palatal region. Major salivary gland infection including acute and chronic bacterial parotitis, viral parotitis (ie, mumps), and other conditions causing salivary gland infection such as tuberculosis and parotid or submandibular actinomycosis is covered elsewhere.


Oral Manifestations of Coronavirus Disease 2019 (COVID-19)

As previously noted, a number of systemic viruses have been implicated in the etiology of oral lesions. This now includes coronavirus 2 (SARS-CoV-2) and its variants. The replication of SARS-CoV-2 appears to be facilitated by angiotensin-converting enzyme 2 (ACE2), and since this enzyme is expressed on epithelial cells of the mucosa, it is thought that this may be one possible reason oral lesions have been periodically identified in the mouths of patients with COVID-19.[14]

In a 2021 review of a limited number of cases (25) taken from 18 studies involving SARS-CoV-2 infection, identified oral lesions included ulceration, depapilation of the tongue, and various maculae, nodules, and plaques.[15]

In another review, oral ulcers were described as aphthous-like, hemorrhagic, and necrotic.[16]

In a systematic review of 40 studies that included cross-sectional and case reports involving 10,228 patients with SARS COVID-19, the most common oral problem was reported as gustatory impairment (hypogeusia, ageusia, and taste disorders). Noted oral lesions included irregular aphthous-like ulcers, erythematous plaques, and small blisters, petechiae involving the tongue, lips, gingiva, palate, and buccal mucosa, and “desquamative” gingivitis. Many of the oral lesions were thought to represent co-morbid secondary effects of COVID-19 or the result of co-morbid infection. In mild cases, lesions appeared about the same time as the initial respiratory symptoms, while in hospitalization cases, lesions developed 7 to 24 days after the onset of symptoms.[17, 18]

The non-specific oral lesions described above occurring in association with COVID-19 are relatively uncommon, but it should be recognized by clinicians involved in the management of these patients that oral disease may develop in patients with mild COVID-19 disease as well as in patients with more severe involvement. Future research should help to identify the possible pathogenic mechanisms underlying these oral conditions, which, in turn, should lead to additional clinical management and treatment considerations.