Introduction
The two chronic autoimmune diseases, psoriasis and psoriatic arthritis afflict people worldwide, are closely connected, and frequently coexist. While psoriatic arthritis causes severe joint inflammation and red, scaly patches on the skin, which can cause stiffness and decreased mobility, psoriasis primarily affects the joints.
According to studies, despite having different symptoms, there is a significant overlap between the two conditions. Psoriatic arthritis affects many people with psoriasis, highlighting the significance of early diagnosis and treatment to avoid future complications. It is still possible to enhance therapies and the quality of life for those who suffer from these related diseases because of ongoing research into the underlying mechanisms that link both conditions.
What Is Psoriasis?
A chronically inflamed and proliferative skin disease is referred to as psoriasis (PsO). Its defining features are erythematous plaques with silvery scales, especially on the scalp and lumbosacral region. Psoriasis has no known treatment, and flare-ups cause the condition to wax and wane. Since the quality of life of people with psoriasis is so terrible, many psoriasis patients experience depression. Psoriasis has various forms, but plaque is the most prevalent and affects the scalp, extremities, and trunk.
The plaques typically have white, silvery scales that can be seen under a microscope. In psoriasis, activated T lymphocytes infiltrate the skin and encourage the growth of keratinocytes (the most prominent cells in the top layer of the skin). Thick plaques are produced as a result of the imbalance in keratinocyte turnover. Emollients and moisturizers may aid in enhancing barrier performance and maintaining moisture. Dithranol, corticosteroids, vitamin D analogs, and retinoids are initially utilized as topical agents. Methotrexate and Cyclosporine can be administered to patients who do not respond to the therapy above. Change to biological therapies and, in certain situations, a healthcare provider may combine them with methotrexate when patients don't respond to methotrexate.
What Is Psoriatic Arthritis?
Chronic inflammatory arthritis, known as psoriatic arthritis (PsA), is connected to psoriasis. Psoriatic arthritis has an etiology and pathogenesis that are complicated interactions of genetic and environmental variables that lead to immune-mediated inflammation of the skin, joints, and other organs. Patients are more likely to develop psoriatic arthritis and psoriasis due to several hereditary risk factors. In these patients, a persistent inflammatory process mainly affecting the joints and skin is set off by an environmental trigger like an infection or mechanical stress, which leads to the creation of IL-23, a key cytokine in the pathogenesis of psoriatic arthritis and psoriasis. Most patients develop psoriasis years before being diagnosed with psoriatic arthritis. However, for some people, joint problems begin either at the same time or earlier than skin patches. Joint pain, stiffness, and edema are the primary symptoms and warning signs of psoriatic arthritis. They can range from minor to severe, affecting any body area, including the fingertips and spine. Disease flare-ups and remissions can occur in both psoriasis and psoriatic arthritis. Psoriatic arthritis has no known treatment option. Treatment aims to control symptoms and prevent joint degeneration. Psoriatic arthritis without therapy can be incapacitating.
What Is the Relationship Between Psoriasis and Psoriatic Arthritis?
Psoriasis is frequently detected before arthritis in patients. Psoriatic skin and PsA joints' chronic inflammatory processes share many immunopathological characteristics.
CD8+T Cells
According to research, CD8+ T cells are the first to populate a skin lesion as it develops. Lymphocyte-specific therapy causes a decrease in CD8+ T cells in the epidermis, which is correlated with clinical improvement. In PsA synovial fluid, CD8+ T cells predominate, which may indicate that these cells are in charge of the immunological response in the joint. T cells initially attach to active endothelium cells (cells in the inner layer of blood vessels) via cell adhesion molecules expressed on their surface before entering the joint. Intercellular adhesion molecule-1 (ICAM-1) and vascular adhesion molecule-1 (VCAM-1) are markedly upregulated in the skin and synovial membrane.
Vascular Changes
Psoriasis and PsA both feature angiogenesis as a prominent early event. Immature vessels are suggested by elongated and tortuous vessels in the skin and joints, which indicate dysregulated angiogenesis. Psoriasis is substantially associated with an increase in angiogenic growth factors, such as transforming growth factor (TGF), platelet-derived growth factor (PDGF), and vascular endothelial growth factor (VEGF). Early PsA also has been reported to have high amounts of VEGF and TGF in the joint fluid. Moreover, angiopoietin expression is increased in perivascular areas of skin with lesional psoriasis.
Tumor Necrosis Factor (TNF)
An essential proinflammatory cytokine that can cause inflammation is TNF. T cells can accomplish the entire inflammatory mechanism either directly or indirectly by signaling the hyperproliferation of keratinocytes by releasing a variety of chemokines and cytokines, including TNF. TNF levels are higher in psoriatic skin lesions, and studies have demonstrated that TNF increases the expression of ICAM-1 on endothelial and keratinocyte cells, which is crucial for cellular adhesion and trafficking. Thus, TNF influences psoriasis's etiology by boosting T cell infiltration, activating T lymphocytes, and keratinocyte proliferation in psoriatic plaques. Also, TNF and other proinflammatory cytokines were expressed at higher levels in the synovial tissue PsA patients than in the normal synovium.
Bone Remodelling
The dynamic interaction between osteoclasts and osteoblasts, an essential process in bone development, maintenance, and repair, controls skeletal remodeling. Osteoblasts (bone-forming cells) develop from mesenchymal lineage and form bone matrix, while osteoclasts (bone-degrading cells) descend from naive B cells, which resorb bone. The delicate balance between bone formation and resorption may become out of whack in pathological situations, leading to excessive bone resorption (osteolysis), new bone deposition, or both. PsA joint radiographs prove that many people have profoundly dysregulated bone remodeling. Additionally, the frequency of precursors to osteoclasts considerably decreased when PsA patients were treated with anti-TNF medications as soon as two weeks into the course of the medication. Consequently, a hypothesis is developing that high levels of TNF, presumably brought on by occurrences in the skin, result in a rise in the frequency of circulating osteoclast precursors.
How Is Psoriatic Arthritis Treated?
The PsA therapies also help with psoriasis. The most vital data to date are supporting TNF-blockers' ability to prevent heart attacks. A medication in that class would be the first line of treatment for those with heart problems. A TNF-blocker would not, however, likely be the first option for a patient with skin cancer because a side effect is an increased chance of squamous cells. Additionally, they indicated that Certolizumab Pegol, a medication that does not contaminate breast milk and does not cross the placenta, may be advantageous for pregnant PsA patients.
Conclusion
It is clear that there is a complicated link between psoriatic arthritis and psoriasis. To promote early intervention and prevent irreparable joint damage, people with psoriasis should be on the lookout for indications of psoriatic arthritis, given that both disorders have similar autoimmune origins. Unraveling the complex mechanisms behind these illnesses will ultimately lead to more potent therapy approaches. Therefore collaboration between medical practitioners and researchers is essential to improve the lives of persons dealing with these connected illnesses by raising awareness, improving research, and offering comprehensive care, giving them hope for a better future.
