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Focal infection the source of the pathology

This article has been cited by other articles in PMC. Abstract Introduction The Focal Infection Theory, originally presented at the beginning of the 20th century, postulates that systemic diseases can be caused by microorganisms that arise from the focus of infection.

Introduction

Foci of infections have been described as sinuses, adenoids, tonsils, teeth, genitourinary tract, gall bladder focal infection the source of the pathology kidneys. A focus of infection is defined as the area that can occur in any part of the body, contains a pathogen microorganism and is usually asymptomatic. There are discordant opinions about the role of focal infections in the pathogenesis of psoriasis and urticaria.

Aim To establish whether there is a higher incidence of focal infections in patients with chronic urticaria and psoriasis. Material and methods We retrospectively reviewed 129 patients with a history of psoriasis and chronic urticaria: Results In the analyzed group, 11 patients had a dental consultation, 58 — laryngological consultation and 29 women had a gynecological consultation.

The most common examples of focal infection were tonsillitis, upper respiratory tract infections, sinusitis, dental caries and genitourinary tract infections.

Aggravating factors were similar to previously described. Conclusions A high incidence of focal infections in patients with psoriasis and urticaria suggests that infections may play a significant role in the pathogenesis of these skin disorders. Treatment of infection foci may play the key role in the remission of skin changes. Chronic urticaria Chronic urticaria is defined by the presence of urticaria, on most days of the week, for at least 6 weeks.

Focal Infection in Dentistry

Urticaria is classified into immunological mediated IgE-dependent and non-IgE dependent and non-immunological mediated ones. Physical urticaria is caused by physical exertion, mechanical, electromagnetic or thermal stimuli such as water, UV light, cold, heat, pressure with nonspecific activation of mast cells [ 2 — 4 ]. There are several theories trying to explain the pathogenesis of urticaria. Chronic urticaria is usually self-limited with a duration of 2-5 years. This subgroup of chronic urticaria is called autoimmune urticaria.

Skin lesions in urticaria are well-circumscribed, raised above the surface of the skin, pale in the middle, with a smooth surface and extreme purities.

The shape of the skin changes plaques, wheals varies: Angioedema in chronic urticaria is an episodic swelling of the mucosa or subcutaneous tissue, asymmetric, developing in a few minutes to a few hours, common in the area of the face [ 11 ]. Aggravating factors include physical factors hot, cold, humidity, etc.

Many autoimmune disorders are associated with chronic urticaria. Patients with chronic urticaria have an increased odds ratio for hypothyroidism, hyperthyroidism, antithyroid antibodies. All examined patients had a high mean platelet volume, positive rheumatoid factor, and antinuclear antibodies.

The common mechanism in previously mentioned diseases is a high prevalence of autoantibodies and the presence of a chronic inflammatory process high mean platelet volume.

The exact role of autoantibodies remains unknown.

The role of focal infections in the pathogenesis of psoriasis and chronic urticaria

It is suggested that patients with chronic urticaria have a higher tendency to develop autoantibodies [ 17 ]. Focal bacterial, viral, parasite infections may play the key role in autoimmunity. In the differential diagnosis of the chronic urticaria, disorders that should be taken into consideration are complement-mediated disorders, malignancies, cutaneous or systemic mastocytosis, connective tissue diseases such as systemic lupus erythematosus, cutaneous blistering disorders e.

Focal infection

The pathogenesis of chronic urticaria has not been fully described yet. The most popular theories include: Autoimmune theory claims that autoantibodies and serum factor present in blood cause release of histamine from skin mast cells and basophiles.

The other theory is supported by the fact that some patients with chronic idiopathic urticaria demonstrate excessive production of platelet-derived clotting factors. This could support the theory that there are histamine releasing factors in the plasma.

Focal infection

The cellular defects theory claims that patients with urticaria have mast cell defects in signaling, trafficking, function [ 19 — 23 ]. Psoriasis Psoriasis is a common and chronic inflammatory skin disease with an incidence of 2. Psoriasis has high potential to reduce the quality of life of the patient. Patients with psoriasis reported reduction in physical functioning and mental functioning comparable to patients with cancer, arthritis, heart disease, hypertension, diabetes and depression [ 26 ].

Psoriasis is characterized by the presence of thick, red skin with flaky, silver-white patches scales derived from excessive growth of skin epithelial cells. In psoriasis we distinguish the following types: Psoriasis is characterized by flare-ups and remissions. Main factors triggering psoriasis are: High prevalence of obesity has been reported in patients with psoriasis [ 32 ]. In differential diagnosis of psoriasis, the following diseases should be considered: Psoriasis is an autoimmune disease focal infection the source of the pathology a great role of genetic and environmental factors in its pathogenesis [ 34 ].

