Coagulating Gland - Inflammation

Image of acute inflammation in the coagulating gland from a male B6C3F1 mouse in a chronic study
Coagulating Gland - Inflammation. Acute inflammation in a male B6C3F1 mouse from a chronic study.
Figure 1 of 4
Image of acute inflammation in the coagulating gland from a male Wistar rat in a chronic study
Coagulating Gland - Inflammation. Acute inflammation in a male Wistar rat from a chronic study.
Figure 2 of 4
Image of inflammation in the coagulating gland from a male Swiss CD-1 mouse in a chronic study
Coagulating Gland - Inflammation. Abscesses in a male Swiss CD-1 mouse from a chronic study.
Figure 3 of 4
Image of chronic to chronic-active inflammation in the coagulating gland from a male F344/N rat in a chronic study
Coagulating Gland - Inflammation. Chronic to chronic-active inflammation in a male F344/N rat from a chronic study.
Figure 4 of 4
next arrow

comment:

Inflammation of the coagulating gland can be acute ( Figure 1image opens in a pop-up window and Figure 2image opens in a pop-up window ), form abscesses ( Figure 3image opens in a pop-up window ), or be chronic to chronic-active ( Figure 4image opens in a pop-up window ). In acute inflammation, the cellular infiltrates are present in the glandular epithelium, stroma, and secretion. In chronic inflammation, the stroma is expanded by mixed cellular exudate, fibroblasts, and collagen. Squamous metaplasia may accompany inflammation in some cases. Coagulating gland inflammation may occur as an incidental finding and is usually unrelated to administration of xenobiotics.

NTP studies have five standard categories of inflammation: acute, suppurative, chronic, chronic-active, and granulomatous. In acute inflammation, 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, but they are aggregated, and many of them are degenerate (suppurative exudate). Cell debris from both the resident cell populations and infiltrating leukocytes, proteinaceous fluid containing fibrin, fewer macrophages, occasional lymphocytes or plasma cells, and, possibly, an infectious agent may also be present in the exudate. Grossly, these lesions would be characterized by the presence of pus. The tissue surrounding the exudate may have 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 there are also a significant number of neutrophils. 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.

recommendation:

Whenever present, inflammation should be diagnosed, classified, and graded. Secondary changes such as squamous metaplasia do not require a separate diagnosis unless warranted by their degree of severity. When both glands are involved, the diagnosis should be qualified as bilateral and the severity based on the more severely affected gland.

references:

Arai Y, Mori T, Suzuki Y, Bern HA. 1983. Long-term effects of perinatal exposure to sex steroids and diethylstilbestrol on the reproductive system of male mammals. Int Rev Cytol 84:235-268.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/6358105

Boorman GA, Elwell MR, Mitsumori K. 1990. Male accessory sex glands, penis, and scrotum. In: Pathology of the Fischer Rat: Reference and Atlas (Boorman GA, Eustis SL, Elwell MR, Montgomery CA, MacKenzie WF, eds). Academic Press, San Diego, 419-428.
Abstract: http://www.ncbi.nlm.nih.gov/nlmcatalog/9002563

Bosland MC. 1992. Lesions in the male accessory glands and penis. In: Pathobiology of the Aging Rat, Vol 1 (Mohr U, Dungworth DL, Capen CC, eds). ILSI Press, Washington, DC, 443-467.
Abstract: http://catalog.hathitrust.org/Record/008994685

Creasy D, Bube A, de Rijk E, Kandori H, Kuwahara M, Masson R, Nolte T, Reams R, Regan K, Rehm S, Rogerson P, Whitney K. 2012. Proliferative and nonproliferative lesions of the rat and mouse male reproductive system. Toxicol Pathol 40:40S-121S.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/22949412

Suwa T, Nyska A, Peckham JC, Hailey JR, Mahler JF, Haseman JK, Maronpot RR. 2001. A retrospective analysis of background lesions and tissue accountability for male accessory sex organs in Fischer-344 rats. Toxicol Pathol 29(4):467-478.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/11560252

Suwa T, Nyska A, Haseman JK, Mahler JF, Maronpot RR. 2002. Spontaneous lesions in control B6C3F1 mice and recommended sectioning of male accessory sex organs. Toxicol Pathol 30(2):228- 234.
Abstract: http://www.ncbi.nlm.nih.gov/pubmed/11950166