A critical review of Rheumatoid Arthritis that affects the musculoskeletal function of the foot and ankle.

A Critical Review of Rheumatoid Arthritis That Affects the Musculoskeletal Function of the Foot and Ankle Student’s Name Institution Course Code: Course Name Professor’s Name Submission Date Table of Contents TOC \o "1-3" \h \z \u Introduction PAGEREF _Toc182957691 \h 3Definition and Overview of Rheumatoid Arthritis PAGEREF _Toc182957692 \h 3Pathogenesis PAGEREF _Toc182957693 \h 4Risk Factors and Aetiology of RA PAGEREF _Toc182957694 \h 4Demographical Factors PAGEREF _Toc182957695 \h 4Age PAGEREF _Toc182957696 \h 4Biological Sex PAGEREF _Toc182957697 \h 5Ethnicity PAGEREF _Toc182957698 \h 6Genetics PAGEREF _Toc182957699 \h 7Lifestyle and Environmental Factors PAGEREF _Toc182957700 \h 7Clinical Presentation of Rheumatoid Arthritis PAGEREF _Toc182957701 \h 8Diagnosis PAGEREF _Toc182957702 \h 8Complications of RA PAGEREF _Toc182957703 \h 9Pathogenesis of The Structural and Functional Foot Problems Associated with RA PAGEREF _Toc182957704 \h 10Patient Assessment of Musculoskeletal Foot Problems Associated with RA Arthritis PAGEREF _Toc182957705 \h 11History-Taking PAGEREF _Toc182957706 \h 12Physical Examination PAGEREF _Toc182957707 \h 12Imaging PAGEREF _Toc182957708 \h 13Functional and Gait Assessments PAGEREF _Toc182957709 \h 14Counterargument PAGEREF _Toc182957710 \h 14Addressing the Argument About Comprehensive Assessment PAGEREF _Toc182957711 \h 14Addressing the Argument About Symptom Interpretation PAGEREF _Toc182957712 \h 15Addressing the Limitations of Imaging and Functional Assessments PAGEREF _Toc182957713 \h 15Disease Activity Score 28 (DAS 28) Appraisal PAGEREF _Toc182957714 \h 16Most Appropriate Methods for Evaluating the Impact of Foot Problems in RA PAGEREF _Toc182957715 \h 17Patient-Reported Outcome Measures (PROMs) PAGEREF _Toc182957716 \h 18Objective Clinical Assessments PAGEREF _Toc182957717 \h 20Key Considerations for Evaluation PAGEREF _Toc182957718 \h 21Conclusion PAGEREF _Toc182957719 \h 21References PAGEREF _Toc182957720 \h 22 Introduction Rheumatoid Arthritis (RA) is an autoimmune disease that features joint damage, pain, and physical functionality impairment (Arthritis Foundation, 2021). It typically affects the small joints of the hands and feet, causing erosion of the joints, cartilage degradation, and deformity. Foot involvement is widespread, and daily activities can become uncomfortable. The deformities resulting from this are hammertoes, hallux abducto valgus (HAV), and collapsed arches, some of which may result in ulcers and infection. These musculoskeletal complications exacerbate functional limitations, which may lead to disability. Management is, therefore, the most effective way of dealing with foot complications associated with RA. The review focuses on RA and foot deformities. This study is validated and supported by NICE Guidelines for RA in adults, and all the arguments presented herein are arrived at after critical consideration of available evidence, as recommended by the National Institute for Health and Care Excellence (2020). This paper discusses musculoskeletal complications associated with this condition and the structural and functional aspects of the foot. In addition, the paper will include factors of aetiology, clinical presentations, pathogenesis, evidence-based evaluation methods, and quality of life among the patients. Definition and Overview of Rheumatoid Arthritis RA is a chronic systemic autoimmune disorder that mainly affects the joints, but other extra-articular systems contribute primarily to its morbidity (Kaeley et al., 2019). The chronic inflammation of the synovial membranes is a feature of RA and leads to the erosion of bones and cartilage, resulting in irreversible destruction of the joints. The driving force behind this autoimmune disorder is an abnormal immune response targeted against the tissues of the joint, leading to the advancement of damage with eventual deformity (Kaeley et al., 2019). Although RA is primarily a synovial-joint disease, inflammation and immune dysregulation may spread beyond the joints within the other body systems, where various complications of RA further increase morbidity and a decline in the quality of life. RA may start at any age into late adulthood. One of the hallmarks of RA is its unpredictable disease course, with periods of exacerbation characterised by an increase in inflammation alternating with periods of remission, during which symptoms may temporarily improve. Pathogenesis RA pathogenesis involves a complex interplay of genetic (HLA-DRB1, PTPN22, TNFAIP3, STAT4, and IL6), environmental, and immunological elements (Cai et al., 2023). An imbalance between pro-inflammatory and anti-inflammatory cytokines forms the basis of the mechanism of RA, initiating inflammation and oxidative stress inside the joints. Inflammation at all such sites furthers the cascade of destruction in the synovium, bone, and cartilage, leading to eventual deformities (Cai et al., 2023). Autoimmune reactions are heavily involved in the pathogenesis of RA, and the production of autoantibodies realises the clinical diagnosis. Immune cells such as CD4+ T and B cells will further fuel inflammation and severity of the disease (Yap et al., 2018). Genetic predisposition and environmental triggers, including smoking and infections, will initiate the disease, leading to chronic inflammation and irreversible joint destruction (Chauhan et al., 2023). Risk Factors and Aetiology of RA Demographical Factors Age According to Lufkin et al. (2021), age remains among the strongest risk factors for RA. The appearance or association of ageing with RA is mainly attributed to the progressive nature of autoimmune