2024-01-17 13:17:21
Systemic diseases to consider during dental treatment A~Z 49
3. Atopic Dermatitis (AD)
There are many types of allergic skin diseases, but the most representative one is atopic dermatitis.
The word ‘atopy’ etymologically means ‘abnormal reaction’, and people with atopic constitution often show urticaria when an intradermal reaction test is performed using a causative protein that can cause an immune response commonly encountered in daily life.
If these causative proteins are eaten, inhaled, or come into contact with the skin, symptoms such as skin itching, hives, and coughing appear within minutes to hours. Atopic constitution is inherited and runs in families, and people with atopic constitution and their family members can be found to have allergic diseases such as asthma, allergic rhinitis, and atopic dermatitis.
As such, atopic dermatitis is a unique allergic skin disease that occurs in people with ‘atopic allergy’.
The cause of atopic dermatitis has not been clearly identified to date, but the occurrence of this disease is due to genetic predisposition, dry skin, the characteristic of feeling itchy more easily than normal people, abnormal skin vascular reaction, white blood cells with abnormal functions, and the patient’s daily life. It is known that infections caused by proteins, bacteria, viruses, and fungi, inflammatory mediators such as histamine, and mental stress interact in a complex manner.
Atopic dermatitis (AD) is a chronic skin disease characterized by itching, redness, lichenification, and skin infection. Causes can be divided into congenital factors (genetic factors) and acquired factors.
Genetic factors such as mutations in genes such as filaggrin are well known, and acquired factors include stimulation from various triggers that can irritate the skin and immunological factors. The biggest characteristics of AD are severe itching and a very sensitive response to external stimuli or allergens.
The cause of itching is not clear, but it is known to be caused by chemical mediators secreted by various inflammatory cells. AD patients have a low threshold for itching, so they itch easily, and the condition gets worse due to allergens, low humidity, excessive sweating, and various irritants (wool, acrylic, soap, detergent).
After scratching or rubbing the skin, eczematous changes appear in the skin, and as the eczema worsens, the vicious cycle of itching occurs once more. The clinical manifestations of AD are very diverse and differ depending on age. In infancy, it occurs most frequently on the cheeks, forehead, and scalp, and often presents with acute eczematous lesions in the form of oozing or crusts, while as childhood progresses, it occurs in the areas in front of the elbows and the popliteal fossa. Lesions become evident on the curved side of the back and often appear in the form of dryness. As puberty and adulthood progress, prurigo and lichenification are commonly observed, not only in the intertriginous region and neck, but also on the face and hands.
1) Cause
AD is a skin disease caused by a complex interaction of genetic factors, skin barrier defects, immune abnormalities, infectious environmental factors, etc., and is caused by abnormalities in the structural proteins, fats, proteolytic enzymes, or decomposition inhibitor enzymes that make up the epidermis. Damage to the barrier, resulting in increased penetration of foreign antigens, and subsequent immune dysregulation are known to be the causes.
1. Genetic factor
Children born to parents with AD have a higher incidence of atopic dermatitis than children born to normal parents. Among many factors, this is most often related to mutations in filaggrin, a key structural protein that makes up the skin barrier.
2. Epidermal barrier defect
The most important role of the skin barrier is to keep the human body, which consists of regarding 80% water, safe from dry external environments, and this function is managed by the epidermis, the outer layer of the skin.
The epidermal layer, including the skin barrier, is the most dynamic organ among the tissues of the human body and maintains epidermal homeostasis by constantly repeating the process of formation, differentiation, and shedding of epidermal cells.
The main constituent cells of the epidermis are keratinocytes, and the differentiation of these cells involves the division process of basal cells, synthesis and maintenance processes in polar cells, autolysis process in granule cells, and remodeling in keratinocytes. The process occurs in four stages, and the final stage of differentiation is the formation of the stratum corneum, which is called the keratinization process.
When the differentiation of keratinocytes occurs abnormally, defects in the skin barrier function occur, which causes skin dryness and chronic skin inflammatory diseases such as atopic dermatitis.
Defects in the skin barrier occur due to genetic causes or various cytokines, which makes it easier for allergens or microorganisms to penetrate through the skin, resulting in a chronic inflammatory skin reaction. There are also reports that various air pollutants can cause damage to the skin barrier and cause or worsen skin inflammation.
1) Reduction of Ceramide; The main lipids that form the lipid membrane between keratinocytes are ceramide, cholesterol, and free fatty acids, with ceramide accounting for regarding 50%. A decrease in ceramide is believed to be the cause of dry skin in all AD patients.
2) increase in serine proteases (SP) and decrease in SP inhibitors; The pH of the skin surface of AD patients is higher than that of normal people, but is higher at the lesion site and becomes even higher as the degree of itching is severe. When the pH of the skin surface increases, the activity of serine protease, which induces exfoliation of keratinocytes, is promoted and SP inhibitors are reduced.
3) Reduction of anti-microbial peptides; Anti-microbial peptides are an important element in maintaining the body’s innate immunity. They are cationic peptides that are produced in epithelial tissue and form a first line of defense that exhibits a wide range of antibacterial effects once morest all germs, including viruses, bacteria, and fungi. do. It also activates adaptive immunity and is involved in the wound recovery function that occurs following biological damage.
4) Mutations in the Filaggrin gene; Filaggrin exists in the form of pro-filaggrin, a protein that composes keratohyalin granules in the granular layer, and is converted to filaggrin during the final differentiation of keratinocytes. When forming the keratinocyte membrane, it aggregates with keratin filament to create a hard, flat structure, forming the skin. It acts as a brick in the barrier that protects the body from the external environment.
Afterwards, as it rises to the upper part of the stratum corneum, it is decomposed into amino acids and becomes a major component of natural moisturizing factors (NMF) such as free amino acids, which are very important for moisturizing, and pyrrolidone carboxylic acid (PCA) and urocanic acid (UCA).
These ingredients exhibit hydration of the stratum corneum, normalization of pH of the stratum corneum, permeability barrier and integrity/cohesion of the stratum corneum, and antibacterial and anti-inflammatory effects.
5) Reduction of tight junctions; Tight junctions exist in epithelial cells and function to fasten the sides of neighboring cell membranes to each other and prevent the flow of moisture between cells. In the epidermis, it exists on the side of the keratinocyte membrane at the top of the granular layer and plays a role in fixing the two cells and maintaining their shape.
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