Overview of Spondyloarthropathies: Difference between revisions

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== Epidemiology / Aetiology ==
== Epidemiology / Aetiology ==
Symptoms associated with spondyloarthropathy typically start before the age of 45.<ref name=":0" /> They affect men and women almost equally, with a 1.1:1 (male:female) ratio although men tend to be younger at diagnosis than women.<ref name=":0" /><ref>Alzate M, Vargas F, Ramirez F, et alSAT0414 Differences in clinical presentation by gender in colombian patients with spondyloarthropathies. Annals of the Rheumatic Diseases 2017;76(2): 928.</ref> With a prevalence rate of 0.5-1.9 percent, they are one of the most common rheumatic diseases - as common as [[Rheumatoid Arthritis|rheumatoid arthritis]].<ref>Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J. How to diagnose axial spondyloarthritis early. Annals of the Rheumatic Diseases. 2004; 63: 535-543.</ref> However, unlike other rheumatic diseases, spondyloarthropathies are seronegative for rheumatoid factor.<ref>Navallas M, Ares J, Beltrán B, Lisbona MP, Maymó J, Solano A. Sacroiliitis associated with axial spondyloarthropathy: new concepts and latest trends. Radiographics. 2013 Jul-Aug;33(4):933-56.</ref>
Symptoms associated with spondyloarthropathy typically start before the age of 45.<ref name=":0" /> They affect men and women almost equally, with a 1.1:1 (male: female) ratio although men tend to be younger at diagnosis than women.<ref name=":0" /><ref>Alzate M, Vargas F, Ramirez F, et al. SAT0414 Differences in a clinical presentation by gender in Colombian patients with spondyloarthropathies. Annals of the Rheumatic Diseases 2017;76(2): 928.</ref> With a prevalence rate of 0.5-1.9 per cent, they are one of the most common rheumatic diseases - as common as [[Rheumatoid Arthritis|rheumatoid arthritis]].<ref>Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J. How to diagnose axial spondyloarthritis early. Annals of the Rheumatic Diseases. 2004; 63: 535-543.</ref> However, unlike other rheumatic diseases, spondyloarthropathies are seronegative for rheumatoid factors.<ref>Navallas M, Ares J, Beltrán B, Lisbona MP, Maymó J, Solano A. Sacroiliitis associated with axial spondyloarthropathy: new concepts and latest trends. Radiographics. 2013 Jul-Aug;33(4):933-56.</ref>


The aetiology and pathogenesis of spondyloarthropathies are complex and not fully understood. There is an initial systemic inflammatory response to a known or unknown source, which causes local tissue changes. These changes can be long-lasting in the local joint environment and the persistent inflammation causes a cycle of unbalanced bone remodelling and axial [[bone]] loss.<ref name=":10">Lassiter W, Allam AE. Inflammatory Back Pain. [Updated 2020 Jun 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK539753/</nowiki></ref>
The aetiology and pathogenesis of spondyloarthropathies are complex and not fully understood. An initial systemic inflammatory response to a known or unknown source causes local tissue changes. These changes can be long-lasting in the local joint environment, and the persistent inflammation causes a cycle of unbalanced bone remodelling and axial [[bone]] loss.<ref name=":10">Lassiter W, Allam AE. Inflammatory Back Pain. [Updated 2020 Jun 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK539753/</nowiki></ref>


While the cause of spondyloarthropathy is not known, research suggests that there are environmental and genetic triggers.<ref name=":1" /> In particular, spondyloarthropathies have been found to share genetic links with the HLA-B27 gene.<ref name=":0" /><ref>Braun, J., Sieper, J. Early diagnosis of spondyloarthritis. ''Nat Rev Rheumatol.'' 2006; 2: 536-45.</ref> 90 percent of patients presenting with axial spondyloarthritis have this gene. However, having this gene is not, in itself, diagnostic of spondyloarthropathy as five to ten percent of patients who carry the HLA-B27 gene do not go on to develop these conditions.<ref name=":0" />
While the cause of spondyloarthropathy is not known, research suggests that there are environmental and genetic triggers.<ref name=":1" /> In particular, spondyloarthropathies have been found to share genetic links with the HLA-B27 gene.<ref name=":0" /><ref>Braun, J., Sieper, J. Early diagnosis of spondyloarthritis. ''Nat Rev Rheumatol.'' 2006; 2: 536-45.</ref> 90 per cent of patients with axial spondyloarthritis have this gene. However, having this gene is not, in itself, diagnostic of spondyloarthropathy, as five to ten per cent of patients who carry the HLA-B27 gene do not go on to develop these conditions.<ref name=":0" />


