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Muscle fibre necrosis, also known as myonecrosis, is a form of muscle degeneration that can be caused by a variety of factors, including trauma, ischemia, infectious agents, myotoxins, and snakebites. It is characterised by swollen, deeply eosinophilic, homogeneous muscle fibres that lack cross-striations. This condition can range in severity from single necrotic fibres to extensive muscle involvement and is often associated with inflammatory myopathies, muscular dystrophies, and other muscle diseases. The process of muscle fibre necrosis involves the death of muscle fibres, infiltration by macrophages, and subsequent repair and regeneration. Understanding the underlying pathophysiology of myonecrosis is crucial for developing effective treatments for muscle diseases and improving patient outcomes.
| Characteristics | Values |
|---|---|
| Other names | Myonecrosis, hyaline degeneration, Zenker's degeneration |
| Causes | Trauma, ischemia, snake bites, extreme exertion, muscular dystrophies, inflammatory myopathies, infectious agents, myotoxins, statin toxicity |
| Histological characteristics | Swollen, deeply eosinophilic, homogeneous myofibers that lack cross striations (hyalinization), pale cytoplasm, absence of nuclear staining, membrane rupture, cell swelling |
| Complications | Contraction of myofibrils, disability, amputation |
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What You'll Learn
Muscle fibre death
Muscle fibre necrosis is characterised by swollen, deeply eosinophilic, homogeneous myofibers that lack cross striations (hyalinization). This is also referred to as hyaline degeneration or Zenker's degeneration. The affected fibres are often fragmented with pyknotic nuclei and can be hypereosinophilic or pale in colour. This process can also lead to dystrophic mineralization.
Sarcolemma destruction, or damage to the sarcolemma, can also lead to muscle fibre necrosis. This results in an influx of calcium ions into the injured muscle fibres, causing contraction of myofibrils and producing contraction bands. This can be observed in cases of hyperacute muscle injury.
Muscle fibre necrosis is often associated with the regeneration process, which can result in the repeated occurrence of necrosis and regeneration, leading to connective tissues filling the spaces between the muscle fibres. This sequence of events is characteristic of muscular dystrophies.
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Causes of muscle fibre necrosis
Muscle fibre necrosis is the degradation of myofibrils and other cytoplasmic components and the sarcolemma. It can range in severity from single necrotic fibres to extensive muscle involvement. There are four categories of muscle necrosis: focal monophasic reactions, multifocal monophasic reactions, focal polyphasic reactions, and multifocal polyphasic reactions.
Muscle fibre necrosis can be caused by a variety of factors, including:
- Ischemia: This refers to a restriction in blood supply to tissues, which can lead to cell death and necrosis.
- Trauma: External trauma, such as a physical injury or needle insertion, can cause focal monophasic reactions leading to muscle fibre necrosis.
- Venom: Snake bites can cause muscle necrosis due to the presence of myotoxins in their venom. These myotoxins can directly damage skeletal muscle fibres.
- Drugs and chemicals: Exposure to myotoxic drugs or chemicals can result in multifocal monophasic reactions and lead to muscle necrosis.
- Metabolic disorders: Disorders that impact metabolism can cause synchronous alterations in the phases of injury and repair, leading to muscle necrosis.
- Inflammatory myopathies: These are inflammatory diseases of the muscle, and they can cause muscle fibre necrosis, especially with extreme exertion or capture myopathy.
- Inherited diseases: Certain inherited diseases, such as muscular dystrophies, can make individuals more susceptible to muscle fibre necrosis.
- Extreme exertion: Also known as capture myopathy, this involves excessive muscle exertion that can lead to muscle fibre necrosis.
- Nutritional deficiencies: Prolonged nutritional deficiencies can result in multifocal polyphasic reactions and cause muscle necrosis.
- Genetic disorders: Genetic disorders, such as muscular dystrophies, can lead to muscle diseases with lesions that are in various stages of necrosis, leukocytic infiltration, and regeneration.
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Histological characteristics
Muscle fibre necrosis is a potential clinical complication of snakebite envenomings, which in severe cases can lead to functional or physical sequelae such as disability or amputation. Snake venom proteins, known as myotoxins, have the ability to directly damage skeletal muscle fibres.
Myofibre necrosis (myonecrosis) is histologically characterised by swollen, deeply eosinophilic, homogeneous myofibers that lack cross striations (hyalinization). This condition is sometimes referred to as hyaline degeneration or Zenker's degeneration. Affected fibres are often vacuolated and fragmented with pyknotic nuclei. Dystrophic mineralization can also occur.
The early stages of necrosis are marked by metabolic failure, with pale muscle fibres that have lost their cytoplasmic structures and staining. Nuclear staining is also absent. Necrotic muscle fibres have a pale cytoplasm and are named liquefied or hyaline fibres. They are phagocytosed and surrounded by inflammatory cells.
There are various stages of myofibre degeneration and regeneration, with regenerating muscle fibres exhibiting basophilic cytoplasm and enlarged nuclei due to vigorous protein synthesis during regenerating myogenesis. The sequence of necrosis and regeneration repeatedly occurs as a chronic process in muscular dystrophies, resulting in rounded muscle fibres and enhanced endomysial connective tissues.
