Understanding the link between viral infections and oral health is crucial for dental professionals. Viral diseases such as influenza, measles, adenovirus, and rubella can cause distinct oral symptoms, which can assist in diagnosis and impact treatment. This overview covers the etiology, epidemiology, pathogenesis, clinical features, complications, diagnosis, and treatment of these viral infections, highlighting their oral manifestations and implications for patient care.

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Influenza

Influenza is a highly contagious acute infectious disease characterized by symptoms of specific intoxication and inflammation of the upper respiratory tract.

Etiology of Influenza
Influenza is an acute respiratory infection caused by RNA viruses of the Orthomyxoviridae family. These viruses are classified into three antigenically distinct types: A, B, and C.

Epidemiology of Influenza
Influenza occurs worldwide and is known for its tendency to spread in epidemics and pandemics. During non-epidemic periods, the disease persists through sporadic cases and localized outbreaks. The primary source of infection is an infected person, who becomes contagious from the late incubation period through the febrile stage. Transmission occurs exclusively via airborne droplets. Infants in their first months of life are relatively resistant to the virus due to maternal immunity. However, in the absence of protective maternal antibodies, even newborns can be susceptible to infection.

Following an influenza infection, a lasting, type-specific immunity develops. Reinfections typically occur due to exposure to new serovars of the influenza virus.

Pathogenesis of Influenza

The pathogenesis of influenza is characterized by the virus's epitheliotropic and systemic toxic effects. Once the virus enters the mucosa of the upper respiratory tract, it invades epithelial cells, where it replicates, causing cell damage that can lead to dystrophy and necrosis. Autoantigens, along with viral antigens, initiate local autoimmune cytotoxic reactions mediated by T-lymphocytes. These reactions aim to eliminate infected cells and viral antigens. Morphologically, this manifests as localized inflammation, while clinically it presents as upper respiratory tract inflammation.

From the initial site of infection, the virus enters the bloodstream, exerting systemic toxic effects and suppressing both cellular and humoral immunity. Its toxic impact primarily targets the central nervous system (CNS).

Clinical Features of Influenza
The incubation period ranges from a few hours to 2–4 days. The disease onset is abrupt, with a sudden rise in body temperature to 39–40°C, chills, dizziness, general weakness, fatigue, and muscle and joint pain. Children may complain of headaches and pain in the eye area. Common symptoms include loss of appetite, sleep disturbances, delirium, nausea, and vomiting. In severe cases, facial flushing, scleral vessel injection, and hyperemia of the tonsils and soft palate are observed.

Specific changes in the oral mucosa include:

Catarrhal stomatitis: Prominent hyperemia, paresthesia, and burning sensations in the oral cavity.
By the first or second day, red pinpoint lesions resembling millet seeds appear on the soft palate due to hyperplasia of the epithelial ducts of salivary glands.
More pronounced changes may occur in the soft palate, uvula, and tonsillar arches, occasionally extending to the cheeks, tongue, and gums.

In some cases, severe hyperemia, petechiae, or desquamation of the oral epithelium may appear. These signs could be accompanied by the development of small hemorrhagic vesicles that rupture, forming bright red erosions or aphthae.

By the third to fourth day, hyperemia and granularity of the soft palate are replaced by vascular injection and petechial hemorrhages, which usually subside by the seventh to eighth day.

Complications of Influenza
During the late stages, large, thin-walled vesicles containing hemorrhagic exudate may form near the transition zone of the hard and soft palates or on the buccal mucosa. These vesicles rupture within hours to two days, leaving large, erosion-free lesions. In individuals with low immunity, these lesions may ulcerate, leading to aphthous or necrotizing ulcerative stomatitis.

Secondary bacterial infections can exacerbate the condition, resulting in more severe complications, including periodontal disease exacerbation, recurrent herpes, or trigeminal and facial nerve damage. Immunodeficiency in the later stages may predispose individuals to acute herpetic stomatitis or candidiasis.
Diagnosis of Influenza
Influenza diagnosis is based on epidemiological data, medical history, clinical manifestations, and laboratory findings (blood tests, cytology, serology, virology, and immunofluorescent studies). A significant diagnostic indicator is the absence of interferon and a marked decrease in lysozyme levels in saliva. Peripheral blood changes are typical of acute inflammatory processes.

Treatment of Influenza
Treatment of influenza-related stomatitis depends on the type of mucosal changes (catarrhal, erosive, ulcerative):

Catarrhal stomatitis: Maintain good oral hygiene and use prophylactic antiseptic rinses.
Erosive and ulcerative lesions: Use numbing agents like benzocaine or lidocaine gels to reduce pain, rinse with solutions containing benzydamine hydrochloride or a mild saline solution to soothe irritation, apply protective agents such as hyaluronic acid gels or lanolin-based ointments to cover and protect lesions.

