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Ulcerated bleeding palisaded encapsulated neuroma of the tongue

Dhanuka S, Rodrigues G, Carnello S

Malays J Pathol, 2019 Aug;41(2):229-232.
PMID: 31427561

INTRODUCTION: Palisaded encapsulated neuroma (PEN) is a benign lesion of Schwann cells and its occurrence in the oral mucosa especially the tongue is very rare.
CASE REPORT: This article describes a case of a 41-year-old male, a chronic smoker with an actively bleeding, ulcerated, solitary, firm lesion on the lateral border of the tongue which had bled thrice before. A differential diagnosis of pyogenic granuloma, haemangioma, fibroma, nerve sheath tumour, salivary gland tumour and malignancy was made and surgically excised. Histopathology of the excised specimen revealed a well-circumscribed lesion with spindle-shaped cells arranged in interlacing fascicles and with the help of immunohistochemical markers confirmed it to be a PEN.
DISCUSSION: To our knowledge, this is the first description of an ulcerated PEN presented with an active bleed.

Matched MeSH terms: Schwann Cells
Fulltext Ancient Schwannoma Of The Facial Nerve: An Unusual Histological Variant Of A Rare Disease

Baharudin, A., Din Suhaimi, S., Omar, E.

International Medical Journal Malaysia, 2006;5(2):1-4.
MyJurnal

Schwannomas are benign slow growing lesions arising from the Schwann cells that ensheath the axons of the peripheral, cranial and autonomic nervous systems. Intracranial schwannomas develop from the facial nerve much more rarely than from the vestibular or trigeminal nerves. Ancient schwannoma is an unusual histological variant of this rare disease. A 48 years old man who had recurrent facial nerve paralysis and right external auditory mass is presented in this case report.

Matched MeSH terms: Schwann Cells
Fulltext Neural-differentiated mesenchymal stem cells incorporated into muscle stuffed vein scaffold forms a stable living nerve conduit

Hassan NH, Sulong AF, Ng MH, Htwe O, Idrus RB, Roohi S, et al.

J Orthop Res, 2012 Oct;30(10):1674-81.
PMID: 22411691 DOI: 10.1002/jor.22102

Autologous nerve grafts to bridge nerve gaps have donor site morbidity and possible neuroma formation resulting in development of various methods of bridging nerve gaps without using autologous nerve grafts. We have fabricated an acellular muscle stuffed vein seeded with differentiated mesenchymal stem cells (MSCs) as a substitute for nerve autografts. Human vein and muscle were both decellularized by liquid nitrogen immersion with subsequent hydrolysis in hydrochloric acid. Human MSCs were subjected to a series of treatments with a reducing agent, retinoic acid, and a combination of trophic factors. The differentiated MSCs were seeded on the surface of acellular muscle tissue and then stuffed into the vein. Our study showed that 35-75% of the cells expressed neural markers such as S100b, glial fibrillary acidic protein (GFAP), p75 NGF receptor, and Nestin after differentiation. Histological and ultra structural analyses of muscle stuffed veins showed attachment of cells onto the surface of the acellular muscle and penetration of the cells into the hydrolyzed fraction of muscle fibers. We implanted these muscle stuffed veins into athymic mice and at 8 weeks post-implantation, the acellular muscle tissue had fully degraded and replaced with new matrix produced by the seeded cells. The vein was still intact and no inflammatory reactions were observed proving the biocompatibility and biodegradability of the conduit. In conclusion, we have successfully formed a stable living nerve conduit which may serve as a substitute for autologous nerves.

Matched MeSH terms: Schwann Cells/cytology*
Complement regulatory proteins (CD46, 55 and 59) expressed on Schwann cells: immune targets in demyelinating neuropathies?

Miyaji K, Paul F, Shahrizaila N, Umapathi T, Yuki N

J Neuroimmunol, 2014 Nov 15;276(1-2):172-4.
PMID: 25156074 DOI: 10.1016/j.jneuroim.2014.08.004

Given their localization and important role in regulating complement, complement regulatory proteins may act as target antigens and their antibodies as biomarkers in demyelinating neuropathies. We investigated the binding of autoantibodies to complement regulatory proteins (CD46, 55 and 59) in demyelinating diseases. In 42 acute inflammatory demyelinating polyneuropathy, 23 chronic inflammatory demyelinating polyneuropathy, 13 acute motor axonal neuropathy, 71 multiple sclerosis, and 19 neuromyelitis optica patients as well as 55 healthy controls, we were unable to detect significant titers of antibodies to CD46, CD55 and CD59. These autoantibodies are unlikely to be biomarkers in acute and chronic inflammatory demyelinating polyneuropathies.

