• Dan Hansen

What is psoriatic arthritis and what causes it? Let's find out!

Updated: Mar 28, 2021

Psoriatic arthritis (PsA)

PsA is an autoimmune disease (AID) that affects joints, soft and connective tissues, and organs. However, arthropathy manifesting as pain, stiffness, redness, swelling, and deformity of the joints is the most common and typically associated manifestation of this disease. What causes this type of disease? Why does this happen? Many AIDs are conditions of chronic (long-term) inflammation that, like PsA typically result in tissue and/or organ damage [1,2,3,4].

Antecedents, Mediators, Triggers (ATMs)

ATMs are factors or agents that are component or integral in the development and continued state of AID. In this way, ATMs can act as initiating or triggering events that when unaddressed continue to perpetuate, exacerbate, and sustain a state of dysfunction. In short, ATMs describe the pathogenesis of disease, or the manner in which disease develops, as well as factors that sustain the disease state.

PSA and Underlying Mechanisms

In PsA, the initiating event/s, exacerbating a state of chronic inflammation can range from genetic, to immunologic, to environmental. For example, bacterial or viral infection, environmental toxins, food hypersensitivity, gut dysbiosis and/or intestinal permeability, obesity, depression, and even chronic stress can function as ATMs. Moreover, genetic predisposition or antecedent factors (e.g. family history) does appear to play a key role in disease expression [5,6,7].

Regardless the wide range of possible ATMs in PsA, culmination of this disease is a result of immune dysfunction. That is, the immune system (IS) is not responding appropriately to ATM stimulus. More specifically the immune system is over-reacting to these stimuli. Why? The IS has a very specific job; to be in charge of deciding whether certain ATMs are friend or foe, whether they will cause harm or if they are harmless. However, in the case of AID, the IS can misidentify certain "friendly" agents as "unfriendly", thereby over-reacting and perpetuating a systemic state of inflammation and often leading to dysfunction. Using food hypersensitivity as an example to explain how the IS can go awry, upon ingestion of food (1) specialized cells called dendritic cells (DCs) and macrophages (m0s) will "sample" food particles from the foods we ingest. At this microscopic, cellular level, these sampled food particles are considered antigens; molecules the immune system must now make a decision upon. (2) DCs and M0s will now present these antigens to specialized immune cells called T cells (TCs). Normally, the TC will not respond any further, effectively giving this food antigen a "pass". However, in autoimmunity (AI), TCs can be autoreactive. This simply means that they are cells that have the capacity to react against self. When this is the case, and a DC or m0 presents food antigen to an autoreactive cell (3) the TC can misidentify the antigen as "unfriendly" and begin an IS chain-reaction. This can trigger two possible conditions. (a) The bystander effect and/ or (b) molecular mimicry. (4) TCs will now begin secreting chemicals, called cytokines, meant to address and destroy the identified "unfriendly" antigen. (5) These cytokines can also activate (a) another type of IS cell called a B cell (BC), as well as other types of TCs call CD8 or cytotoxic/ killer TCs. (6) BCs, once activated against an antigen begin to secrete their own products called immunoglobulins or antibodies. In this case, BCs will secrete immunoglobulin G, or IgG. (7) IgG will bind to these food antigens and attract more m0s. (8) M0s will now seek out to engulf (effectively destroy) anything that has been "tagged" by IgG. (9) The aforementioned CD8 cytotoxic TCs are also out to now destroy anything that "looks" like the antigen that has been identified as "foe". In the case of AID, this triggering food antigen can resemble self-tissues. That is to say, bodily tissues (proteins) can "look" like the tagged food antigen. In this case, CD8 TCs will not only (a) attack the food antigen, but also (b) any self-tissue that resembles said antigen. This is, as mentioned above, molecular mimicry. The bottom line TC involvement is a major driver in the state of AID. In other words, activated TCs are understood as a mechanism driving inflammatory AID conditions. The result of activated TCs, BCs, and their immunoglobulin and cytokine products is the associated symptoms of PsA: pain, stiffness, redness, swelling, and joint and tissue damage and deformity [1,2,3,4].

Diagnosis and Differential

Although there are currently no definitive tests, there are a number of diagnostic criteria used to confirm PsA. One such tool is known as the Classification of Psoriatic Arthritis (CASPAR) criteria [8]. PsA is confirmed when three of five possible CASPAR criteria are present: (1) confirmed skin psoriasis (PsO), (2) Psoriatic nail dystrophy, (3) Dactylitis (severe inflammation of the finger and toe joints), (4) Negative test result for presence of rheumatoid factor, a diagnostic criteria of exclusion; ruling out the possibility of rheumatoid arthritis (RA), (5) Radiographic evidence (x-Ray evidence of joint destruction).