Adenovirus Infection

Adenovirus infection is an acute respiratory illness characterized by fever, moderate intoxication, and inflammation of the respiratory mucosa, conjunctiva, and lymphoid tissue. This condition holds a significant place in the pathology of young children. By the age of five, nearly all children have experienced adenovirus infection, with approximately half enduring it more than once.

Etiology of Adenovirus Infection

Adenoviruses are DNA-containing pathogens known for their resilience in external environments. There are 57 identified types of adenoviruses, associated with human disease. Initial signs of cell damage, primarily in the nucleus, manifest within 12 hours of infection.

Epidemiology of Adenovirus Infection

The infection's sources include symptomatic patients, individuals with subclinical forms of the disease, and asymptomatic carriers. The risk is highest during the acute phase of illness. The primary mode of transmission is airborne, though alimentary transmission (resembling gastrointestinal infections) is also possible. Newborns are largely protected by passive transplacental immunity, but susceptibility increases markedly after six months. Adenovirus infections are common year-round but peak during colder months, often appearing sporadically or in outbreaks, particularly in child care settings.

Pathogenesis of Adenovirus Infection

The upper respiratory tract, conjunctiva, or gastrointestinal tract often serves as the entry point for adenoviruses. They penetrate epithelial cells via pinocytosis, reaching the cytoplasm and nucleus of susceptible cells and regional lymph nodes. Viral DNA synthesis begins in the cell nucleus, producing mature viral particles within 16–20 hours. Viral replication in epithelial cells and lymph nodes corresponds to the incubation period. The virus then spreads via the bloodstream, affecting nasal and pharyngeal mucosa, tonsils, and regional lymph nodes. Advanced stages involve viremia, which can impact the respiratory system, gastrointestinal tract, kidneys, liver, and spleen.

Clinical Presentation of Adenovirus Infection

The incubation period ranges from 2 to 14 days, with symptoms often developing suddenly. The illness begins with fever and upper respiratory catarrh. Fever gradually intensifies, peaking at 39°C by the second or third day. Intoxication symptoms, such as lethargy, headache, and mild muscle or joint pain, are moderate. Appetite may decline, and some children may exhibit oral mucosal changes resembling acute candidal or herpetic stomatitis, complicating the course of the illness.

Abdominal pain, nausea, and vomiting are less common symptoms. Pharyngeal involvement is prominent, marked by moderate redness and swelling of the tonsillar arches and soft palate. A distinctive feature is "granular pharyngitis," where the posterior pharyngeal wall appears swollen and hyperemic with bright, enlarged follicles, often coated with whitish plaques and thick mucus.

Oral mucosal changes include redness, swelling, petechiae, and fine hemorrhages. The soft palate may appear granular, with enhanced vascular patterns.

A hallmark of adenovirus infection is conjunctival involvement. Conjunctivitis may be catarrhal, follicular, or membranous, emerging either on the first day or later (days 3–5). Membranous conjunctivitis is particularly diagnostic. Examination often reveals puffy facial features, swollen eyelids, purulent eye discharge, and profuse nasal secretions. Cervical lymph nodes are frequently mildly enlarged. Young children may also experience gastrointestinal symptoms, including loose stools.

Peripheral blood tests in the early stages may show mild leukocytosis with neutrophilia, lymphopenia, and slightly elevated ESR.

Adenovirus infections can be prolonged. Fever typically subsides by days 5–7, while respiratory catarrh symptoms resolve within 2–4 weeks. Conjunctivitis may persist for 7–14 days. In some cases, corneal involvement (keratitis) may cause symptoms to linger longer, even up to several weeks.

Complications of Adenovirus Infection

Complications often arise from secondary bacterial infections. The overall prognosis is favorable.

Diagnosis of Adenovirus Infection

The diagnosis of adenovirus infection is based on fever, upper respiratory symptoms, lymphoid tissue hyperplasia in the oropharynx, cervical lymph node enlargement, and characteristic conjunctival inflammation. Rapid diagnostic methods include fluorescent antibody techniques. Differential diagnosis should consider other viral respiratory infections, infectious mononucleosis, and acute herpetic stomatitis.

Treatment of Adenovirus Infection

Children with adenovirus infections are usually treated at home. Nutrition should be high in calories, with reduced fat and meat intake. Generous hydration is essential.

Treatment is primarily supportive and symptomatic under pediatric supervision. No specific dental treatment is typically required, but good oral hygiene and rinsing with herbal decoctions (e.g., chamomile) are advised.

Measles (morbilli)

Measles is a highly contagious viral infection caused by a filterable virus belonging to the Paramyxoviridae family. Transmission occurs through airborne droplets, making infected individuals contagious from the last two days of the incubation period until the third day of the rash.