Matched MeSH terms: Schwann Cells/metabolism*
Fulltext Rapidly Growing Huge Lower Back Malignant Peripheral Nerve Sheath Tumour

Abuzarifa N, Al-Chalabi MMM, Wan Sulaiman WA

Cureus, 2021 Mar 05;13(3):e13712.
PMID: 33842103 DOI: 10.7759/cureus.13712

Malignant peripheral nerve sheath tumours (also called neurofibrosarcomas) are a rare, highly aggressive soft tissue sarcomas that arise from the peripheral nerves or cells associated with the nerve sheath, such as Schwann cells, peri-neural cells and fibroblasts. It is representing 10% of all soft tissue sarcomas in which it is considered as an extremely rare malignancy, especially in patients with neurofibromatosis type I. In the general population, it affects approximately 1 in 100,000 people. This article is reporting a 56-year-old Malay female patient who is a known case of neurofibromatosis type I for 20 years, presented with a lower back, pruritic, gradually increasing swelling during the last five months. Last month before the presentation, the lesion rapidly grows, reaching a size of (15×15 cm), accompanied by foul-smelling discharge and pain exacerbated with movement. Although no history of preceding trauma or accident, the mass bleeds within contact. In conclusion, only a few cases of giant malignant peripheral nerve sheath tumours reported in the literature describing its location and growth progression. We present a massive, extremely rapid growth of cutaneous exophytic malignant peripheral nerve sheath tumours over the lower back.

Matched MeSH terms: Schwann Cells
Fulltext Major cellular events in peripheral nerve regeneration: A brief overview

Naidu, M., David, P.

International Medical Journal Malaysia, 2009;8(1):61-64.
MyJurnal

Injury to a peripheral nerve leads to degeneration of the segment distal to the site of lesion, a process referred to as Wallerian degeneration. During Wallerian degeneration, axons and myelin sheaths undergo degeneration and are phagocytosed by macrophages and Schwann cells. The Schwann cells proliferate and the endoneurial tubes persist, together the whole structure is known as the band of BÃ¼ngner. Within few hours, the damaged axons in the proximal stump initiate a regeneration response, with formation of new growth cones. During Wallerian degeneration, neurotrophins, neural cell adhesion molecules, cytokines and other soluble factors are upregulated to facilitate regeneration. The recovery of the target in mammals is often variable, but almost never complete. In humans, scar tissue forms at the site of lesion and this often results in poor recovery of the target. The major events underlying this regenerative process is highlighted and discussed in this review.

Matched MeSH terms: Schwann Cells
Fulltext Sodium phenylbutyrate inhibits Schwann cell inflammation via HDAC and NFκB to promote axonal regeneration and remyelination

Yadav A, Huang TC, Chen SH, Ramasamy TS, Hsueh YY, Lin SP, et al.

J Neuroinflammation, 2021 Oct 16;18(1):238.
PMID: 34656124 DOI: 10.1186/s12974-021-02273-1

BACKGROUND: Epigenetic regulation by histone deacetylases (HDACs) in Schwann cells (SCs) after injury facilitates them to undergo de- and redifferentiation processes necessary to support various stages of nerve repair. Although de-differentiation activates the synthesis and secretion of inflammatory cytokines by SCs to initiate an immune response during nerve repair, changes in either the timing or duration of prolonged inflammation mediated by SCs can affect later processes associated with repair and regeneration. Limited studies have investigated the regulatory processes through which HDACs in SCs control inflammatory cytokines to provide a favorable environment for peripheral nerve regeneration.
METHODS: We employed the HDAC inhibitor (HDACi) sodium phenylbutyrate (PBA) to address this question in an in vitro RT4 SC inflammation model and an in vivo sciatic nerve transection injury model to examine the effects of HDAC inhibition on the expression of pro-inflammatory cytokines. Furthermore, we assessed the outcomes of suppression of extended inflammation on the regenerative potential of nerves by assessing axonal regeneration, remyelination, and reinnervation.
RESULTS: Significant reductions in lipopolysaccharide (LPS)-induced pro-inflammatory cytokine (tumor necrosis factor-α [TNFα]) expression and secretion were observed in vitro following PBA treatment. PBA treatment also affected the transient changes in nuclear factor κB (NFκB)-p65 phosphorylation and translocation in response to LPS induction in RT4 SCs. Similarly, PBA mediated long-term suppressive effects on HDAC3 expression and activity. PBA administration resulted in marked inhibition of pro-inflammatory cytokine secretion at the site of transection injury when compared with that in the hydrogel control group at 6-week post-injury. A conducive microenvironment for axonal regrowth and remyelination was generated by increasing expression levels of protein gene product 9.5 (PGP9.5) and myelin basic protein (MBP) in regenerating nerve tissues. PBA administration increased the relative gastrocnemius muscle weight percentage and maintained the intactness of muscle bundles when compared with those in the hydrogel control group.
CONCLUSIONS: Suppressing the lengthened state of inflammation using PBA treatment favors axonal regrowth and remyelination following nerve transection injury. PBA treatment also regulates pro-inflammatory cytokine expression by inhibiting the transcriptional activation of NFκB-p65 and HDAC3 in SCs in vitro.

Matched MeSH terms: Schwann Cells/drug effects; Schwann Cells/metabolism; Schwann Cells/pathology
Fulltext The role of cells, neurotrophins, extracellular matrix and cell surface molecules in peripheral nerve regeneration

Naidu M

Malays J Med Sci, 2009 Apr;16(2):10-4.
PMID: 22589652 MyJurnal

Wallerian degeneration is a complicated process whereby axons and myelin sheaths undergo degeneration, and eventually are phagocytosed by macrophages and Schwann cells following nerve damage. Schwann cells proliferate and the endoneural tubes persist. In addition, neurotrophins, neural cell adhesion molecules, cytokines and other soluble factors are upregulated to facilitate regeneration. The important role of cellular components, neurotrophins, and extracellular matrix components, including cell surface molecules involved in this regenerative process, is highlighted and discussed in this review.

