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19
Pathology ofInfection andInfectious Diseases
oftheOro- FacialComplex
Nagamani Narayana and John Casey
Department of Oral Biology, University of Nebraska Medical Centre, Nebraska, USA
19.1 Introduction
The spectrum of orofacial infections affecting the orofacial structures is quite diverse. These
infections may be conveniently categorised as odontogenic and non- odontogenic. Odontogenic
infections include dental caries, periodontal disease and suppurative deep space infections. Nonodontogenic infections include infections of the mucosal and neck. This chapter briefly discusses
mechanisms of tissue injury caused by microorganisms and the more common infections of the
odontogenic and non- odontogenic sources.
19.2 Mechanisms ofTissue Injury Caused by Microorganisms:
AnOverview
While the complexity of tissue injury and the inflammatory/immune response induced by bacterial,
fungal and viral organisms is complex and beyond the scope of this chapter, general mechanisms
of infectious tissue damage will be incorporated into the following discussion.
Pathogenicity is the ability of a microorganism to cause disease in a host. The degree to which
that organism can cause disease is termed virulence, a continuum from low to high. Various virulence factors determine the degree to which an infectious organism can damage host tissues
directly. The stages of virulence are exposure, adhesion, invasion and infection. These stages are
facilitated by the following examples(1):
1) The ability to use motility to interact with host cells:
● Motile bacteria can traverse the surface mucus covering mucosal epithelial cells using
flagellaand chemotaxis.
2) The ability to adhere to and invade host cells(2):
● Bacteria may produce pili with a specifically shaped tip structure corresponding to a receptor
on the host cell for attachment to that cell. Cell wall adhesion molecules and biofilm production
also enable bacterial– host cell attachment. Some bacteria and fungi can produce molecules,
Pathological Basis of Oral and Maxillofacial Diseases, First Edition. Edited by S. R. Prabhu, Syed Ali Khurram,
Omar Kujan and Merva Soluk Tekkesin.
© 2025 John Wiley & Sons Ltd. Published 2025 by John Wiley & Sons Ltd.
t.me/Dr_Mouayyad_AlbtousH
called Invasins, which activate the host cell’s cytoskeletal mechanisms, allowing cell penetration
by phagocytosis.
● Exoenzymes, including hyaluronidase, collagenase and deoxyribonuclease (DNase), damage
and liquefy the host extracellular matrix, enabling the invading organisms to spread more
quickly.
● Coagulase, a characteristic of Staph aureus, activates the coagulation cascade to form a fibrin
clot around the organisms, protecting them from neutrophils and macrophages.
● Bacterial kinases, streptokinase and staphylokinase, will dissolve fibrin clots, releasing
entrapped bacteria to facilitate the expansion of the infection.
3) The ability to evade innate and adaptive host defences:
● The capsules of certain bacteria, Streptococcus pneumoniae, for example, interfere with the
complement pathway host defence, preventing immune cells from attaching. The capsule
also increases the size of the bacterium, making it more difficult for phagocytes to engulf the
organism.
● Formation of biofilm prevents phagocytosis by neutrophils and monocytes.
● The production of proteases interferes with antibody- mediated defences by digesting the
attached antibody molecule.
4) The ability to compete for host nutrition:
● Bacteria develop specific transport systems to utilise host cellular nutrients, especially iron,
thereby competing with and depriving the host cells of critical nutrition.
In addition to the factors mentioned above, the endotoxins of certain gram- negative organisms
activate a systemic immune response by producing high levels of cytokines, which, if severe,
results in sepsis with end- organ dysfunction/failure, decreased cardiac function, hypotension and
sometimes death. Likewise, the ‘superantigens’, toxic shock syndrome toxin produced by some
strains of Staphylococcus aureus and the streptococcal mitogenic exotoxin of Streptococcus pyo-
genes also may result in severe sepsis via a similar mechanism(3).