Etiology of Measles
Measles (morbilli) is caused by a filterable virus belonging to the Paramyxoviridae family. The pathogen, which contains RNA, is highly sensitive to heat, ultraviolet light, and disinfectants. Infection occurs through airborne droplets, making measles highly contagious. Individuals with measles are infectious from the last two days of the incubation period to the first four days after the onset of the rash.

Epidemiology of Measles
Humans are the sole reservoir of the measles virus. The disease predominantly affects unvaccinated individuals, particularly young children, although susceptibility persists throughout life for those not previously infected or immunized. Measles outbreaks are more common in colder seasons (autumn, winter, and early spring). The virus spreads through coughing or sneezing and can travel significant distances indoors, even between rooms or apartments.

Pathogenesis of Measles
The virus typically enters the body through the mucous membranes of the upper respiratory tract or the conjunctiva. Initial viral replication occurs at these sites, followed by viremia, which can be detected from the earliest stages of infection. The highest viral load is observed during the prodromal phase and the first day of the rash. Measles exhibits a particular affinity for the central nervous system (CNS), respiratory tract, and gastrointestinal tract.

The infection significantly impairs both general and local immunity, with notable depletion of vitamins C and A. Respiratory complications are common, such as laryngotracheobronchitis and pneumonia, caused by widespread inflammation of the nasal, laryngeal, tracheal, and bronchial mucosa. Neurological involvement may lead to encephalopathy, while gastrointestinal symptoms often involve the oral and colonic mucosa. The characteristic papular rash results from exudative processes in the epidermis, leading to cell necrosis, keratinization, and eventual desquamation.

Clinical Features of Measles

The incubation period for measles typically lasts 8–12 days. The illness progresses through three phases: the prodromal (catarrhal) stage, the rash stage, and the pigmentation stage.

During the prodromal phase, patients experience fever (38–39°C), fatigue, reduced appetite, and an intensifying dry, persistent, hacking cough. Nasal discharge becomes prominent, and conjunctivitis causes photophobia, scleral redness, and eyelid swelling. The characteristic Koplik’s spots emerge in this phase as tiny, white or grayish specks surrounded by a red halo, often appearing on the buccal mucosa near the molars. These spots resemble sprinkled lime droplets and are pathognomonic for measles.

The prodromal phase can be recognized by "three Cs" of measles:

Cough
Coryza (runny nose)
Conjunctivitis

The rash stage begins on days 3–4 with maculopapular eruptions starting on the face and behind the ears, then spreading to the trunk and extremities. The rash often coalesces but spares some areas of normal skin. Fever and systemic symptoms worsen. Over the next 3–4 days, the rash fades, leaving pigmented spots and fine desquamation.

Complications of Measles
Measles weakens the immune system, predisposing individuals to secondary infections such as otitis media, pneumonia, laryngitis, encephalitis, and stomatitis. In severe cases, complications like mastoiditis or herpes reactivation may occur.

Diagnosis of Measles
Koplik’s spots are a definitive early sign of measles, facilitating prompt diagnosis and prevention efforts. Differential diagnosis includes conditions such as scarlet fever, rubella, acute herpetic stomatitis, and candidiasis. The absence of features like aphthous lesions, strawberry tongue (scarlet fever), or multinucleated giant cells (herpes) aids in differentiation.

Treatment of Measles
Uncomplicated cases are typically managed at home with symptomatic care. Bed rest, hydration, and a nutrient-rich diet (especially vitamins A and C) are essential. Gentle oral hygiene and antiseptic mouth rinses (e.g., sodium bicarbonate or chlorhexidine) are recommended. Antihistamines may help alleviate discomfort. Antiviral ointments can prevent herpes recurrence. Complicated cases may require hospitalization for targeted interventions.

This disease is more commonly seen in pediatric populations due to their higher exposure, lower vaccination rates in some areas, and the nature of children’s immune systems, which may still be developing or may not have had the chance to develop immunity to certain viral infections. In general, children are particularly susceptible to viral infections, and as pediatric dentists, it's crucial to be prepared for the unique challenges these little patients bring. Our course, "Daily Manipulations of a Pediatric Dentist: From Communication to Restoration," covers everything from effective behavior management to advanced restorative techniques, ensuring you are equipped to handle all aspects of pediatric dental care.

Rubella

Rubella, commonly known as German measles, is an acute viral infection characterized by a fine-spotted (measles-like) rash, generalized lymphadenopathy, mild fever, and significant risk to fetal health in pregnant women. There are two main forms of rubella based on the transmission mechanism: acquired and congenital. Among these, congenital rubella is the most dangerous due to the teratogenic effects of the virus, which can lead to severe fetal abnormalities.

Etiology of Rubella

The rubella virus belongs to the Togaviridae family, classified as an RNA-containing virus. It is unstable in external environments, quickly inactivated at temperatures above 56°C, through drying, pH fluctuations below 6.8 or above 8, ultraviolet radiation, and disinfectants (e.g., chlorine-based and alcohol-based solutions).