disorders, which always demonstrates more significance later in life. It can be viewed in many aspects, which include the accumulation of environmental exposures, changing function of the immune system, and greater possible comorbidities across the life span. Ageing itself, despite this fact, is a reported risk factor; a critical analysis would expose specific restrictions on the generalisation of this relationship. It also occurs in people in their 30s, meaning it is not possible for the age factor alone to be the predictor of the disease. Because of genetic predisposition and other risk factors, the mechanisms from ageing to RA may also be greatly different from person to person and thus should be nuanced and depend on the individual rather than age variability. Biological Sex Biologically, according to Lufkin et al. (2021), RA affects women 2-3 times more than men, and such a trend opens the avenues for a critical discussion of various hormonal influences and genes and social behaviours that explain such discrepancies. It has been revealed that immune responses may be influenced by estrogen, which could imply the susceptibility to autoimmune diseases in females. However, Lufkin et al. (2021) correctly point out that, as important as the hormonal factors are, such a simplistic explanation of the differences based on biology alone overlooks the role of socio-cultural variables. For instance, lifestyle habits, health-care-seeking behaviours, and access to and utilisation of health resources may differ by sex and thus could influence the prevalence of diseases and outcomes of their management. Moreover, the interrelation of biological sex with age further complicates the risks of RA, whereby the diagnosis and treatment would present special challenges in older women due to the added load of age-related health problems (Lufkin et al., 2021). Sexual dimorphism in immune response does not suggest just higher prevalence in females, but severity and disease course may also be different, with females presenting more incapacitating complaints than males. One of the key objectives of Lufkin et al.’s (2021) study was to search for and characterise important high-order interactions of risk factors that play a critical role in the prediction of RA. In conducting such a study, one of the challenges was that the number of synthetic variables increased exponentially with the inclusion of higher-order interactions, which congruently increased the cost of computation. This drawback prompted Lufkin and colleagues to limit their research to as many third-order interactions as possible. Lufkin et al.’s (2021) use of FAMD also decreased the amount of predictor parameters assessed using regression, which significantly reduced the computation requirement. FAMD also offered room for categorical and continuous variables of risk factors for consideration in the model. Ethnicity Ethnicity, as reported by Molokhia and McKeigue 2000, is one of the most solid risk factors in rheumatoid arthritis and is significantly variable in prevalence between populations. This RA prevalence is the highest among Native Americans, whereas generally, Afro-Caribbean and East Asian populations have lower prevalence rates compared to Europeans. They illustrate that ethnicity is a critical risk factor for RA: the disease prevalence is high among Native Americans, whereas it is reportedly low among Afro-Caribbean, East Asian, and European populations. Although genetic factors, such as HLA alleles, are partial explanations for these differences, environmental influences and disparities in healthcare access also play critical roles. Generally, it was found that the prevalence of RA is higher among African Americans than European Americans, but variability in diagnosis and unequal access to healthcare complicate the interpretation of those differences. Such an understanding implies that RA risk is the product of a very complex interplay of genetic, environmental, and social factors; focusing only on genetic predisposition will not take into account other major contributors, such as lifestyle and healthcare disparities. It also reflects difficulties in accurately comparing different ethnic groups in the absence of standardised methodologies and the consideration of socio-environmental variables. Genetics Molokhia and McKeigue (2000) noted that there are two of the most potent risk factors for rheumatoid arthritis, which are the presence of certain genetic alleles within the human leucocyte antigen region. Strong associations of increased liability to RA in some ethnic groups were accounted for by certain alleles, especially members of the HLA-DR family. That means carriers of such high-susceptibility alleles have a higher probability of developing RA compared with carriers of low-susceptibility genotypes, thus pointing to the role of genetic predisposition in the aetiology. These genetic associations may provide a basis for some understanding of the individuals at higher risk and could potentially guide targeted prevention and treatment strategies for RA among various populations. Lifestyle and Environmental Factors Saevarsdottir et al. (2015) conducted a review on smoking as a risk factor in the aetiology of RA. They gathered original work SWEFOT trial (n=487). They identified genetic factors such as HLA-DRB1, PTPN22 and PADI4 (Ishikawa & Terao, 2020) and smoking as a significant risk factor with a 12–63% risk gradient (Saevarsdottir et al., 2015) and correlations between RA and Cigarette Smoking increases the risk of RA development by 26% in those who smoked 1–10 pack-years (Ishikawa & Terao,2020). The 14% attribution of RA to smoking, with a significant increase in risk for current smokers, points to the pressing need