Parakeratosis

Place of parakeratosis in the structure of dyskeratosis

In pathological anatomy, parakeratosis is not considered an isolated disease, but rather a crucial histological symptom. According to modern concepts, it belongs to the group of dyskeratoses. The most illustrative example of the clinical realization of this process is cervical leukoplakia. Translated literally from Greek, this term means "white plaque".

In current clinical guidelines, leukoplakia is interpreted as keratosis or hyperkeratosis, which essentially represents abnormal keratinization of an epithelium type that does not normally keratinize (non-keratinizing stratified squamous epithelium). It is important to note that in some cases, this local keratinization process may not occur independently, but rather be accompanied by prominent signs of dysplasia in deeper, underlying tissue layers.

Pathomorphological picture

Histological examination of tissues in local keratinization processes demonstrates a characteristic triad of signs. Pathomorphology necessarily includes:

• Parakeratosis — disruption of the keratinization process.
• Hyperkeratosis — excessive thickening of the stratum corneum.
• Acanthosis — thickening of the epidermis due to proliferation of cells in the stratum spinosum.

In addition to changes within the stratified squamous epithelium itself, the pathological process also affects the underlying stroma. Specific lymphohistiocytic infiltrates form around the blood vessels of the stromal tissue, indicating a tissue reaction to the developing dyskeratosis.

Etiology and classification of the process

Among the risk factors triggering the mechanisms of keratinization and parakeratosis, viral agents unconditionally lead, primarily human papillomavirus (HPV). A somewhat lesser but significant impact is exerted by concomitant endocrine disorders, changes in the body's immune status, and infectious factors, among which chlamydial infection is particularly highlighted.

Depending on the nature of cellular changes, morphologists divide leukoplakia into two fundamentally different categories:

1. Simple leukoplakia. In clinical practice, it is considered exclusively as a background process.
2. Proliferating leukoplakia with cellular atypia. This condition is already classified as a precancerous lesion of the cervix. The severity of precancer directly depends on the degree of cellular atypia. Characteristic features of this form are a sharp increase in the mitotic activity of cells and the appearance of atypical cellular elements localized predominantly in the basal and parabasal layers of the stratified squamous epithelium.

Clinical manifestations and diagnostics

The insidious nature of local keratinization processes lies in the fact that the disease proceeds completely asymptomatically. Patients present with no specific complaints. Upon visual inspection with the naked eye, the pathology can only be noticed in clinically apparent cases—when characteristic raised white plaques are discovered on the ectocervix.

In all other situations, colposcopy helps detect areas of parakeratosis and hyperkeratosis. The colposcopic picture is specific: the pathological lesion looks like a whitish, shiny film (which can be either completely smooth or bumpy), caused by the development of the epithelial stratum corneum. The key visual markers are:

• Punctation — multiple red dots against the background of the plaque.
• Mosaicism — lines that intertwine and form peculiar polygons.

These patterns are caused by translucent blood vessels running within the connective tissue papillae and projections that deeply penetrate the altered epithelial layers.

Diagnostics is necessarily supplemented by the Schiller test. In leukoplakia, it is negative (iodine-negative zone). This occurs because normal intermediate cells capable of accumulating glycogen are absent in the keratinized areas.

It is important to remember that standard cytologic examination does not allow reliable differentiation of the simple form from the proliferating form with atypia. Surface keratinizing cells simply do not reflect the pathological processes occurring in the deep basal layers. That is why the gold standard of diagnostics is a mandatory targeted cervical biopsy followed by detailed histological examination.

Class and exam questions

What else to study on this topic

• Pathogenesis of HPV's effect on the keratinization processes of non-keratinizing epithelium.
• Histological differences between the basal and parabasal layers of stratified squamous epithelium.
• The concept of cervical intraepithelial neoplasia (CIN) and its grades.
• Morphological characteristics of stromal lymphohistiocytic infiltrates.

Other topics in the "Additional Topics" section

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