Indirect host cellular injury occurs by activating a localised antimicrobial inflammatory immune
response surrounding the infection, contributing to tissue injury and destruction as an unfortunate
byproduct. As a reaction to bacterial and fungal invasion, activation and recruitment of neutrophils
and monocytes release reactive oxygen and nitrogen species, lysosomal enzymes, proteases, elastases
and collagenases, resulting in purulent exudate, abscess formation (suppuration) and ulceration
known as acute inflammation dominated by neutrophils (Figure19.1). If the organism is eliminated, healing will proceed in an orderly fashion with restoration of the tissue architecture. If the
microorganism persists or if healing does not occur as expected, a state of ongoing or chronic inflam-
mation results, widening the zone of injury with lymphocytes, plasma cells and macrophages predominating (Figure19.2). Ongoing vascular proliferation and fibrosis may result in scar tissue(4, 5).
The immune response to infection by mycobacteria and some intracellular fungi, Histoplasma,
for example, relies on activated macrophages, which may fuse to form ‘multinucleated giant cells’
rather than neutrophils, as part of the granulomatous/granuloma response pattern (Figures19.3
and19.4). This reaction may help wall off the organisms, rendering them inert but not necessarily
destroying them. As the granulomatous reaction expands, the target organ is progressively injured
by expanding central cellular necrosis and the granulomatous response, especially in the lung.
How this action plays out depends on the infected individual’s immunocompetency. Those
individuals with impaired T- cell function, especially involving the CD- 4lymphocytes, may not be
able to mount the expected granulomatous response from the CD- 4/activated macrophage interplay,
thus allowing the infections and tissue injury to proliferate unchecked(6).
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Figure19.1 Acute inflammation.
H&E- stained image showing a dense
infiltrate of neutrophils (suppuration)
and oedema.
Figure19.2 Chronic inflammation.
H&E- stained image showing a dense
infiltrate of lymphocytes, plasma cells
and macrophages.
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Figure19.3 Granulomatous
inflammation. H&E- stained image
showing granulomas with epithelioid
macrophages and giant cells.
Figure19.4 Granulomatous
inflammation. H&E- stained image
showing granulomas with epithelioid
macrophages and giant cells and
coagulation necrosis.
Injury from viruses results from intracellular viral replication producing ‘ballooning degeneration’ and death of the infected cells and from the adaptive immune response of cytotoxic T cells
recognising and destroying the infected cells(7). Along with the viral injury itself, this process
activates pro- inflammatory cytokines responsible for immune system activation and tissue injury.
In some instances, the host cellular damage caused by the immune reaction accounts for more
significant damage than the direct viral injury as in hepatitis, for example. Apoptosis of the infected
cells may be initiated by viral replication and the recognition and contact with sensitised killer
T- cells. Viral injury also promotes secondary bacterial infection.
An indirect type of tissue injury occurs when the infection stimulates autoantibody production
directed against a specific organ or cellular component. Most of these reactions are associated with
viral infections, either proven or suspected. A well- documented example of a bacterial infection
causing this type of injury is group Streptococcus pyogenes, the causative agent of rheumatic heart
disease, stimulating the production of antibodies which cross- react with cardiac antigens in the aortic and mitral valves as well as in cardiac myocytes causing both acute and chronic injury to the heart.
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19.2.1 Oral andMaxillofacial Bacterial Infections
It is increasingly apparent that the commensal bacteria of the head, neck and oral cavity are critical
in maintaining human health. New DNA sequencing techniques have shown commensal organisms ubiquitous throughout the oral cavity and contiguous spaces. These commensals can become
infective when host defences, including the protective epithelial barrier of the surface, are
damaged.
19.2.1.1 Dental Caries
The most common infections of the oro- facial region are dental caries and periodontal disease
that develop after a proliferation of bacterial commensals and subsequent upregulation of
virulence factors or exchange of genetic information between more pathogenic species
andthese commensals. Bacterial infections in the oral cavity include caries, gingivitis, periodontitis and osteomyelitis. These diseases are caused by normal oral flora. Microbiologic
identification is usually not required as managing these conditions does not generally require
antibiotics(8, 9).