{{#ev:youtube|https://www.youtube.com/watch?v=1Fgi7whO7NQ|width}}<ref>USME Spondyloarthropathy Available from: https://www.youtube.com/watch?v=1Fgi7whO7NQ (last accessed 8.11.2020) </ref>  
{{#ev:youtube|https://www.youtube.com/watch?v=1Fgi7whO7NQ|width}}<ref>USME Spondyloarthropathy Available from: https://www.youtube.com/watch?v=1Fgi7whO7NQ (last accessed 8.11.2020) </ref>  


== Characteristics / Clinical Presentation ==
== Characteristics / Clinical Presentation ==
[[Low Back Pain|Back pain]] is extremely prevalent. <ref name=":4">Poddubnyy D. [https://academic.oup.com/rheumatology/article/59/Supplement_4/iv6/5923432 Classification vs diagnostic criteria: the challenge of diagnosing axial spondyloarthritis]. Rheumatology. 2020 Oct;59(Supplement_4):iv6-17.</ref> The occurrence of back pain lasting for three months or longer and back pain onset before 45 years of age is a starting point for the diagnosis of spondyloarthritis.<ref name=":4" /> It is important to be able to differentiate between different types of back pain ([[Differentiating Inflammatory and Mechanical Back Pain|i.e. mechanical or inflammatory]]), and the different types of spondyloarthropathy. The specific features of each type of spondyloarthropathy are discussed below.
[[Low Back Pain|Back pain]] is extremely prevalent. <ref name=":4">Poddubnyy D. [https://academic.oup.com/rheumatology/article/59/Supplement_4/iv6/5923432 Classification vs diagnostic criteria: the challenge of diagnosing axial spondyloarthritis]. Rheumatology. 2020 Oct;59(Supplement_4):iv6-17.</ref> The occurrence of back pain lasting for three months or longer and back pain onset before 45 years of age is a starting point for the diagnosis of spondyloarthritis.<ref name=":4" /> It is important to be able to differentiate between different types of back pain ([[Differentiating Inflammatory and Mechanical Back Pain|, i.e. mechanical or inflammatory]]), and the different types of spondyloarthropathy. The specific features of each type of spondyloarthropathy are discussed below.


== Axial Spondyloarthritis ==
== Axial Spondyloarthritis ==
Axial spondyloarthritis refers to patients who have both non-radiographic and radiographic axial spondyloarthritis. Radiographic axial spondyloarthritis is also called [[Ankylosing Spondylitis (Axial Spondyloarthritis)|ankylosing spondylitis]].<ref name=":3">Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017 Jul 1;390(10089):73-84. </ref> While non-radiographic axial spondyloarthritis does not show on x-ray, there are changes on MRI.<ref name=":0" />
Axial spondyloarthritis refers to patients who have both non-radiographic and radiographic axial spondyloarthritis. Radiographic axial spondyloarthritis is also called [[Ankylosing Spondylitis (Axial Spondyloarthritis)|ankylosing spondylitis]].<ref name=":3">Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017 Jul 1;390(10089):73-84. </ref> While non-radiographic axial spondyloarthritis does not show on x-ray, there are changes on MRI.<ref name=":0" />


Axial spondyloarthritis tends to start when patients are aged in their 20s. There is a male to female ratio of 2:1 for radiographic axial spondyloarthritis and of 1:1 for non-radiographic axial spondyloarthritis.<ref name=":3" />
Axial spondyloarthritis tends to start when patients are aged in their 20s. There is a male-to-female ratio of 2:1 for radiographic axial spondyloarthritis and 1:1 for non-radiographic axial spondyloarthritis.<ref name=":3" />


Axial spondyloarthritis predominantly affects the spine, with inflammatory changes causing pain, stiffness and a loss of motion in the back.<ref name=":0" /><ref name=":2">Wenker KJ, Quint JM. Ankylosing Spondylitis. [Updated 2022 Apr 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK470173/</nowiki></ref> Patients will often present with impaired spinal movement, abnormal [[posture]], buttock and hip pain, peripheral arthritis, enthesitis and dactylitis.<ref name=":2" />  
Axial spondyloarthritis predominantly affects the spine, with inflammatory changes causing pain, stiffness and a loss of motion in the back.<ref name=":0" /><ref name=":2">Wenker KJ, Quint JM. Ankylosing Spondylitis. [Updated 2022 Apr 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: <nowiki>https://www.ncbi.nlm.nih.gov/books/NBK470173/</nowiki></ref> Patients will often present with impaired spinal movement, abnormal [[posture]], buttock and hip pain, peripheral arthritis, enthesitis and dactylitis.<ref name=":2" />  
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{{#ev:youtube|iN2EiKKKJss}}<ref>Novartis. More than just back pain, what is Axial Spondyloarthritis (axSpA)? Available from: https://www.youtube.com/watch?v=iN2EiKKKJss [last accessed 9/11/2020]</ref>   
{{#ev:youtube|iN2EiKKKJss}}<ref>Novartis. More than just back pain, what is Axial Spondyloarthritis (axSpA)? Available from: https://www.youtube.com/watch?v=iN2EiKKKJss [last accessed 9/11/2020]</ref>   


