Introduction And Importance: A terminal extensor tendon disruption, with or without bony avulsion, may lead to a mallet deformity. In most cases, trauma precedes deformity. Non-traumatic causes are less probable. Several reports showed non-traumatic causes include villonodular tumors or chronic inflammation/infection. Conversely, osteochondroma, a benign tumor, typically develops from the growth plate of the long bones during the first two decades of life.
Case Presentation: We describe an unusual case of osteochondroma and mallet deformity in a child's finger. The child was only 4 years old at the time of the first presentation, and there was no clear injury before the symptom. The parent reported that the left little finger was crooked. Over the past year, the painless deformity has gradually progressed. At the physical examination, a palpated bony mass was found proximal to the angulated DIP joint. A radiograph was inconclusive and suggested an old fracture of the middle phalanx. Intraoperatively, a sessile-type exostosis at the epi-metaphysis of the middle phalanx pushed the intact terminal extensor ulnarwards.
Clinical Discussion: After removing the exostosis, the biopsy confirmed the presence of osteochondroma. We reconstruct the terminal extensor tendon and skin. During the 2-year follow-up, there was no evidence of infection, deformity relapse, or tumor recurrence.
Conclusion: Our goal is to raise awareness of osteochondroma, an extremely rare cause of a non-traumatic mallet finger in a very young child. Surgical resection remains the mainstay treatment for the tumor, with additional soft tissue reconstruction to overcome the secondary deformity.
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http://dx.doi.org/10.1016/j.ijscr.2025.111105 | DOI Listing |
Int J Surg Case Rep
March 2025
Pathology Anatomy Department, Eka Hospital, Bekasi, West Java, Indonesia.
Introduction And Importance: A terminal extensor tendon disruption, with or without bony avulsion, may lead to a mallet deformity. In most cases, trauma precedes deformity. Non-traumatic causes are less probable.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
March 2025
Randall Centre for Cell and Molecular Biophysics and British Heart Foundation Centre of Research Excellence, New Hunt's House, Guy's Campus, King's College London, London SE1 1UL, United Kingdom.
Muscle contraction is driven by myosin motors from the thick filaments pulling on the actin-containing thin filaments of the sarcomere, and it is regulated by structural changes in both filaments. Thin filaments are activated by an increase in intracellular calcium concentration [Ca] and by myosin binding to actin. Thick filaments are activated by direct sensing of the filament load.
View Article and Find Full Text PDFJ Muscle Res Cell Motil
January 2025
School of Molecular and Cellular Biology, University of Leeds, Leeds, LS2 9JT, UK.
Biallelic mutations in multiple EGF domain protein 10 (MEGF10) gene cause EMARDD (early myopathy, areflexia, respiratory distress and dysphagia) in humans, a severe recessive myopathy, associated with reduced numbers of PAX7 positive satellite cells. To better understand the role of MEGF10 in satellite cells, we overexpressed human MEGF10 in mouse H-2k-tsA58 myoblasts and found that it inhibited fusion. Addition of purified extracellular domains of human MEGF10, with (ECD) or without (EGF) the N-terminal EMI domain to H-2k-tsA58 myoblasts, showed that the ECD was more effective at reducing myoblast adhesion and fusion by day 7 of differentiation, yet promoted adhesion of myoblasts to non-adhesive surfaces, highlighting the importance of the EMI domain in these behaviours.
View Article and Find Full Text PDFMuscle Nerve
March 2025
Division of Plastic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri, USA.
Introduction: Motor recovery following nerve injury is dependent on time required for muscle reinnervation. This process is imperfect, however, and recovery is often incomplete. At the neuromuscular junction (NMJ), macrophage signaling aids muscle reinnervation.
View Article and Find Full Text PDFJ Hand Surg Glob Online
November 2024
Department of Orthopaedics, The University of North Carolina School of Medicine, Chapel Hill, NC.
Purpose: Terminal extensor tenotomy or Dolphin tenotomy, is a described treatment for the management of distal interphalangeal (DIP) joint hyperextension in chronic boutonniere deformity. The purpose of this study was to investigate the effects of incremental partial Dolphin tenotomy in correcting boutonniere deformity, with a focus on evaluating the improvement in DIP joint hyperextension deformity and documenting the development of iatrogenic mallet finger.
Methods: Thirty-eight fingers from 10 cadaveric hands were used.
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