Proliferative Myositis

Another pseudosarcomatous lesion is proliferative myositis, a reactive fibroproliferative lesion of injured striated muscle.  Some authorities consider it to be an early stage of heterotopic ossification or myositis ossificans, while others consider it to be a separate clinical and histopathologic entity. As with nodular fasciitis, accurate microscopic diagnosis is extremely important. In some investigations, more than 40% of proliferative myositis cases have been erroneously diagnosed as sarcoma, especially rhabdomyosarcoma.  This reactive lesion is usually seen in the flat muscles of the shoulder girdle, but occasionally presents in the head and neck region, particularly in the sternocleidomastoid muscle.  It was first described by Kern in 1960.

Proliferative myositis of the oral region is a rapidly enlarging, immovable, perhaps tender submucosal mass. Children are rarely affected and the typical patient is 45-65 years of age at tumor onset.  There is a slight female predilection. The lesion is usually 1.5-5.0 cm. in greatest dimension at the time of diagnosis and involves the muscle in a diffuse, infiltrative fashion.

This lesion appears almost scar-like on gross examination, with a poorly circumscribed periphery and a grayish-white cut surface. Microscopically, plump fibroblast-like cells are the predominant cell type, but giant ganglion-like cells with deeply staining basophilic cytoplasm and prominent nucleoli are the hallmark of proliferative myositis. These cells are also myofibroblasts but are often so bizarre as to impart a strong similarity to rhabdomyosarcoma or other sarcoma. Likewise, atrophic or degenerated muscle cells may contribute to the overall impression of striated muscle malignancy.

Fibrosis is seen to involve the endomysium, perimysium and epimysium. Lesional cells are immunoreactive for vimentin, actin, smooth-muscle actin, factor XIIIa, and fibronectin, and are usually not reactive for desmin or myosin.  Occasionally, however, they will also react for desmin and myosin. Ultrastructurally, they appear to be myofibroblasts.  Focal ossification or dystrophic calcification may be observed in some cases, but never is it as pronounced as in heterotopic ossification.

Spontaneous regression and disappearance has been rarely reported. Treatment of this self-limiting lesion is conservative surgical excision and recurrence should not be expected.  The major prognostic difficulty is the arrival at a correct diagnostic interpretation of the tissue, hence, recurrent lesions should be carefully evaluated for an alternative diagnosis.

Ushigome S, Takakuwa T, Takagi M, et al. Proliferative myositis and fasciitis. Report of five cases with an ultrastructural and immunohistochemical study. Acta Pathol Jpn 1986; 36:963.

Dent CD, DeBoom GW, Hamlin ML. Proliferative myositis of the head and neck. Report of a case and review of the literature. Oral Surg Oral Med Oral Pathol 1994; 78:354-358.

Turner R, Robson A, Motley R. Proliferative myositis - an unusual cause of multiple subcutaneous nodules. Clin Exper Dermatol 1997; 22:101-103.