It has been estimated that axial spondyloarthritis has 90 percent heritability, with the HLA-B27 gene being the most significant genetic factor.<ref name=":3" /><ref name=":2" /><ref>Ebrahimiadib N, Berijani S, Ghahari M, Pahlaviani FG. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358754/pdf/jovr-16-462.pdf Ankylosing Spondylitis]. J Ophthalmic Vis Res. 2021 Jul 29;16(3):462-469.</ref> The actual role of HLA-B27 in the pathogenesis of axial spondyloarthritis remains unclear, but evidence suggests that the [[cytokines]], tumour necrosis factor (TNF)-α and interleukin-17 are involved.<ref name=":3" />
It has been estimated that axial spondyloarthritis has 90 per cent heritability, with the HLA-B27 gene being the most significant genetic factor.<ref name=":3" /><ref name=":2" /><ref>Ebrahimiadib N, Berijani S, Ghahari M, Pahlaviani FG. [https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8358754/pdf/jovr-16-462.pdf Ankylosing Spondylitis]. J Ophthalmic Vis Res. 2021 Jul 29;16(3):462-469.</ref> The actual role of HLA-B27 in the pathogenesis of axial spondyloarthritis remains unclear, but evidence suggests that the [[cytokines]], tumour necrosis factor (TNF)-α and interleukin-17 are involved.<ref name=":3" />


Radiographic axial spondyloarthritis has also been linked to an increased risk of cardiovascular disease, potentially due to the systemic inflammation associated with this condition. Because it results in diminished chest wall expansion and decreased spinal mobility, it can lead to a restrictive pulmonary pattern in individuals with this condition. These individuals are also more prone to vertebral [[Insufficiency Fracture|fragility fractures]], [[Atlantoaxial Osteoarthritis|atlantoaxial]] subluxation, [[Spinal Cord Injury|spinal cord injury]] and, occasionally, [[Cauda Equina Syndrome|cauda equina syndrome]].<ref name=":2" />
Radiographic axial spondyloarthritis has also been linked to an increased risk of cardiovascular disease due to the systemic inflammation associated with this condition. Because it results in diminished chest wall expansion and decreased spinal mobility, it can lead to a restrictive pulmonary pattern in individuals with this condition. These individuals are also more prone to vertebral [[Insufficiency Fracture|fragility fractures]], [[Atlantoaxial Osteoarthritis|atlantoaxial]] subluxation, [[Spinal Cord Injury|spinal cord injury]] and, occasionally, [[Cauda Equina Syndrome|cauda equina syndrome]].<ref name=":2" />


{{#ev:youtube|a23A3nAaO0E}}<ref>Zero To Finals. Ankylosing Spondylitis: Visual Explanation for Students. Available from https://www.youtube.com/watch?v=a23A3nAaO0E [last accessed: 8/11/2020]</ref>
{{#ev:youtube|a23A3nAaO0E}}<ref>Zero To Finals. Ankylosing Spondylitis: Visual Explanation for Students. Available from https://www.youtube.com/watch?v=a23A3nAaO0E [last accessed: 8/11/2020]</ref>
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== Psoriatic Arthritis ==
== Psoriatic Arthritis ==
Psoriatic Arthritis (PsA) is a chronic, immune-mediated inflammatory joint disease that is associated with psoriasis.<ref name=":5">Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2018; 391(10136): 2273-2284. </ref> Individuals present with joint and entheses inflammation in both the axial skeleton and peripheral joints. It affects multiple organs, including the skin and is associated with increased risk of mortality from cardiovascular disease.<ref name=":5" /><ref>Van den Bosch F, Coates L. Clinical management of psoriatic arthritis. Lancet. 2018; 391(10136): 2285-2294.</ref>  
Psoriatic Arthritis (PsA) is a chronic, immune-mediated inflammatory joint disease associated with psoriasis.<ref name=":5">Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2018; 391(10136): 2273-2284. </ref> Individuals present with joint and entheses inflammation in both the axial skeleton and peripheral joints. It affects multiple organs, including the skin and is associated with an increased risk of mortality from cardiovascular disease.<ref name=":5" /><ref>Van den Bosch F, Coates L. Clinical management of psoriatic arthritis. Lancet. 2018; 391(10136): 2285-2294.</ref>  