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19.2.1.2 Etiopathogenesis
The principal bacteria responsible for tooth decay are Streptococcus mutans and Lactobacillus. The
infection of tooth decay differs from most infections as changes manifest only when the infection
reaches the pulp(8). Viridans streptococci are implicated in the formation of dental caries and are
pathogenic when introduced into the fascial planes of the head and neck, forming abscesses.
The pathogenetic mechanisms underlying the development of dental caries have continuously
evolved since the late 1800s. Advances in understanding biofilm formation and maintenance have
significantly contributed to the precise mechanisms leading to the enamel demineralisation caused
by cariogenic bacteria. Although many species of bacteria have been implicated in the development of caries, Streptococcus mutans and Lactobacillus spp have consistently been shown to be the
major players. The natural habitat of S. mutans is the human oral cavity, more specifically, the
dental plaque formed on the hard surfaces of the tooth. In the mouth, the polysaccharides produced by exoenzymes from S. mutans are the main constituents of the insoluble matrix on which
plaque biofilms form and dental caries develop. S. mutans is principally responsible for initiating
the formation and maintenance of the dental biofilm, whilst Lactobacillus, along with S. mutans,
contributes to the acidification of the biofilm with the production of organic acids, principally
lactic acid, from dietary carbohydrates, especially sugars.
Lactobacilli spp. are gram- positive facultative anaerobic, rod- shaped bacteria which can convert
lactose and other sugar substrates to lactic acid and survive in a low- pH environment (as low as 3).
This disturbance in the symbiotic oral microbiome allows the proliferation of cariogenic, acidogenic bacteria, resulting in dysbiosis(10– 12).
19.2.1.3 Clinical Features
Dental caries begins as a soft, opaque or brown spot on the enamel. Dental caries is initially asymptomatic. Once the tooth structure is disrupted, odontoblastic processes are exposed to the oral
environment, and these expand and contract in response to heat, cold and other environmental
shifts, transmitting pain via sensory nerves in the odontoblast layer. As the lesion progresses, caries
reaches the pulp, resulting in pulpitis with pain, usually when reclining. The tooth will be vital if
caries is restricted to dentin. The tooth will test non- vital as soon as the pulp is necrotic. A radiograph of the tooth will demonstrate a well- defined radiolucency at the apex. Radiographs are taken
to identify the extent of decay, although they do not aid in distinguishing between periapical granuloma and cysts. Abscess and cellulitis may be present if the tooth is painful and soft tissue swelling is noted(13, 14).
19.2.1.4 Management
The treatment of dental decay depends on the stage of decay. If it involves enamel or dentine, a
restoration with amalgam or composite is needed. If the caries has reached the pulp, the tooth
should undergo root canal treatment or be extracted, depending on the extent of the pulp involvement. The root canal treatment may be followed by apicoectomy when a periapical granuloma, a
periapical cyst, or a periapical abscess is present. Managing an abscess and cellulitis may require
incision, drainage and tooth extraction under antibiotic cover. It is a common practice to use penicillin or clindamycin for 5– 10days.
19.2.1.5 Dental Abscesses: Periapical andPeriodontal Abscesses
The terms dental abscess, dentoalveolar abscess and odontogenic abscess are often used synonymously to describe abscesses formed in the tissues around the tooth. The cause may be an endodontic
infection (acute apical abscess) or a periodontal infection (periodontal abscess and pericoronitis).
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19.2.1.6 Periapical Abscess
A periapical abscess is also known as a dentoalveolar abscess because of a localised collection of
pus in the alveolar bone at the root apex of the tooth. This arises secondary to dental caries, trauma
or failed dental root canal treatment. It is a localised collection of pus associated with a tooth.
The pathogenesis of periapical abscess is polymicrobial, comprising various facultative anaerobes, such as the viridans group streptococci and the Streptococcus anginosus group, and strict
anaerobes, especially anaerobic cocci, Prevotella and Fusobacterium species(15).
