Stomatitis

Candidal stomatitis: etiology and mechanisms of development

Stomatitis often represents a localized form of candidomycosis—a typical opportunistic mycotic infection that manifests exclusively against the background of declining immune reactivity. The primary causative agents of oral mucosal inflammation are yeast-like fungi belonging to the genus Candida. Although about two hundred species of these microorganisms are known to science, Candida albicans is unquestionably recognized as the dominant pathogen.

In the vast majority of clinical scenarios, the endogenous route of infection occurs. Fungi of this genus are not absolute aggressors initially; they coexist peacefully with humans as natural representatives of the normal mucosal microflora. However, at the slightest decrease in immune defense, they transform, acquire pronounced pathogenic properties, actively invade tissues, and provoke autoinfection.

Exogenous routes of pathogen transmission are significantly less common in practice. These include the vertical mechanism, where infection of the newborn infant occurs directly during childbirth or in the process of breastfeeding.

Predictors and risk factors

Oral mucosal inflammation does not occur spontaneously. The development of a candidal lesion is always provoked by specific conditions that severely disrupt the systemic or local homeostasis of the body. Key risk factors include:

• Iatrogenic dysbiosis. Most commonly, it becomes a direct consequence of irrational or prolonged antibiotic therapy, which destroys beneficial microflora and provides fungi with space for unimpeded proliferation.
• Immunodeficiency states. This includes a wide spectrum of pathologies, including HIV infection, in which stomatitis becomes a striking marker of profound immunosuppression.
• Endocrine and metabolic disorders. Metabolic disturbances create a favorable nutrient medium for fungal invasion.
• Mechanical injuries. Trauma to the skin and mucous membranes, especially if it occurs under conditions of high humidity or maceration, opens direct portals of entry for infection.

Clinical manifestations depending on immune status

The symptoms and severity of stomatitis depend directly on the patient's immune defense status.

In immunocompetent individuals, the disease proceeds in a superficial form, commonly known as classical "thrush". The pathological process is localized on the buccal, labial, and lingual mucosa. Patients complain of pronounced itching and a burning sensation. Objectively, tissue hyperemia, exudation, and the appearance of characteristic white curdy plaques are observed. This condition is frequently associated with antibiotic administration. With a rational approach, it is characterized by rapid involution (regression)—it is sufficient to discontinue the antibacterial drug and prescribe adequate antimycotic therapy.

In HIV-infected patients, the picture is completely different. The clinical presentation of stomatitis here strictly correlates with the current stage of HIV infection and the degree of immune decline. Lesions are persistent and recurrent in nature. With the progression of immunosuppression, superficial stomatitis may be only the first stage, followed by severe visceral forms of candidiasis (involving the gastrointestinal tract and respiratory system) and even disseminated forms up to candidal sepsis with multi-organ involvement.

Stomatitis as a manifestation of hematological pathologies

In addition to a purely fungal etiology, severe inflammatory oral lesions may have a completely different nature. They often act as a formidable symptom of systemic blood diseases, specifically aplastic anemia in children.

In this pathology, total suppression of various hematopoietic lineages occurs in the bone marrow. If the pathological process affects granulocytopoiesis, the patient inevitably develops a syndrome of infectious complications. Its main laboratory marker and criterion is a sharp drop in the leukocyte level in peripheral blood (values often drop below 2 × 10⁹/L).

Such profound neutropenia catastrophically reduces the non-specific resistance of the child's body to any external and internal pathogens. As a result, the child develops frequent and extremely severe bacterial as well as fungal infections. Stomatitis in this case becomes one of the most striking clinical manifestations, along with pneumonia, severe tonsillitis, and even sepsis. An important differential diagnostic sign pointing specifically to bone marrow aplasia is the absence of enlargement of the liver, spleen, and lymph nodes (hepatosplenomegaly and lymphadenopathy), which distinguishes this condition from leukemias.

Class and exam questions

What else to study on this topic

• Invasive and disseminated forms of candidiasis (candidal sepsis)
• Anemic and hemorrhagic syndromes in aplastic anemia
• Prevention of Pneumocystis pneumonia in case of CD4 lymphocyte count drop
• Differential diagnosis of pancytopenia without hepatosplenomegaly
• Odontogenic maxillary sinusitis and its anatomical prerequisites

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Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.