Laboratory Testing

Considering the aforementioned range of ATM contributors, and given that PsA is an AID of chronic inflammation, assessing for the presence of inflammatory markers as well as potential infection can be used to further confirm the presence of disease. This type of testing typically involves blood and urine samples analyzed (screened) to identify specific types of compounds that suggest there is a state of inflammation and, or infection. The following lab testing can be used to this end. (1) Complete blood count/ differential and platelet count, looking at blood cells, their expected number and value can be used to identify infection and other contributing issues, (2) Blood urea nitrogen, creatinine, uric acid, and a urinalysis used to assess inflammation and kidney function, (3) Erythrocyte sedimentation rate (ESR), and CRP used to assess inflammation, (4) Rheumatoid factor (RF), anti-cyclic citrullinated peptide (anti-CCP) antibody, and anti-mutated citrullinated vimentin (anti-MCVs). As stated above these are a criterion of exclusion and inclusion with anti-MCVs shown to be significantly higher in PsA and PsO to controls [9], (4) HLA-B27 testing. Associations of PsO and the presence of Human leukocyte antigen B27 (HLA-B27) in blood serum can be used to further confirm genetic predisposition [10].

Nutritional therapy

In an attempt to restore balance to an overactive TC involvement, it would be necessary to (a) remove problematic ATMs, (b) provide support to assist with the aforementioned restoration and rebalance, and (c) help to repair damage. To achieve these goals, and aligned with the example of food hypersensitivity described early, the first step would be to remove problematic foods while simultaneously providing nutritive and anti-inflammatory whole foods to help reduce inflammation, restore balance, and repair damage. Therefore, adherence to nutritional interventions that prioritize elimination of inflammatory foods while promoting high intakes of nutrient-dense, anti-inflammatory foods would be the foundational component of a multi-layered strategy to address PsA.

- Dan Hansen​ Mission Healing Engage​ © 2021

For further discussion on these topics


1. Cai, Y., Fleming, C., & Yan, J. (2012). New insights of T cells in the pathogenesis of psoriasis. Cellular & molecular immunology, 9(4), 302–309. Retrieved from

2. Merola, J. F., Espinoza, L. R., & Fleischmann, R. (2018). Distinguishing rheumatoid arthritis from psoriatic arthritis. RMD Open, 4(2), e000656. Retrieved from

3. Mc Ardle, A., Flatley, B., Pennington, S. R., & FitzGerald, O. (2015). Early biomarkers of joint damage in rheumatoid and psoriatic arthritis. Arthritis Research & Therapy, 17, 141. Retrieved from

4. Veale, D. J., Ritchlin, C., & FitzGerald, O. (2005, March 1). Immunopathology of psoriasis and psoriatic arthritis. Annals of the Rheumatic Diseases, 64(3), 26. Retrieved from

5. Ogdie, A., & Gelfand, J. M. (2015). Clinical Risk Factors for the Development of Psoriatic Arthritis Among Patients with Psoriasis: A Review of Available Evidence. Current rheumatology reports, 17(10), 64. Retrieved from

6. Lewinson, R. T., Vallerand, I. A., Lowerison, M. W., Parsons, L. M., Frolkis, A. D., Kaplan, G. G., Bulloch, A. G. M., Swain, M. G., Patten, S. B., & Barnabe, C. (2017). Depression Is Associated with an Increased Risk of Psoriatic Arthritis among Patients with Psoriasis: A Population-Based Study. Journal of Investigative Dermatology, 137(4), 828–835. Retrieved from

7. Xie, W., Huang, H., Deng, X., Gao, D., & Zhang, Z. (2021). Modifiable lifestyle and environmental factors associated with onset of psoriatic arthritis in patients with psoriasis: A systematic review and meta-analysis of observational studies. Journal of the American Academy of Dermatology, 84(3), 701–711. Retrieved from

8. Taylor, W., Gladman, D., Helliwell, P., Marchesoni, A., Mease, P., Mielants, H., & CASPAR Study Group (2006). Classification criteria for psoriatic arthritis: development of new criteria from a large international study. Arthritis and rheumatism, 54(8), 2665–2673. Retrieved from

9. Dalmády, S., Kiss, M., Képíró, L., Kovács, L., Sonkodi, G., Kemény, L., & Gyulai, R. (2013). Higher levels of autoantibodies targeting mutated citrullinated vimentin in patients with psoriatic arthritis than in patients with psoriasis vulgaris. Clinical & Developmental Immunology, 2013, 474028. Retrieved from

10. Ruiz, D. G., Azevedo, M. N., & Lupi, O. (2012). HLA-B27 frequency in a group of patients with psoriatic arthritis. Anais brasileiros de dermatologia, 87(6), 847–850. Retrieved from

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