The signs and symptoms of the acute dental abscess are pain, swelling and erythema, usually localised to the affected tooth. Other features include extraoral and intraoral swelling,
erythema, tenderness to palpation, trismus and fever. The spread of bacteria from periapical
(endodontic) abscesses to other tissues may give rise to fascial plane infections involving the
sublingual, submandibular, buccal and pterygomandibular spaces. The spread of infections
into the fascial spaces is determined by the location of the tip of the root involved in relation
to its overlying buccal or lingual cortical plate, the overlying bone’s thickness and the apex’s
relationship to the attachment of a muscle. If the infection affects the sublingual and submandibular spaces bilaterally and the submental space, a life- threatening condition known as
Ludwig’s angina may occur (see later). Infections of the midface can result in a life- threatening
condition called cavernous sinus thrombosis. Treatment of acute apical abscesses involves the
use of antibiotics, incision for drainage, root canal treatment or extraction of the involved
tooth to remove the source of infection. Most bacterial species involved with endodontic infections, including abscesses, are susceptible to penicillin. Clindamycin and Moxifloxacin also
offer good antibacterial activity.
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19.2.1.7 Periodontal Abscess
A periodontal abscess involves the supporting structures of the teeth (periodontal ligaments and
alveolar bone). It is a pocket of pus in the gingival and periodontal tissues usually caused by periodontal bacterial infections. Local factors that increase the risk of a periodontal abscess include
invaginated tooth, root grooves, cracked tooth and external root resorption.
The microbiology of periodontal abscesses includes gram- negative anaerobic bacteria
(GNABS). The most prevalent bacteria found in periodontal abscesses is Porphyromonas gin-
givalis. Other bacteria implicated in the condition include Prevotella intermedia, Prevotella
melaninogenica, Fusobacterium nucleatum, Tannerella forsythia, Treponema species,
Campylobacter species, Capnocytophaga species, Aggregatibacter actinomycetemcomitans and
gram- negative enteric rods. Most periodontal abscesses originate due to the blockage or
obstruction of a periodontal pocket, usually due to calculus accumulation, dislodged calculus
during debridement pushed into the soft periodontal tissues, or a foreign body impaction like
dental floss or a piece of toothpick. This leads to periodontal pocket closure, which impedes
the clearance of gingival crevicular fluid, causing an accumulation of bacteria. However,
most of the tissue damage in periodontal abscesses is due to the release of lysosomal enzymes
from host neutrophils(16).
Clinical features of a periodontal abscess include a swelling of the gingiva; pain, with the area of
swelling tender to touch; a purulent exudate; and increased probing depth. The involved tooth may
be sensitive to percussion and may be mobile. Treatment considerations include establishing
drainage by debriding the pocket, removing plaque, calculus, and other irritants, and possibly
incising the abscess. Systemic antibiotics may be indicated when signs of systemic involvement are
present and if complete drainage cannot be established. Penicillin is the choice. Tetracyclines and
metronidazole have also been advocated.
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19.2.1.8 Ludwig’s Angina
Ludwig’s angina is a severe form of diffuse cellulitis presenting with an acute onset and spreading
rapidly, affecting the submandibular, sublingual and submental spaces obstructing the airway.
19.2.1.9 Etiopathogenesis
Odontogenic infections, especially those originating in the second and third mandibular molars,
are the most common origins of infection. Other causes include respiratory infections, especially
in children, oral piercing or laceration, osteomyelitis, peritonsillar or parapharyngeal abscess, and
submandibular sialadenitis. Patients with diabetes, alcoholism, malnutrition and immunosuppression may be at greater risk for Ludwig’s angina(17– 19).
The condition is usually polymicrobial principally from the oral cavity, including both aerobes
and anaerobes. Staphylococcus, Streptococcus Peptostreptococcus, Fusobacterium, Bacteroides and
Actinomyces are the most frequent organisms. Diabetic patients presenting with Ludwig angina are
prone to infection with Klebsiella pneumoniae, and individuals with diabetes, undergoing haemodialysis, and recovering from recent hospitalisation (within a year) are at increased risk of
methicillin- resistant Staphylococcus aureus (MRSA) infection(17).
