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Skeletal Muscle - Inflammation

Image of inflammation in the skeletal muscle from a female Swiss CD-1 mouse in a chronic study
Skeletal muscle - Inflammation, Acute in a female Swiss CD-1 mouse from a chronic study. A neutrophilic infiltrate has led to necrosis and loss of muscle fibers.
Figure 1 of 8
Image of inflammation in the skeletal muscle from a female Swiss CD-1 mouse in a chronic study
Skeletal muscle - Inflammation, Acute in a female Swiss CD-1 mouse from a chronic study (higher magnification of Figure 1). There is loss of muscle fibers and a hypereosinophilic degenerative fiber (arrow).
Figure 2 of 8
Image of inflammation in the skeletal muscle from a male B6C3F1/N mouse in a chronic study
Skeletal muscle - Inflammation, Suppurative in a male B6C3F1/N mouse from a chronic study. A localized collection of intact and degenerating neutrophils is present in the muscle.
Figure 3 of 8
Image of inflammation in the skeletal muscle from a male B6C3F1/N mouse in a chronic study
Skeletal muscle - Inflammation, Suppurative in a male B6C3F1/N mouse from a chronic study (higher magnification of Figure 3). There is a localized collection of intact and degenerating neutrophils, as well as early neutrophilic infiltration between adjacent muscle fibers.
Figure 4 of 8
Image of inflammation in the skeletal muscle from a female F344/N rat in a chronic study
Skeletal muscle -Inflammation, Chronic in a female F344/N rat from a chronic study. A mixed mononuclear cellular response is associated with degeneration and loss of muscle fibers.
Figure 5 of 8
Image of inflammation in the skeletal muscle from a female F344/N rat in a chronic study
Skeletal muscle - Inflammation, Chronic in a female F344/N rat from a chronic study (higher magnification of Figure 5).
Figure 6 of 8
Image of inflammation in the skeletal muscle from a male Sprague Dawley rat in a subchronic study
Skeletal muscle - Inflammation, Granulomatous in a male Sprague Dawley rat from a subchronic study. A mixture of mononuclear cells, along with multinucleated giant cells, has replaced muscle fibers, and muscle fiber degeneration and mineralization within multinucleated giant cells (arrows) can be seen in the area of inflammation.
Figure 7 of 8
Image of inflammation in the skeletal muscle from a male Tg.Ac (FVB/N) mouse in a subchronic study
Skeletal muscle - Inflammation, Chronic-active in a male Tg.Ac (FVB/N) homozygous mouse from a subchronic study. A circumscribed area of granulomatous inflammation with multinucleated giant cells (arrow) and neutrophils within an extensive area of chronic-active inflammation surrounds a foreign body consistent with plant material.
Figure 8 of 8
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comment:

Inflammation of skeletal muscle can occur as a result of numerous types of injury, including physical trauma (e.g., injection sites, bite wounds, and blunt trauma), exposure to myotoxins or infectious agents, and ischemia, thrombosis, or myofiber necrosis. Inflammation can exhibit various morphologic patterns. It can be primarily interstitial, with little or no myofiber necrosis, or can be the predominant feature, with little inflammation.

In NTP studies, there are five standard categories of inflammation: acute, suppurative, chronic, chronic-active, and granulomatous; abscesses are diagnosed as suppurative inflammation. In acute inflammation ( Figure 1image opens in a pop-up window and Figure 2image opens in a pop-up window ), the predominant infiltrating cell is the neutrophil, though fewer macrophages and lymphocytes may also be present. There may also be evidence of edema or hyperemia. The neutrophil is also the predominant infiltrating cell type in suppurative inflammation ( Figure 3image opens in a pop-up window and Figure 4image opens in a pop-up window ), but the neutrophils are aggregated, and many of them are degenerate (suppurative exudate). Cell debris (both from the resident cell populations and from infiltrating leukocytes); proteinaceous fluid containing fibrin, fewer macrophages, occasional lymphocytes, and/or plasma cells; and possibly an infectious agent may also be present within the exudate. Grossly, these lesions would be characterized by the presence of pus. In the tissue surrounding the exudate, there may be fibroblasts, fibrous connective tissue, and mixed inflammatory cells, depending on the chronicity of the lesion. Lymphocytes predominate in chronic inflammation. Lymphocytes also predominate in chronic-active inflammation, but a significant number of neutrophils are also present ( Figure 5image opens in a pop-up window and Figure 6image opens in a pop-up window ). Both lesions may contain macrophages. Granulomatous inflammation is another form of chronic inflammation, but this diagnosis requires the presence of a significant number of aggregated, large, activated macrophages, epithelioid macrophages, or multinucleated giant cells ( Figure 7image opens in a pop-up window and Figure 8image opens in a pop-up window ).

