Introduction: Osteoarthritis (OA) and haemophilic arthropathy (HA) are clinically similar, but pathologically distinct conditions which result in joint pain and loss of function. Distinguishing their disease mechanisms is therefore a key step in the development of curative therapy, as opposed to current symptomatic treatments. A disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS) 4 is a metzincin‐family member proteoglycan with known local involvement in OA pathogenesis.Aim: To investigate the potential differences and discriminatory potential of ADAMTS‐4 between OA and HA patients.Methods: We determined ADAMTS‐4 plasma concentrations by ELISA in patients with HA and OA. This pilot cross‐sectional study included N = 40 male participants equally divided across four subgroups: haemophilia patients with severe or mild HA and control subjects with severe or mild/no OA.Results: Our study showed a striking elevation in plasma ADAMTS‐4 expression levels in HA patients as compared to OA, as well as an increase in patients with severe as compared to mild HA. By performing the binomial logistical analysis and fitting the receiver–operator curve (ROC) (cut‐off probability .5), ADAMTS‐4 had a sensitivity of 95% and specificity of 50% in discriminating between HA and OA among our study participants.Conclusion: Uncovering the marked differences in plasma levels of ADAMTS‐4 in patients with HA versus OA potentially sheds new light on the mechanisms of HA pathogenesis and could foster more research into the roles ADAMTS‐4 and other matrix metalloproteinases (MMPs) play in HA versus OA.

Hemophilia is an X-linked genetic disorder that predominantly affects males, with females typically serving as asymptomatic carriers. Hemophilia A results from a deficiency or dysfunction of coagulation factor VIII, while a deficiency in factor IX causes hemophilia B. A less common condition, factor XI deficiency (formerly hemophilia C), is categorized as a rare bleeding disorder. The severity of hemophilia is classified based on the activity concentration of factors VIII and IX: severe (<1 IU/dL), moderate (1–5 IU/dL), and mild (6–<40 IU/dL). One of the most prevalent complications of hemophilia is hemarthrosis, bleeding into joint cavities, which, if unrecognized or untreated, can lead to hemophilic arthropathy. The pathophysiology of hemophilic arthropathy involves two key mechanisms: the accumulation of iron from blood in synovial joints, which cannot be cleared due to repeated bleeding, and the inflammatory response, resulting in synovial hyperplasia and the progressive destruction of cartilage and bone. Hemophilic arthropathy significantly impairs quality of life, causing chronic pain, joint deformities, and sometimes requiring surgical intervention. This thesis will examine the pathophysiology and management strategies for hemophilic arthropathy.

Background and Aims: The pathophysiology of haemophilic arthropathy (HA) is complex and largely undefined. Proteomic analyses provide insights into the intricate mechanisms of the HA.Our study aimed to identify differentially expressed proteins in relation to the severity of HA, explore their pathophysiological roles, and evaluate their potential as HA biomarkers.Methods: Our cross‐sectional observational study encompassed 30 HA patients and 15 healthy subjects. Plasma samples were pooled into three groups of 15 samples from those with severe haemophilic arthropathy (sHA), mild haemophilic arthropathy (mHA) and healthy controls. Proteomic analysis was performed using liquid chromatography‐mass spectrometry. The severity of HA was assessed using the World Federation of Haemophilia Physical Examination Score and ultrasonography following the Haemophilia Early Arthropathy Detection with Ultrasound (HEAD‐US) guidelines.Results: A total of 788 proteins were identified, with 97% of the uniquely identified proteins being expressed in all analysed groups. We identified several up and downregulated proteins across the groups that were mainly related to inflammatory and immunity‐modulating processes, as well as joint degeneration. We highlighted ten proteins relevant for the development of HA: cathepsin G, endoplasmic reticulum aminopeptidase 2, S100‐A9, insulin‐like growth factor I, apolipoprotein (a), osteopontin, pregnancy zone protein, cartilage oligomeric matrix protein, CD44, and cadherin‐related family member 2.Conclusion: Our analysis identified several proteins that shed further light on the distinctive pathogenesis of HA and could serve for biomarker research. However, these results need to be validated on a larger patient group.

Objectives: This study aims to assess the impact of a Tai Chi exercise program (TCEP) on pain, spinal flexibility, muscle strength, stability and balance, functional status, and quality of life (QoL) among home-dwelling patients with osteoarthritis (OA) or inflammatory arthritis (iA). Patients and methods: Between October 2018 and April 2019, a total of 28 participants (4 males, 24 females; median age: 62 years; range, 34 to 79 years) who completed the training program participating in at least 18 sessions were included. The TCEP consisted of 50 sessions for 60 min twice a week. The average attendance rate was high (78%, 39 sessions). Results: Chest mobility (breathing index, p<0.001), sagittal mobility of cervical (p<0.001), thoracic (p=0.009), and lumbar spine (Schober’s test, p<0.001) improved significantly in participants with OA and iA. The improvement in functional status was significant only in participants with OA (Lequesne index, p=0.014). Although the change in Lequesne index was statistically significant, the median value remained in the range of severe disability and the change did not reach the minimal clinically important difference. Although the trends were positive, the changes in pain (Visual Analog Scale pain, p=0.599), stability and balance (functional reach test, p=0.341), muscular strength (wall sit test, p=0.069), and health-related QoL (15D, p=0.065) were non-significant in participants with OA and iA. Conclusion: Our study results suggest that a 25-week TCEP is safe and can improve chest and spinal mobility in home-dwelling individuals with OA or iA.