19.2.1.10 Clinical Features
Ludwig angina originates in the floor of the mouth and extends to the submandibular space
(Figure19.5). The mylohyoid muscle divides the floor of the mouth into the sublingual space above
the muscle and the submandibular space below the muscle. The roots of the mandibular molars
are located inferior to the attachment of the mylohyoid muscle, allowing the spread of odontogenic
infection into the submandibular space. Extension of the infection into these spaces may enlarge
or elevate the tongue and obstruct the airway. Cellulitis, characteristic of Ludwig’s angina, is
responsible for erythema, warmth, oedema and tenderness to palpation resulting from the
Figure19.5 Ludwig’s Angina. Clinical appearance with bilateral involvement of the submandibular,
sublingual and submental spaces shows brawny swelling induration. Courtesy of Professor
S R Prabhu, Brisbane, Australia.
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inflammatory response to bacteria. The infection may progress, resulting in oedema of the airway
structures and may extend to the parapharyngeal space, retropharyngeal space and superior mediastinum via the styloglossus muscle. The infection spreads to the neck via spaces between the fascial layers and not through the lymphatic system(17– 19).
19.2.1.11 Osteomyelitis
Osteomyelitis is an acute or chronic inflammatory process involving the bone and its structures
secondary to infection with pyogenic organisms. In the maxillofacial complex, mandibular osteomyelitis occurs more frequently than maxillary involvement.
19.2.1.12 Pathogenesis
Osteomyelitis means ‘inflammation of the bone marrow’. Healthy, intact bones are resistant to
infection. The bone becomes susceptible to disease by introducing a large inoculum of bacteria
from trauma, ischemia or the presence of foreign bodies. Most frequently, osteomyelitis of the
jawbones is a sequala of dental, periodontal or periapical abscess. Staphylococcus aureus is the
most common organism causing jaw osteomyelitis, but Streptococci (both α- and β- haemolytic)
are occasionally implicated. The process presents as an acute or chronic polymicrobial infection. In acute osteomyelitis, the organisms excite acute inflammation in the medullary bone.
This results in oedema and exudation that causes pus to be forced under pressure through the
medullary bone, resulting in artery thrombosis, reducing the vascular supply to the bone, which
then necroses. Eventually, pus bursts through the cortical plate to drain via sinuses in the skin
or mucosa. Where pus penetrates the cortex, it may spread subperiosteally, stripping the periosteum and thus further reducing the blood supply. Necrotic pieces of bone become sequestra,
surrounded by pus, which either spontaneously discharges or remains and perpetuates infection. The periosteum lays down new bone to form an involucrum encasing the infected and
sequestrated bone. The involucrum may prevent sequestra from being shed. Osteomyelitis has
a range of clinical manifestations depending on the virulence of the infecting organisms, host
resistance and the reaction of the periosteum to inflammation (21). Chronic osteomyelitis
presents with intermittent pain and swelling, relieved by the discharge of pus through
long- standing sinuses. Bone destruction is localised; often, a single sequestrum may be the
source of chronic infection.
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19.2.1.13 Clinical Features
Jaw osteomyelitis presents with deep- seated, boring pain and swelling. Teeth in the affected area
become loose and tender to percussion, with pus oozing from the gingival crevices. The pain
becomes less intense once pus penetrates the cortical plate and discharges intraorally or extraorally,
often through several sinuses. Labial anaesthesia is a characteristic feature because of pressure on
the inferior dental nerve. Radiographic changes are seen only after there has been significant
decalcification of bone. Early cases may not be detected. Blood tests show leucocytosis with neutropenia and a raised erythrocyte sedimentation rate (ESR).
19.2.1.14 Management
Treatment of osteomyelitis is with antibiotics and drainage. Penicillin was the drug of choice, but
since many staphylococci are now penicillin- resistant, flucloxacillin or fusidic acid may be used.
Extraction of the offending tooth is necessary. In chronic osteomyelitis, removal of the sequestrum
and curettage of the associated granulation tissue usually produces complete resolution.
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19.2.1.15 Actinomycosis
Actinomycosis is a bacterial infection usually caused by Actinomyces israelii. Actinomyces are part
of the normal flora of the human oral cavity, gastrointestinal (GI) tract and female urogenital tract.