Since inflammation can occur in response to, or result in, myofiber necrosis, myopathic changes in addition to edema and/or hemorrhage often occur concurrently. An inflammatory response is necessary to effectively repair damaged tissues; however, the nature, duration, and intensity of this response will crucially influence the overall outcome of repair.

recommendation:

Inflammation should be diagnosed and graded whenever it is considered a primary lesion. It may be diagnosed as a secondary lesion (e.g., secondary to necrosis) if it is particularly severe or more severe than expected relative to the severity of the primary lesion. The diagnosis should include the type of inflammation (e.g., acute, chronic, chronic-active) as a modifier. Generally it is not necessary to include a site modifier unless it is needed to separate two distinct lesions. Associated lesions, such as vascular lesions, foreign bodies, or infectious agents, should be diagnosed separately. Lesions secondary to the inflammation (e.g., necrosis) and lesions that are part of the inflammatory process (e.g., edema or hemorrhage) should not be diagnosed separately unless warranted by severity but should be described in the pathology narrative.

references:

Berridge BR, Van Vleet JF, Herman E. 2013. Cardiac, vascular, and skeletal muscle systems. In: Haschek and Rousseaux’s Handbook of Toxicologic Pathology, 3rd ed (Haschek WM, Rousseaux CG, Wallig MA, Bolon B, Ochoa R, Mahler MW, eds). Elsevier, Amsterdam, 1635-1665.

Greaves P. 2007. Musculoskeletal system. In: Histopathology of Preclinical Toxicity Studies, 3rd ed. Elsevier, Oxford, 160-214.

Greaves P, Seely JC. 1996. Non-proliferative lesions of soft tissues and skeletal muscle in rats, MST-1. In: Guides for Toxicologic Pathology. STP/ARP/AFIP, Washington, DC.

Greaves P, Chouinard L, Ernst H, Mecklenburg L, Pruimboom-Brees IM, Rinke M, Rittinghausen S, Thibault S, von Erichsen J, Yoshida T. 2013. Proliferative and non-proliferative lesions of the rat and mouse soft tissue, skeletal muscle, and mesothelium. J Toxicol Pathol 26(3 suppl):1S-26S.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/25035576

Leininger JR. 1999. Skeletal muscle. In: Pathology of the Mouse (Maronpot R, Boorman G, Gaul BW, eds). Cache River Press, St Louis, 637-643.

Mann CJ, Perdiguero E, Kharraz Y, Aguilar S, Pessina P, Serrano AL, Muñoz-Cánoves P. 2001. Aberrant repair and fibrosis development in skeletal muscle. Skelet Muscle 1:21.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/21798099

McDonald MM, Hamilton BF. 1990. Bones, joints, and synovia. In: Pathology of the Fischer Rat: Reference and Atlas (Boorman G, Eustis SL, Elwell MR, Montgomery CA, MacKenzie WF, eds). Academic Press, San Diego, 193-207.

Percy DH, Barthold SW. 2007. Mouse. In: Pathology of Laboratory Rodents and Rabbits, 3rd ed. Blackwell, Ames, IA, 88-89.

Vahle JL, Leininger JR, Long PH, Hall DG, Ernst H. 2013. Bone, muscle, and tooth. In: Toxicologic Pathology: Nonclinical Safety Assessment (Sahota PS, Popp JA, Hardisty JF, Gopinath C, eds). CRC Press, Boca Raton, FL, 561-587.

Van Vleet JF, Valentine BA. 2007. Muscle and tendon. In: Jubb, Kennedy, and Palmer’s Pathology of Domestic Animals, 5th ed, Vol 1 (Grant MG, ed). Elsevier, Edinburgh, 185-280.

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Web page last updated on: March 13, 2015