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Snake bites and venom
Snake bites and the resulting venom introduced into the body can cause muscle fibre necrosis. Snake venom is a mixture of different proteins with diverse functions, and one of these major protein groups present in viper venoms are metalloproteases that primarily induce muscle damage. The venom is generally delivered at the bite site by subcutaneous or intramuscular injection. Once in the tissue, various types of toxins can cause tissue damage of rapid onset, especially in viperid species and some elapid species.
Snake bite is often associated with localised soft tissue necrosis. Less frequently, victims may suffer extensive muscle damage leading to rhabdomyolysis and the loss of muscle-specific protein. Local inflammation and pain are important characteristics of snakebite envenomations inflicted by viperid and crotalid species, whose venoms are rich sources of myotoxic PLA2s. Phospholipases A2 (PLA2) are important myotoxic components in these venoms, inducing a similar pattern of degenerative events in muscle cells. Myotoxic PLA2s bind to acceptors in the plasma membrane, which might be lipids or proteins and may differ in their affinity for the PLA2s. Upon binding, myotoxic PLA2s disrupt the integrity of the plasma membrane by catalytically dependent or independent mechanisms, provoking a pronounced Ca2+ influx that, in turn, initiates a complex series of degenerative events associated with hypercontraction, activation of calpains and cytosolic Ca2+-dependent PLA2s, and mitochondrial Ca2+ overload.
In addition to metalloproteases, snake venom serine proteases (SVSPs) also cause systemic envenomation effects such as altering blood pressure, activating or inhibiting coagulation factors, and degrading fibrinogen. Snake venom metalloproteases (SVMPs) are a predominant component of viper venoms and are involved in the degradation of basement membrane proteins (particularly collagen) surrounding the tissues around the bite site. Although their collagenolytic properties have been established, the molecular mechanisms through which SVMPs induce permanent muscle damage are poorly understood.
Snakebite envenomation is a neglected tropical disease that causes around 100,000 deaths annually and innumerable permanent disabilities, predominantly in the rural population living in the lower-income regions of the world. The significant rate of mortality and morbidity occurs due to the difficulties associated with the treatment of snakebites, which vary depending on the species, geographical location, age of the snake, the quantity of venom injected, correct diagnosis, and mode of treatment.
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Treatment strategies
Muscle fibre necrosis is a degenerative process that can range in severity from single necrotic fibres to extensive muscle involvement. It has four categories: focal monophasic reactions, multifocal monophasic reactions, focal polyphasic reactions, and multifocal polyphasic reactions. This condition can be caused by various factors, including ischemia, trauma, inherited diseases, inflammatory myopathies, and extreme exertion.
Now, let's discuss some treatment strategies for muscle fibre necrosis:
The treatment approach for muscle fibre necrosis will depend on the underlying cause and the extent of the condition. Here are some potential strategies:
- Anti-inflammatory medications: For cases where muscle necrosis is caused or aggravated by an inflammatory reaction, anti-inflammatory drugs can be administered to reduce local muscle damage. In particular, inhibitors of eicosanoid formation have shown promise in reducing inflammation and protecting muscle tissue.
- Inhibition of necroptosis: In inflammatory myopathies, such as polymyositis, muscle fibres undergo necroptosis, releasing pro-inflammatory molecules that accelerate muscle injury. Inhibiting necroptosis, such as through the use of necroptosis inhibitors or anti-HMGB1 antibodies, can suppress muscle injury and inflammation, improving muscle weakness and cell death.
- Treatment of snakebites: In cases where muscle necrosis is a result of snakebite envenomings, improving treatments for snakebites is crucial. Understanding the mechanism of action of Lys49 myotoxins, which are found in viperid species, can lead to the development of effective treatments to prevent or mitigate muscle necrosis caused by snake venom.
- Regenerative repair: Effective regenerative repair is possible following ischemic injury, provided that satellite cells remain viable. Regeneration is most successful in lesions with intact basal laminae. However, in cases of crush injury, the muscle basal lamina may be damaged, hindering the regenerative process.
- Nutritional interventions: In cases of multifocal polyphasic reactions, nutritional deficiencies can play a role in the development of muscle necrosis. Addressing nutritional deficiencies and ensuring adequate nutrient intake can help mitigate ongoing insults to the muscles and support their recovery.
- Genetic counselling: For individuals with inherited diseases such as muscular dystrophies, genetic counselling can be beneficial. Understanding the genetic basis of the disease can help in developing targeted treatments and potentially preventing or delaying the onset of muscle fibre necrosis.
- Exercise caution with medical procedures and medications: Focal monophasic reactions can result from medical procedures like needle insertion, while multifocal monophasic reactions can be caused by exposure to myotoxic drugs or chemicals. It is important for healthcare providers to be aware of these risks and take appropriate measures to minimise muscle damage during procedures and when prescribing medications.
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Frequently asked questions
Muscle fibre necrosis is the death of muscle fibres, which is a key feature of inflammatory myopathies. It can be caused by numerous types of injury, including trauma, ischemia, infectious agents, and myotoxins.
The four categories of muscle necrosis are focal monophasic reactions, multifocal monophasic reactions, focal polyphasic reactions, and multifocal polyphasic reactions.
Under a microscope, muscle fibre necrosis is characterised by swollen, deeply eosinophilic, homogeneous myofibers that lack cross striations (hyalinization).