The organism is not virulent and only invades the body to cause deeper infections when there is
tissue injury and a subsequent break in the normal mucosal barrier. Infection is mostly polymicrobial. The infection is established with the help of a companion bacteria by inhibiting host defences,
reducing oxygen tension or producing a toxin that facilitates the inoculation of actinomycoses.
In the mouth, this normal commensal of the oral cavity is in the supra and subgingival plaques.
This anaerobic gram- positive organism causes disease when there is disruption of normal flora due
to dental caries, extractions or trauma.
Around 60% of infections are cervicofacial and are described as ‘lumpy jaw syndrome’. The predisposing risk factors for cervicofacial infection include infection in erupting teeth, dental caries,
gingivitis, dental extraction, diabetes, alcohol use disorder, malnutrition and malignancy.
Actinomycosis usually follows root canal treatment, dental implant procedures, osteonecrosis and
periodontitis(22).
Once Actinomyces spp. have invaded tissues, they develop a chronic granulomatous infection characterised by the formation of tiny clumps called sulphur granules because of their yellow colour.
These formations of 0.1– 1 mm in diameter, composed of an internal tangle of mycelial fragments
(Figure 19.6) and a rosette of peripheral clubs, are stabilised by a protein– polysaccharide complex,
which is supposed to provide a resistance mechanism to host defences by inhibiting phagocytosis.
19.2.1.16 Clinical Features
Actinomycosis results in pain and swelling leading to osteomyelitis with multiple sinus tracts
discharging yellow ‘sulphur’ granules.
19.2.1.17 Management
Dental radiographs help evaluate apical abscesses. Computed tomography (CT) and magnetic
resonance imaging (MRI) studies may show osteolysis in the chronic form of infection. The treatment is controversial. Penicillin used for 6weeks to 12months is adequate, although antibiotics
may be avoided by surgical curettage of the infected area.
Figure19.6 H&E image exhibiting
filamentous organisms, dead bone
and infiltrate of inflammatory cells.
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19.2.2 Periodontal Diseases
Periodontal diseases affect the gingiva, periodontal ligament and the alveolar bone. Gingivitis,
inflammation of the gingiva, usually originates from bacteria in the dental plaque. Periodontitis
occurs due to the extension of gingival inflammation into the surrounding periodontal structures,
resulting in bone loss and gingival recession(9).
19.2.2.1 Pathogenesis
Periodontal disease can be viewed as dysbiosis of the oral microbiota and dysregulation of the host
immune response directed against the subgingival microbiota, leading to gingival inflammation,
bleeding or suppuration (Figure 19.7) upon probing, periodontal pocket formation and loss of supporting structures(23).
Microorganisms mainly cause gingivitis and periodontal disease within the subgingival dental
plaque, penetrating the gingival epithelium and eliciting an inflammatory host response. The microflora associated with gingivitis is predominated by Actinomyces species such as A. viscosus, A. naeslundii
and Porphyromonas gingivalis. Other species, such as S. sanguis and S. anginosus, are also found. As
periodontal disease advances, Porphyromonas gingivalis, Prevotella intermedia, Bacteroides forsythus,
Campylobacter species and Treponema denticola become predominant. Two specific clinical entities,
namely localised juvenile periodontitis (LJP) and acute necrotising ulcerative gingivitis (ANUG), are
associated with specific pathogens. Microorganisms include Actinobacillus actinomycetemcomitans in
localised juvenile periodontitis, Fusobacterium nucleatum, and Treponema denticola in NUG.
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19.2.2.2 Clinical Features
Findings are dependent upon whether the gingivitis is localised or generalised. Marginal gingiva
may appear red, and patients may complain of sensitivity and bleeding. When inflammation
reaches the periodontal structures, there will be increased bleeding and mobility of teeth. Halitosis
may be noted in some patients. The radiograph will show bone loss, and the amount of bone loss
will help in assessing the prognosis. Occasionally, a patient will present with abscesses and sinus
tracts. The abscess harbours plaque bacteria, including Streptococcus mutans, Actinomyces,
Fusobacteria and Prevotella(9, 24, 25).
Figure19.7 Clinical photograph showing periodontal
abscess in relation to #3.
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