There is a wide variation in the annual incidence of PsA, ranging from 0.1 to 23.1 cases per 100,000. Prevalence rates also vary between countries, as does the mean age at diagnosis (40.7 to 52.0 years).<ref name=":6">Kerschbaumer A, Fenzl KH, Erlacher L, Aletaha D. An overview of psoriatic arthritis - epidemiology, clinical features, pathophysiology and novel treatment targets. Wien Klin Wochenschr. 2016; 128(21-22): 791-795.</ref>
There is a wide variation in the annual incidence of PsA, ranging from 0.1 to 23.1 cases per 100,000. Prevalence rates also vary between countries, as does the mean age at diagnosis (40.7 to 52.0 years).<ref name=":6">Kerschbaumer A, Fenzl KH, Erlacher L, Aletaha D. An overview of psoriatic arthritis - epidemiology, clinical features, pathophysiology and novel treatment targets. Wien Klin Wochenschr. 2016; 128(21-22): 791-795.</ref>
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* Inflammatory arthritis
* Inflammatory arthritis
* Absence of [[Blood Tests|serological tests]] for rheumatoid arthritis
* Absence of [[Blood Tests|serological tests]] for rheumatoid arthritis
Between 60 and 70 percent of patients will develop psoriasis prior to PsA. However, in 15 to 20 percent of patients, symptoms of arthritis develop first. For 15 to 20 percent of individuals, psoriasis and arthritis will begin within a year of each other.<ref name=":6" />
Between 60 and 70 per cent of patients will develop psoriasis before PsA. However, in 15 to 20 per cent of patients, symptoms of arthritis develop first. For 15 to 20 per cent of individuals, psoriasis and arthritis will begin within a year.<ref name=":6" />


For more information on PsA, please [[Psoriatic Arthritis|click here]].  
For more information on PsA, please [[Psoriatic Arthritis|click here]].  
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== Enteropathic Arthritis ==
== Enteropathic Arthritis ==
Enteropathic Arthritis (EnA) is a spondyloarthropathy that occurs in patients who also have [[Irritable Bowel Syndrome|inflammatory bowel disease]] (IBD) and / or other gastrointestinal diseases, such as ulcerative colitis and [[Crohn's Disease|Crohn’s disease]].<ref name=":7">Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment. Clin Dev Immunol. 2013; 2013: 631408. </ref>
Enteropathic Arthritis (EnA) is a spondyloarthropathy that occurs in patients who also have [[Irritable Bowel Syndrome|inflammatory bowel disease]] (IBD) and/or other gastrointestinal diseases, such as ulcerative colitis and [[Crohn's Disease|Crohn’s disease]].<ref name=":7">Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment. Clin Dev Immunol. 2013; 2013: 631408. </ref>


There is no gold standard test for EnA, so diagnosis generally relies on medical history and physical examination.<ref name=":7" /> Typically, patients who have IBD and then go on to develop inflammatory back pain and / or synovitis (predominantly in the lower limbs) are diagnosed as having spondyloarthropathy.<ref name=":7" /> Women are more likely to have peripheral joint involvement, whereas men are more likely to experience axial skeleton symptoms.<ref name=":7" />
There is no gold standard test for EnA, so diagnosis generally relies on medical history and physical examination.<ref name=":7" /> Typically, patients who have IBD and then go on to develop inflammatory back pain and/or synovitis (predominantly in the lower limbs) are diagnosed as having spondyloarthropathy.<ref name=":7" /> Women are more likely to have peripheral joint involvement, whereas men are more likely to experience axial skeleton symptoms.<ref name=":7" />


Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.<ref name=":7" />
Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.<ref name=":7" />


Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 percent, but the pathogenesis is not fully understood.<ref name=":7" /> However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.<ref name=":7" />
Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 per cent, but the pathogenesis is not fully understood.<ref name=":7" /> However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.<ref name=":7" />