for targeted public health interventions for smoking cessation and lifestyle modification (Gianfrancesco & Crowson, 2021). The results suggest that smoking was the strongest independent risk factor for developing RA in people with genetic susceptibility. Clinical Presentation of Rheumatoid Arthritis Rheumatoid arthritis is a systemic disease of uncertain aetiology characterised by the involvement of both joint-specific and systemic manifestations; the clinical features are varied. Hallmarks include pain, stiffness, and swelling in symmetrical small peripheral joints of the wrist, metacarpophalangeal (MCPs), and metatarsophalangeal (MTPs) (Leeden et al., 2008). General morning stiffness lasting more than one hour is a characteristic symptom and demonstrates an actively inflamed joint. Over time, affected joints may undergo destructive changes leading to deformity and loss of functionality, often accompanied by profound limitations to mobility. Besides the symptoms related to the joints, other systemic features include fatigue, low-grade fever, malaise, anorexia, and weight loss, common and arising from the inflammatory features of RA (Garrow et al., 2000). The extra-articular complications include rheumatoid nodules, vasculitis with leg ulcers, mononeuropathies, and pulmonary problems, including pleural effusion, nodules, infiltrates, or fibrosis, contributing to significant respiratory morbidity. Cardiovascular features include pericarditis and myocarditis, while lymphadenopathy also underlines the systemic effect of RA. Other specific syndromes related to RA involve Felty syndrome, which involves splenomegaly and neutropenia, and Sjögren syndrome, which includes symptomatology of dry eyes and mouth (Patel & Akhondi, 2021). Diagnosis RA diagnosis is made by combining clinical assessments, laboratory tests, imaging studies, analysis for joint inflammation, and a review of symmetrical joint involvement. It is confirmed by detecting specific autoantibodies with particular prominence for rheumatoid factor and anti-cyclic citrullinated peptide antibodies that help identify inflammation through acute-phase reactants. Confirmation is by blood tests that detect the presence of rheumatoid factor, anti-cyclic citrullinated peptide antibodies (repetition, but this reads better than above), along with inflammation markers such as erythrocyte sedimentation rate and C-reactive protein. Siddle et al. (2010) further mention that imaging diagnostic techniques include X-rays, ultrasounds, or MRI for an appropriate overview of the joint damage assessment by measuring lesion development in bone and cartilage. An early and accurate diagnosis is necessary because delayed treatment results in higher levels of joint destruction and poorer outcomes (Chauhan et al., 2023). Complications of RA Rheumatoid arthritis may present many complications, especially concerning the foot, which usually causes structural deformities. Joint deformities with RA include subluxation of MTP joints, hallux abducto valgus, and pes planus. These structural deformities result as a direct consequence of chronic inflammation, which causes the foot's ligaments, tendons, and bones to be misaligned and without the normal architectural appearance of the foot. Ciofoaia et al. (2022) give an extensive review of complications associated with RA, therefore underlining the complex nature of the disease, which is much more than the consequences of joint damage. Generally speaking, RA can be considered a severe autoimmune disease that primarily affects joints, though systemic impacts are not trivial either. The authors point out that RA patients have a high risk of developing several extra-articular manifestations, including cardiovascular disease, pulmonary complications, and mental health disorders. Inflammatory markers associated with RA are strongly associated with increased cardiovascular risks; therefore, controlling RA may improve outcomes in cardiovascular disorders. Ciofoaia et al. (2022) do, however, emphasise that pulmonary complications are a major feature; interstitial lung disease is more common in RA patients compared to the general population. Current awareness and screening of respiratory health are, therefore, low among RA patients, and this is something the clinician needs to be aware of with appropriate proactive management strategies. Pathogenesis of The Structural and Functional Foot Problems Associated with RA The foot problems in RA result from synovitis or inflammation of the synovial membrane, abnormal immune response, overproduction of synovial fluid, joint swelling, increased intra-articular pressure, cartilage and bone erosion, and severe disruption of joints, particularly MTP joints. According to Wechalekar et al. (2012), such ensuing joint injuries and inflammation provide the ideal conditions for manifesting a wide range of foot deformities that eventually alter biomechanics and impair functionality. As the disease progresses, the chronic inflammatory processes in RA culminate in typical joint deformities. Moreover, the pathogenesis of the structural and functional foot problems related to rheumatoid arthritis is inextricably linked to the multifactorial nature of both pain and joint damage emphasised by Sarzi-Puttini et al. (2014). The typical inflammation in RA is confined to the synovial membrane of joints of the feet, which leads to synovitis, which is also responsible for the pain, swelling, and stiffness, especially of the metatarsophalangeal and ankle joints. The inflammatory process can cause profound structural changes, including erosions and joint deformities such as hallux valgus and hammer toes, which impede function and further complicate the assessment of disease activity by the i...