Matched MeSH terms: Schwann Cells
Approaches to deriving Schwann cells from human bone marrow for neural tube regeneration in a clinical setting

Hidayah HN, Mazzre M, Ng AM, Ruszymah BH, Shalimar A

Med J Malaysia, 2008 Jul;63 Suppl A:39-40.
PMID: 19024973

Bone marrow derived Mesenchymal stem cells (MSCs) were evaluated as an alternative source for tissue engineering of peripheral nerves. Human MSCs were subjected to a series of treatment with a reducing agent, retinoic acid and a combination of trophic factors. This treated MSCs differentiated into Schwann cells were characterized in vitro via flow cytometry analysis and immunocytochemically. In contrast to untreated MSCs, differentiated MSCs expressed Schwann cell markers in vitro, as we confirmed by flow cytometry analysis and immunocytochemically. These results suggest that human MSCs can be induced to be a substitute for Schwann cells that may be applied for nerve regeneration since it is difficult to grow Schwann cells in vitro.

Matched MeSH terms: Schwann Cells/transplantation*
Fulltext Sciatic nerve repair with tissue engineered nerve: Olfactory ensheathing cells seeded poly(lactic-co-glygolic acid) conduit in an animal model

Tan CW, Ng MH, Ohnmar H, Lokanathan Y, Nur-Hidayah H, Roohi SA, et al.

Indian J Orthop, 2013 Nov;47(6):547-52.
PMID: 24379458 DOI: 10.4103/0019-5413.121572

BACKGROUND AND AIM: Synthetic nerve conduits have been sought for repair of nerve defects as the autologous nerve grafts causes donor site morbidity and possess other drawbacks. Many strategies have been investigated to improve nerve regeneration through synthetic nerve guided conduits. Olfactory ensheathing cells (OECs) that share both Schwann cell and astrocytic characteristics have been shown to promote axonal regeneration after transplantation. The present study was driven by the hypothesis that tissue-engineered poly(lactic-co-glycolic acid) (PLGA) seeded with OECs would improve peripheral nerve regeneration in a long sciatic nerve defect.
MATERIALS AND METHODS: Sciatic nerve gap of 15 mm was created in six adult female Sprague-Dawley rats and implanted with PLGA seeded with OECs. The nerve regeneration was assessed electrophysiologically at 2, 4 and 6 weeks following implantation. Histopathological examination, scanning electron microscopic (SEM) examination and immunohistochemical analysis were performed at the end of the study.
RESULTS: Nerve conduction studies revealed a significant improvement of nerve conduction velocities whereby the mean nerve conduction velocity increases from 4.2 ΁ 0.4 m/s at week 2 to 27.3 ΁ 5.7 m/s at week 6 post-implantation (P < 0.0001). Histological analysis revealed presence of spindle-shaped cells. Immunohistochemical analysis further demonstrated the expression of S100 protein in both cell nucleus and the cytoplasm in these cells, hence confirming their Schwann-cell-like property. Under SEM, these cells were found to be actively secreting extracellular matrix.
CONCLUSION: Tissue-engineered PLGA conduit seeded with OECs provided a permissive environment to facilitate nerve regeneration in a small animal model.

Matched MeSH terms: Schwann Cells
Fulltext Melatonin promotes Schwann cell dedifferentiation and proliferation through the Ras/Raf/ERK and MAPK pathways, and glial cell-derived neurotrophic factor expression

Tiong YL, Ng KY, Koh RY, Ponnudurai G, Chye SM

Exp Ther Med, 2020 Nov;20(5):16.
PMID: 32934681 DOI: 10.3892/etm.2020.9143

Upon peripheral nerve injury (PNI), continuous proliferation of Schwann cells is critical for axon regeneration and tubular reconstruction for nerve regeneration. Melatonin is a hormone that is able to induce proliferation in various cell types. In the present study, the effects of melatonin on promoting Schwann cell proliferation and the molecular mechanism involved were investigated. The present results showed that melatonin enhanced the melatonin receptors (MT1 and MT2) expression in Schwann cells. Melatonin induced Schwann cell dedifferentiation into progenitor-like Schwann cells, as observed by immunofluorescence staining, which showed Sox2 marker expression. In addition, melatonin enhanced Schwann cell proliferation, mediated by the upregulation of glial cell-derived neurotropic factor (GNDF) and protein kinase C (PKC). Furthermore, the Ras/Raf/ERK and MAPK signaling pathways were also involved in Schwann cell dedifferentiation and proliferation. In conclusion, melatonin induced Schwann cell dedifferentiation and proliferation via the Ras/Raf/ERK, MAPK and GDNF/PKC pathways. The present results suggested that melatonin could be used to enhance the recovery of PNI.

Matched MeSH terms: Schwann Cells