For more information on EnA, please [[Enteropathic Spondylitis|click here]].
For more information on EnA, please [[Enteropathic Spondylitis|click here]].
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Reactive arthritis (ReA) is a seronegative spondyloarthropathy, which occurs after an extra-articular [[Infectious Disease|infection]] (usually of the gastrointestinal or [[Urinary Tract Infection|genitourinary tract]]).<ref>Courcoul A, Brinster A, Decullier E, Larbre JP, Piperno M, Pradat E et al. A bicentre retrospective study of features and outcomes of patients with reactive arthritis. Joint Bone Spine. 2018; 85(2): 201-205.</ref><ref name=":8">Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014; 13(4-5): 546-9. </ref> It is associated with inflammatory back pain, oligoarthritis, and extra-articular symptoms.<ref name=":8" /> It tends to develop between one and six weeks after a urogenital or gastrointestinal infection.<ref name=":8" /><ref>Ono K, Kishimoto M, Shimasaki T, Uchida H, Kurai D, Deshpande GA et al. Reactive arthritis after COVID-19 infection. RMD Open 2020; 6: e001350.</ref>
Reactive arthritis (ReA) is a seronegative spondyloarthropathy, which occurs after an extra-articular [[Infectious Disease|infection]] (usually of the gastrointestinal or [[Urinary Tract Infection|genitourinary tract]]).<ref>Courcoul A, Brinster A, Decullier E, Larbre JP, Piperno M, Pradat E et al. A bicentre retrospective study of features and outcomes of patients with reactive arthritis. Joint Bone Spine. 2018; 85(2): 201-205.</ref><ref name=":8">Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014; 13(4-5): 546-9. </ref> It is associated with inflammatory back pain, oligoarthritis, and extra-articular symptoms.<ref name=":8" /> It tends to develop between one and six weeks after a urogenital or gastrointestinal infection.<ref name=":8" /><ref>Ono K, Kishimoto M, Shimasaki T, Uchida H, Kurai D, Deshpande GA et al. Reactive arthritis after COVID-19 infection. RMD Open 2020; 6: e001350.</ref>


A classic triad of symptoms have been identified, which are:<ref name=":9">Wu IB, Schwartz RA. Reiter's syndrome: the classic triad and more. J Am Acad Dermatol. 2008; 59(1): 113-21.</ref>
A classic triad of symptoms has been identified:<ref name=":9">Wu IB, Schwartz RA. Reiter's syndrome: the classic triad and more. J Am Acad Dermatol. 2008; 59(1): 113-21.</ref>
* [[Arthritis]]
* [[Arthritis]]
* Urethritis
* Urethritis
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== Undifferentiated Spondyloarthritis ==
== Undifferentiated Spondyloarthritis ==
The diagnosis of undifferentiated spondyloarthropathy is used in cases where individuals exhibit features of spondyloarthropathy, but they do not fit into any of the conditions discussed above.<ref>Chou CT, Lin KC, Wei JCC, Tsai WC, Ho HH, Hwang CM et al. Study of undifferentiated spondyloarthropathy among first-degree relatives of ankylosing spondylitis probands. Rheumatology. 2005; 44(5): 662-5.</ref> It usually occurs in less than five joints, but generally will include the knee joint.<ref>Hauk L. Spondyloarthritis: NICE Releases Guidelines on Diagnosis and Treatment. Am Fam Physician. 2017; 96(10): 677-678.</ref>  
The diagnosis of undifferentiated spondyloarthropathy is used in cases where individuals exhibit features of spondyloarthropathy but they do not fit into any of the conditions discussed above.<ref>Chou CT, Lin KC, Wei JCC, Tsai WC, Ho HH, Hwang CM et al. Study of undifferentiated spondyloarthropathy among first-degree relatives of ankylosing spondylitis probands. Rheumatology. 2005; 44(5): 662-5.</ref> It usually occurs in less than five joints but generally will include the knee joint.<ref>Hauk L. Spondyloarthritis: NICE Releases Guidelines on Diagnosis and Treatment. Am Fam Physician. 2017; 96(10): 677-678.</ref>  


== Summary ==
== Summary ==
Spondyloarthropathy is an umbrella term that encompasses five inflammatory rheumatic diseases. These conditions can impact multiple areas of the body, including joints and entheses, as well as other organs.
Spondyloarthropathy is an umbrella term that encompasses five inflammatory rheumatic diseases. These conditions can impact multiple areas of the body, including joints and entheses, as well as other organs.


While the specific aetiology remains unknown, current research suggests a strong [[Genetic Disorders|genetic]] component, as well as specific environmental triggers.
While the specific aetiology remains unknown, current research suggests a strong [[Genetic Disorders|genetic]] component and specific environmental triggers.


== References ==
== References ==

Revision as of 22:54, 25 October 2022

Original Editor - Jess Bell Top Contributors - Jess Bell, Kim Jackson, Ewa Jaraczewska, Tarina van der Stockt and Lucinda hampton

Introduction[edit | edit source]

Spondyloarthropathy (or spondyloarthritis) is an umbrella term for a group of inflammatory rheumatic diseases.[1][2] Spondyloarthropathies are progressive and painful. They often involve the axial skeleton (i.e. the spine and the sacroiliac joints), but they can also affect the peripheral skeleton.[1] They are associated with enthesitis (inflammation of the site where tendons / ligaments insert into bone[3]) and dactylitis (i.e. diffuse swelling of the digits[4]). Other areas affected include the heart, eyes, lungs, skin, gut and genitourinary tract.[2]

There are five types of spondyloarthritis:[1]

Epidemiology / Aetiology[edit | edit source]

Symptoms associated with spondyloarthropathy typically start before the age of 45.[1] They affect men and women almost equally, with a 1.1:1 (male: female) ratio although men tend to be younger at diagnosis than women.[1][8] With a prevalence rate of 0.5-1.9 per cent, they are one of the most common rheumatic diseases - as common as rheumatoid arthritis.[9] However, unlike other rheumatic diseases, spondyloarthropathies are seronegative for rheumatoid factors.[10]

The aetiology and pathogenesis of spondyloarthropathies are complex and not fully understood. An initial systemic inflammatory response to a known or unknown source causes local tissue changes. These changes can be long-lasting in the local joint environment, and the persistent inflammation causes a cycle of unbalanced bone remodelling and axial bone loss.[11]

While the cause of spondyloarthropathy is not known, research suggests that there are environmental and genetic triggers.[2] In particular, spondyloarthropathies have been found to share genetic links with the HLA-B27 gene.[1][12] 90 per cent of patients with axial spondyloarthritis have this gene. However, having this gene is not, in itself, diagnostic of spondyloarthropathy, as five to ten per cent of patients who carry the HLA-B27 gene do not go on to develop these conditions.[1]

[13]

Characteristics / Clinical Presentation[edit | edit source]

Back pain is extremely prevalent. [14] The occurrence of back pain lasting for three months or longer and back pain onset before 45 years of age is a starting point for the diagnosis of spondyloarthritis.[14] It is important to be able to differentiate between different types of back pain (, i.e. mechanical or inflammatory), and the different types of spondyloarthropathy. The specific features of each type of spondyloarthropathy are discussed below.

Axial Spondyloarthritis[edit | edit source]

Axial spondyloarthritis refers to patients who have both non-radiographic and radiographic axial spondyloarthritis. Radiographic axial spondyloarthritis is also called ankylosing spondylitis.[15] While non-radiographic axial spondyloarthritis does not show on x-ray, there are changes on MRI.[1]

Axial spondyloarthritis tends to start when patients are aged in their 20s. There is a male-to-female ratio of 2:1 for radiographic axial spondyloarthritis and 1:1 for non-radiographic axial spondyloarthritis.[15]

Axial spondyloarthritis predominantly affects the spine, with inflammatory changes causing pain, stiffness and a loss of motion in the back.[1][16] Patients will often present with impaired spinal movement, abnormal posture, buttock and hip pain, peripheral arthritis, enthesitis and dactylitis.[16]

[17]

It has been estimated that axial spondyloarthritis has 90 per cent heritability, with the HLA-B27 gene being the most significant genetic factor.[15][16][18] The actual role of HLA-B27 in the pathogenesis of axial spondyloarthritis remains unclear, but evidence suggests that the cytokines, tumour necrosis factor (TNF)-α and interleukin-17 are involved.[15]

Radiographic axial spondyloarthritis has also been linked to an increased risk of cardiovascular disease due to the systemic inflammation associated with this condition. Because it results in diminished chest wall expansion and decreased spinal mobility, it can lead to a restrictive pulmonary pattern in individuals with this condition. These individuals are also more prone to vertebral fragility fractures, atlantoaxial subluxation, spinal cord injury and, occasionally, cauda equina syndrome.[16]

[19]

For more information on axial spondyloarthritis, please click here.

Psoriatic Arthritis[edit | edit source]

Psoriatic Arthritis (PsA) is a chronic, immune-mediated inflammatory joint disease associated with psoriasis.[20] Individuals present with joint and entheses inflammation in both the axial skeleton and peripheral joints. It affects multiple organs, including the skin and is associated with an increased risk of mortality from cardiovascular disease.[20][21]

There is a wide variation in the annual incidence of PsA, ranging from 0.1 to 23.1 cases per 100,000. Prevalence rates also vary between countries, as does the mean age at diagnosis (40.7 to 52.0 years).[22]

Hallmark features of PsA are:[22]

  • The presence of psoriasis
  • Inflammatory arthritis
  • Absence of serological tests for rheumatoid arthritis

Between 60 and 70 per cent of patients will develop psoriasis before PsA. However, in 15 to 20 per cent of patients, symptoms of arthritis develop first. For 15 to 20 per cent of individuals, psoriasis and arthritis will begin within a year.[22]

For more information on PsA, please click here.

[23]

Enteropathic Arthritis[edit | edit source]

Enteropathic Arthritis (EnA) is a spondyloarthropathy that occurs in patients who also have inflammatory bowel disease (IBD) and/or other gastrointestinal diseases, such as ulcerative colitis and Crohn’s disease.[24]

There is no gold standard test for EnA, so diagnosis generally relies on medical history and physical examination.[24] Typically, patients who have IBD and then go on to develop inflammatory back pain and/or synovitis (predominantly in the lower limbs) are diagnosed as having spondyloarthropathy.[24] Women are more likely to have peripheral joint involvement, whereas men are more likely to experience axial skeleton symptoms.[24]

Between 17 and 39 percent of patients with IBD develop rheumatic manifestations. Between two and 16 percent of IBD patients develop EnA in the axial skeleton. The prevalence of sacroiliitis in this population is between 12 and 20 percent of patients.[24]

Like other spondyloarthropathies, there is an association with the HLA-B27 gene, ranging from 3.9 to 18.9 per cent, but the pathogenesis is not fully understood.[24] However, it has been observed that joint inflammation occurs in patients who are genetically predisposed and who have bacterial gut infections. This, therefore, suggests that there is some relationship between inflammation of the gut mucosa and arthritis.[24]

For more information on EnA, please click here.

Reactive Arthritis[edit | edit source]

Reactive arthritis (ReA) is a seronegative spondyloarthropathy, which occurs after an extra-articular infection (usually of the gastrointestinal or genitourinary tract).[25][26] It is associated with inflammatory back pain, oligoarthritis, and extra-articular symptoms.[26] It tends to develop between one and six weeks after a urogenital or gastrointestinal infection.[26][27]

A classic triad of symptoms has been identified:[28]

Dermatological manifestations (such as keratoderma blennorrhagicum, circinate balanitis, ulcerative vulvitis, changes in nails, and oral lesions) can occur.[28] It can also affect the heart and eyes although symptom severity is varied.[26]

ReA is more common in men[28] and typically affects young adults.[26] Its exact pathophysiology is not yet understood, but it appears likely that infectious and immune factors are involved.[28] Again, those affected are more likely to carry the HLA-B27 gene.[26]

[29]

Clinical symptoms can be distinguished from septic arthritis. Key signs of septic arthritis are:[26]

  • Fever
  • Systemic signs of infection
  • Monoarthritis

For more information on ReA, please click here.

Undifferentiated Spondyloarthritis[edit | edit source]

The diagnosis of undifferentiated spondyloarthropathy is used in cases where individuals exhibit features of spondyloarthropathy but they do not fit into any of the conditions discussed above.[30] It usually occurs in less than five joints but generally will include the knee joint.[31]

Summary[edit | edit source]

Spondyloarthropathy is an umbrella term that encompasses five inflammatory rheumatic diseases. These conditions can impact multiple areas of the body, including joints and entheses, as well as other organs.

While the specific aetiology remains unknown, current research suggests a strong genetic component and specific environmental triggers.

References[edit | edit source]

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 1.6 1.7 1.8 Martey C. Overview of Spondyloarthropathies Course. Plus2020.
  2. ↑ 2.0 2.1 2.2 Ehrenfeld M, Infection and spondyloarthropathies. In: Shoenfeld Y, Agmon-Levin N, Rose NR editors. Infection and autoimmunity. Elsevier B.V. 2015. p745-57.
  3. ↑ Schett G, Lories R, D'Agostino M, Elewaut D, Krikham B, Soriano ER et al. Enthesitis: from pathophysiology to treatment. Nat Rev Rheumatol. 2017; 13: 731–741.
  4. ↑ Girolimetto N, Giovannini I, Crepaldi G, De Marco G, Tinazzi I, Possemato N, Macchioni P, McConnell R, McGonagle D, Iagnocco A, Zabotti A. Psoriatic Dactylitis: Current perspectives and new insights in ultrasonography and magnetic resonance imaging. Journal of Clinical Medicine. 2021 Jun 12;10(12):2604.
  5. ↑ Fragoulis GE, Siebert S. Treatment strategies in axial spondyloarthritis: what, when and how?. Rheumatology. 2020 Oct;59(Supplement_4):iv79-89.
  6. ↑ Ogdie A, Coates LC, Gladman DD. Treatment guidelines in psoriatic arthritis. Rheumatology. 2020 Mar 1;59(Supplement_1):i37-46.
  7. ↑ Bentaleb I, Abdelghani KB, Rostom S, Amine B, Laatar A, Bahiri R. Reactive arthritis: update. Current clinical microbiology reports. 2020 Dec;7(4):124-32.
  8. ↑ Alzate M, Vargas F, Ramirez F, et al. SAT0414 Differences in a clinical presentation by gender in Colombian patients with spondyloarthropathies. Annals of the Rheumatic Diseases 2017;76(2): 928.
  9. ↑ Rudwaleit M, van der Heijde D, Khan MA, Braun J, Sieper J. How to diagnose axial spondyloarthritis early. Annals of the Rheumatic Diseases. 2004; 63: 535-543.
  10. ↑ Navallas M, Ares J, Beltrán B, Lisbona MP, Maymó J, Solano A. Sacroiliitis associated with axial spondyloarthropathy: new concepts and latest trends. Radiographics. 2013 Jul-Aug;33(4):933-56.
  11. ↑ Lassiter W, Allam AE. Inflammatory Back Pain. [Updated 2020 Jun 22]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK539753/
  12. ↑ Braun, J., Sieper, J. Early diagnosis of spondyloarthritis. Nat Rev Rheumatol. 2006; 2: 536-45.
  13. ↑ USME Spondyloarthropathy Available from: https://www.youtube.com/watch?v=1Fgi7whO7NQ (last accessed 8.11.2020)
  14. ↑ 14.0 14.1 Poddubnyy D. Classification vs diagnostic criteria: the challenge of diagnosing axial spondyloarthritis. Rheumatology. 2020 Oct;59(Supplement_4):iv6-17.
  15. ↑ 15.0 15.1 15.2 15.3 Sieper J, Poddubnyy D. Axial spondyloarthritis. Lancet. 2017 Jul 1;390(10089):73-84. 
  16. ↑ 16.0 16.1 16.2 16.3 Wenker KJ, Quint JM. Ankylosing Spondylitis. [Updated 2022 Apr 9]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470173/
  17. ↑ Novartis. More than just back pain, what is Axial Spondyloarthritis (axSpA)? Available from: https://www.youtube.com/watch?v=iN2EiKKKJss [last accessed 9/11/2020]
  18. ↑ Ebrahimiadib N, Berijani S, Ghahari M, Pahlaviani FG. Ankylosing Spondylitis. J Ophthalmic Vis Res. 2021 Jul 29;16(3):462-469.
  19. ↑ Zero To Finals. Ankylosing Spondylitis: Visual Explanation for Students. Available from https://www.youtube.com/watch?v=a23A3nAaO0E [last accessed: 8/11/2020]
  20. ↑ 20.0 20.1 Veale DJ, Fearon U. The pathogenesis of psoriatic arthritis. Lancet. 2018; 391(10136): 2273-2284.
  21. ↑ Van den Bosch F, Coates L. Clinical management of psoriatic arthritis. Lancet. 2018; 391(10136): 2285-2294.
  22. ↑ 22.0 22.1 22.2 Kerschbaumer A, Fenzl KH, Erlacher L, Aletaha D. An overview of psoriatic arthritis - epidemiology, clinical features, pathophysiology and novel treatment targets. Wien Klin Wochenschr. 2016; 128(21-22): 791-795.
  23. ↑ Zero To Finals. Psoriatic Arthritis. Available from: https://www.youtube.com/watch?v=fQCU7rQbovk [last accessed 8/11/2020]
  24. ↑ 24.0 24.1 24.2 24.3 24.4 24.5 24.6 Peluso R, Di Minno MN, Iervolino S, et al. Enteropathic spondyloarthritis: from diagnosis to treatment. Clin Dev Immunol. 2013; 2013: 631408.
  25. ↑ Courcoul A, Brinster A, Decullier E, Larbre JP, Piperno M, Pradat E et al. A bicentre retrospective study of features and outcomes of patients with reactive arthritis. Joint Bone Spine. 2018; 85(2): 201-205.
  26. ↑ 26.0 26.1 26.2 26.3 26.4 26.5 26.6 Selmi C, Gershwin ME. Diagnosis and classification of reactive arthritis. Autoimmun Rev. 2014; 13(4-5): 546-9. 
  27. ↑ Ono K, Kishimoto M, Shimasaki T, Uchida H, Kurai D, Deshpande GA et al. Reactive arthritis after COVID-19 infection. RMD Open 2020; 6: e001350.
  28. ↑ 28.0 28.1 28.2 28.3 Wu IB, Schwartz RA. Reiter's syndrome: the classic triad and more. J Am Acad Dermatol. 2008; 59(1): 113-21.
  29. ↑ Zero To Finals. Reactive Arthritis: Visual Explanation for Students. Available from: https://www.youtube.com/watch?v=snjGL2x6Eus [last accessed 8/11/2020]
  30. ↑ Chou CT, Lin KC, Wei JCC, Tsai WC, Ho HH, Hwang CM et al. Study of undifferentiated spondyloarthropathy among first-degree relatives of ankylosing spondylitis probands. Rheumatology. 2005; 44(5): 662-5.
  31. ↑ Hauk L. Spondyloarthritis: NICE Releases Guidelines on Diagnosis and Treatment. Am Fam Physician. 2017; 96(10): 677-678.
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