Epidemiology of Rubella

The infection source is typically an individual infected with rubella. Although the disease can occur at any age, children aged 1 to 7 years are most commonly affected. Asymptomatic carriers, particularly those with subclinical forms or congenital rubella, pose significant risks since the virus can persist in their systems for 18 months or longer. Rubella often appears in epidemic outbreaks, with peak incidence occurring between April and June. During outbreaks, both children and adults can contract the virus. Transmission occurs via airborne droplets, with the virus being released into the environment up to a week before and after the rash appears.

Pathogenesis of Rubella

The rubella virus enters the body through the mucous membranes of the upper respiratory tract and replicates in the lymph nodes (particularly occipital and posterior cervical nodes), which enlarge towards the end of the incubation period. The virus then spreads into the bloodstream, leading to the characteristic rash about two weeks after infection.

Besides its affinity for skin tissue (dermatotropism), the rubella virus also targets endothelial cells, nervous tissue, and embryonic structures. After recovery, individuals develop lifelong immunity.

Clinical Features of Rubella

The incubation period of rubella ranges from 11 to 24 days. Symptoms of systemic toxicity are generally mild, with the rash being the first noticeable sign. The rash initially appears on the face and neck, rapidly spreading to the trunk and extremities within hours. It is most prominent on the face, extensor surfaces of limbs, back, lower back, and buttocks. The rash consists of small spots measuring 2–4 mm in diameter, sometimes slightly raised, which rarely merge and may cause mild itching. The rash fades without leaving pigmentation.

Patients may experience slight weakness, malaise, moderate headache, and occasionally muscle pain. Fever is usually low-grade but can occasionally reach 38–39°C, lasting 1–3 days. Physical examination reveals mild symptoms of upper respiratory tract inflammation, slight throat redness, swollen tonsils, and conjunctival vessel injection. Oral manifestations include generalized catarrhal stomatitis and submandibular lymphadenitis. Pale pink spots (enanthema) may appear on the soft and hard palate. Desquamation of the tongue’s epithelium leads to a “lacquered” appearance after 2–4 days. Lips may become swollen and intensely red, developing erosions and cracks by the fourth or fifth day.

A hallmark of rubella is the enlargement of peripheral lymph nodes, particularly occipital and posterior cervical nodes. These nodes are firm and may be tender, enlarging before the rash appears and persisting after its resolution.

Complications of Rubella

The most common complication of rubella is arthritis. Less frequent complications include thrombocytopenic purpura and, more severely, rubella encephalitis.

Diagnosis of Rubella

Differential diagnosis includes adenovirus and enterovirus infections, measles, infectious mononucleosis, drug-induced exanthema, enteroviral rashes, and herpesvirus infections. Clinical presentation, laboratory tests, and epidemiological data aid in distinguishing rubella from these conditions.

Treatment of Rubella

Rubella is primarily managed at home. During the rash phase, patients are advised to rest and follow a milk-vegetarian diet, supplemented with vitamins and ample fluids. Local treatment involves maintaining oral hygiene and, when necessary, using antiseptics, pain relievers, antiviral agents, and epithelialization-promoting remedies.

Summary table of the oral manifestations of Influenza, Adenovirus, Measles, and Rubella:

Viral Infection	Oral Manifestations
Influenza	Catarrhal stomatitis: Hyperemia, paresthesia, and burning sensations in the oral cavity. Red pinpoint lesions (resembling millet seeds) on the soft palate. Hyperemia, petechiae, or desquamation of the oral epithelium. Small hemorrhagic vesicles that may rupture, leaving red erosions or aphthae. Severe hyperemia and granularity of the soft palate replaced by vascular injection and petechial hemorrhages by day 3-4.
Adenovirus	Redness, swelling, petechiae, and fine hemorrhages in the oral mucosa. Granular appearance of the soft palate with enhanced vascular patterns.
Measles	Koplik's spots: Small white or grayish specks surrounded by a red halo on the buccal mucosa. Generalized oral mucosal changes accompanying the rash.
Rubella	Generalized catarrhal stomatitis. Pale pink enanthem spots on the soft and hard palate. Lacquered tongue due to epithelial desquamation. Swollen, intensely red lips with erosions and cracks.

While these viral infections may cause temporary gingival irritation or inflammation as part of their broader oral manifestations, they are not primary causes of gingivitis or periodontitis. Do you want to enhance your periodontal expertise? Then join our comprehensive course, "Non-Surgical Periodontal Therapy and Minimally Invasive Protocols"! You'll master clinical protocols for non-surgical treatments, including minimally invasive techniques and the use of specialized instruments for supra- and subgingival instrumentation and gain in-depth knowledge on the biological rationale behind therapy steps, the expected outcomes, and how to implement Supportive Periodontal Therapy (SPT) effectively.

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