Inflammation, angiogenesis and sensory nerve sprouting in the synovium of bony ankylosed and not bony ankylosed knees with end‐stage haemophilic arthropathy

Haemophilia ◽  
2021 ◽  
Author(s):  
Jiaxin Huang ◽  
Haijia Zhu ◽  
Shuaijie Lv ◽  
Peijian Tong ◽  
Liu Xun ◽  
...  
2019 ◽  
Vol 4 (5) ◽  
pp. 165-173 ◽  
Author(s):  
E. Carlos Rodríguez-Merchán

The musculoskeletal problems of haemophilic patients begin in infancy when minor injuries lead to haemarthroses and haematomas. Early continuous haematological primary prophylaxis by means of the intravenous infusion of the deficient coagulation factor (ideally from cradle to grave) is of paramount importance because the immature skeleton is very sensitive to the complications of haemophilia: severe structural deficiencies may develop quickly. If primary haematological prophylaxis is not feasible due to expense or lack of venous access, joint bleeding will occur. Then, the orthopaedic surgeon must aggressively treat haemarthrosis (joint aspiration under factor coverage) to prevent progression to synovitis (that will require early radiosynovectomy or arthroscopic synovectomy), recurrent joint bleeds, and ultimately end-stage osteoarthritis (haemophilic arthropathy). Between the second and fourth decades, many haemophilic patients develop articular destruction. At this stage the main possible treatments include arthroscopic joint debridement (knee, ankle), articular fusion (ankle) and total joint arthroplasty (knee, hip, ankle, elbow).Cite this article: EFORT Open Rev 2019;4:165-173. DOI: 10.1302/2058-5241.4.180090


2011 ◽  
Vol 1 (1) ◽  
pp. 51-59 ◽  
Author(s):  
Karin Knobe ◽  
Erik Berntorp

In patients with haemophilia, regular replacement therapy with clotting factor concentrates (prophylaxis) is effective in preventing recurrent bleeding episodes into joints and muscles. However, despite this success, intra-articular and intramuscular bleeding is still a major clinical manifestation of the disease. Bleeding most commonly occurs in the knees, elbows, and ankles, and is often evident from early childhood. The pathogenesis of haemophilic arthropathy is multifactorial, with changes occurring in the synovium, bone, cartilage, and blood vessels. Recurrent joint bleeding causes synovial proliferation and inflammation (haemophilic synovitis) that contribute to end-stage degeneration (haemophilic arthropathy); with pain and limitation of motion severely affecting patients’ quality of life. If joint bleeding is not treated adequately, it tends to recur, resulting in a vicious cycle that must be broken to prevent the development of chronic synovitis and degenerative arthritis. Effective prevention and management of haemophilic arthropathy includes the use of early, aggressive prophylaxis with factor replacement therapies, as well as elective procedures, including restorative physical therapy, analgesia, aspiration, synovectomy, and orthopaedic surgery. Optimal treatment of patients with haemophilia requires a multidisciplinary team comprising a haematologist, physiotherapist, orthopaedic practitioner, rehabilitation physician, occupational therapist, psychologist, social workers, and nurses.


1992 ◽  
Vol 6 (1) ◽  
pp. 41-52 ◽  
Author(s):  
Margaret R. Byers ◽  
Esther F. Wheeler ◽  
Mark Bothwell

1998 ◽  
Vol 89 (6) ◽  
pp. 1055-1057 ◽  
Author(s):  
Allan J. Belzberg ◽  
James N. Campbell

✓ Division of a peripheral nerve produces an axotomy leading to neurite outgrowth from the proximal stump and wallerian degeneration in the distal stump. Because there is no longer a connection between the distal stump and neuronal cell bodies in the anterior spinal cord or dorsal root ganglion, it is assumed that no neurites should exist in the distal stump. The authors present the case of a patient who unexpectedly had a neuroma on the proximal end of the distal segment of a previously severed nerve. The lateral antebrachial cutaneous nerve had been surgically severed. Innervated by the radial nerve, a neuroma subsequently formed in the distal segment. Our hypothesis is that the proximal end of the distal portion of a severed nerve may be innervated by collateral sprouts of axons that branch at points of more distal plexus formation. This invokes a similar pathophysiology to the controversial notion of end-to-side nerve sprouting. Neuromas that develop on the “wrong side” of a nerve become an additional potential source of pain in patients with injured nerves.


Haemophilia ◽  
2013 ◽  
Vol 20 (1) ◽  
pp. e97-e99 ◽  
Author(s):  
J. F. Baker ◽  
F. Maleki ◽  
J. M. Broderick ◽  
J. McKenna

Author(s):  
Paul W Ackermann ◽  
Phinit Phisitkul ◽  
Christopher J Pearce

Achilles tendinopathy (AT), which is increasing in prevalence, continues to puzzle clinicians around the world. AT comprises insertional and non-insertional AT (NIAT). This review will deal with NIAT, which is often related to changes in activities in sports and occupation, but can also be unrelated to activities that load the Achilles tendon. Recent studies demonstrate that extrinsic risk factors such as errors in training and occupational activities and intake of drugs that interact in tendon metabolism may lead to tendinopathy. In combination with intrinsic risk factors, lower limb biomechanical abnormalities and metabolic, inflammatory conditions, for example, diabetes, hypercholesterolaemia and genetic deviations, the risk of of AT is increased. Therefore, dysregulated mechanical loading and aberrant cellular signalling due to systemic metabolic/inflammatory imbalance and local hypoxia are suggested to cause NIAT. The exact aetiology and pathophysiology of NIAT are, however, not fully known and warrant further studies. NIAT is a condition that increases with ageing and characterised by pain during activity. Recent findings demonstrate that tendinosis is characterised by a fibrotic, failed healing response associated with pathological ingrowth of blood vessels and sensory nerves into a normally aneuronal/avascular tendon proper. This pathological sensory nerve sprouting may partly explain increased pain signalling, and partly by release of neuronal mediators contribute to causing the fibrotic alterations observed in NIAT. Establishing the differential underlying risk factors of NIAT should give better preventive strategies in patient education and counselling. Unravelling the common pathophysiological processes of NIAT may provide the means for future targeted therapies using combined surgical and biological approaches.


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