Factors playing a key role in the pathogenesis of psoriasis are: The main hypothesis assumes that the disease starts with the activation of the T cell by an unknown antigen and subsequent secretion of the cytokines by activated T cells, inflammatory cells and keratinocytes.

The T cells may become antigen-specific memory cells and may react with keratin cross-reaction, molecular mimicry. There are many studies supporting the role of genetic factors in the pathogenesis of psoriasis.

The role of focal infections in the pathogenesis of psoriasis has been described for decades [ 3637 ]. There are single case reports of remission of skin changes after tonsillectomy [ 38 — 44 ]. Focus of infection as the cause of systemic response The Focal Infection Theory, with its simplicity, has been the point of interest to scientists for decades. The first description of focal infection influencing the whole organism was the cure of the arthritis in a patient after tooth extraction, reported by Hippocrates.

The physician Frank Billings presented the theory in the form of case reports. For the first time, he showed the role of tonsillectomy and dental extractions in the cure of systemic diseases [ 4142 ]. The theory's golden years were the twenties, when a large number of diseases were treated with management of the focal infection [ 43 ]. A systemic response may be caused by dissemination of microorganisms from the focus. The possible role of foci in the pathogenesis of systemic diseases has been attributed to inflammatory processes such as: More recent studies mention among diseases caused by microorganisms from focus of infection: Infections are one of the most common preventable causes of cancer [ 50 ].

Autoimmunity occurs when the immune system of the host recognizes focal infection the source of the pathology attacks its own tissues. There are many factors responsible for the autoimmune response, such as genetics, age and environment. Environmental factors triggering the development of the immune system response include bacterial and viral infections [ 51 ].

Serum of the patients with the positive result of the autologous serum skin test had significantly increased histamine release compared with skin test-negative chronic urticaria sera, as well as higher induction of basophile CD63 surface expression and sulfidoleukotriene production. Additionally, incubation with chloroquine, dapsone, and lidocaine caused reduction in the histamine release, CD63 expression, and sulfidoleukotriene production [ 57 ].

As a part of the Focal Infection Theory, host infection by the pathogen virus, bacteria leads to autoimmunity. If the pathogen carries amino acids similar focal infection the source of the pathology the self-antigen, lymphocytes T or B are activated due to cross-reaction and lead to the damage and activation of the other parts of the immune system.

Persisting pathogens stimulate the immune response and the lysis process, which leads to release in antigens. Antigens from the damaged tissues interact with antigen-presenting cells APC and cause self-specific immune response. Several pathogens have been described in the chronic urticaria, but only in Helicobacter pylori, streptococcal, staphylococcal and Yersinia infections those mechanisms have been proved [ 5859 ].

A streptococcal infection is an example of molecular mimicry between hemolytic streptococcus group A antigens and proteins of the host. This leads to both humoral and cell-mediated autoimmune reactions and clinical consequences of rheumatic fever and heart disease [ 60 ].

The majority of the studies emphasize the role of Helicobacter pylori as the exacerbating factor of the chronic urticaria. The prevalence of Helicobacter pylori is higher when an additional thyroid autoimmunity process occurs [ 61 ].

Eradication of Helicobacter pylori causes often remission of chronic urticaria. Studies show that the remission rate is 61. Treatment with quinolones led in some cases to remission of urticaria [ 62 ]. Norovirus is a viral cause of urticaria [ 63 ]. Infections of oropharynx Several studies show an increased incidence of tonsillitis, sinusitis and dental infections among patients with chronic urticaria. Ten percent of the patients had anti staphylolysin antibodies [ 57 ]. There have been single cases of the recurrence of chronic urticaria after antibiotic treatment [ 57 ].

  • Treatment of infection foci may play the key role in the remission of skin changes;
  • Serum of the patients with the positive result of the autologous serum skin test had significantly increased histamine release compared with skin test-negative chronic urticaria sera, as well as higher induction of basophile CD63 surface expression and sulfidoleukotriene production;
  • Norovirus is a viral cause of urticaria [ 63 ];
  • Skin lesions in urticaria are well-circumscribed, raised above the surface of the skin, pale in the middle, with a smooth surface and extreme purities;
  • There are several theories trying to explain the pathogenesis of urticaria.

Aim There are discordant opinions about the role of focal infections in the pathogenesis of psoriasis and urticaria. The aim of the study was to establish whether there is a higher incidence of focal infections in patients with chronic urticaria and psoriasis. We collected the following data: We examined 101 patients with psoriasis: The median age of the patients was 47. Psoriasis men and women The medium age of patients with psoriasis was 48.

Seventy-seven patients had plaque psoriasis, 16 presented with psoriatic arthritis, 4 with pustular psoriasis and 4 with psoriatic erythroderma. In different types of psoriasis, the percentage of women and men was as follows: