A lipoma is the most common type of soft tissue tumor and solitary lipomas have been classified into two types; cutaneous/superficial and deep-seated/subfascial. In spite of some descriptions about superficial lipomas [8
], little is known about the etiology or histogenesis of intramuscular lipomas, which are the deep-seated type. Intramuscular and intermuscular lipomas are relatively rare as compared to superficial lipomas, and have been reported to comprise 1.8% and 0.3% of all fatty tumors, respectively [9
]. Microscopically, an intramuscular lipoma is composed of mature lipocytes, the same as lipomas found in other areas. Macroscopically, intramuscular lipomas are not always as well circumscribed as the superficial type and such cases have been designated as infiltrating lipomas. Fletcher and Martin-Bates noted that an intramuscular lipoma could also be subdivided into infiltrative and well-circumscribed types [7
], however, the factors contributing to these variations are not well understood.
Fat cell overgrowth due to muscular damage is not uncommon and has been reported in several orthopedic diseases such as muscular dystrophy [10
] and rheumatoid arthritis [11
], as well as other joint diseases and various neuropathies [3
]. The present study was performed to investigate the association between lipomatous cell growth and surrounding muscular degeneration in intramuscular lipomas, and evaluate the contribution of focal muscular atrophy to the infiltrating growth of these tumors.
Interestingly, type-selective muscle fiber atrophy or degenerative change was found in 70% of the present tumors (11/17 cases), most of which (10/11 case) were the infiltrating type. Type-selective muscle involvement in these 11 cases strongly suggests that they have had any neurogenic or myogenic disorders, [4
] at the focal lesions, and endomysial fat overgrowth could be explained as a result of muscle involution. Type-selectivity was not the same in these 11 cases and the fundamental disease mechanism seems to be heterogeneous. Further, increases of immunoreactivity to cathepsin-D, a lysosomal catabolic enzyme, was corresponded to the degree of degenerative or atrophic changes in these specimens, and ultrastructural analysis also revealed degeneration in the surrounding muscle fibers of the lesion.
The main factor determining the differences in muscle pathology between the various disorders is the time course, and chronic or longstanding disorders offer more opportunity various histological aspects than those that are rapidly progressive. The relatively big size and the longstanding of the intramuscular lipomas might be promoting disuse atrophy in the surrounding muscle fibers, and rarely muscle type-selective atrophy. An intramuscular lipoma itself may cause the surrounding muscle atrophy due to compressive growth, but such a case of muscle atrophy will often likely be presented without muscle types-selectivity. Neither cathepsin-D reactivity nor muscle types-selectivity was found in the control sections of our study, i.e., traumatic muscles. Our immunohistochemical analyses revealed type-selective muscular atrophy in a majority of the present intramuscular lipomas, suggesting any association of focally neurogenic or myogenic disorders in the lesions. Ultrastructural analysis revealed degenerative findings of the surrounding muscle, but could not demonstrate any specific findings involved with neurogenic or myogenic disorders. Patterns in the involved muscle fibers in the intramuscular lipomas could be divided into different groups and it was presumable that pathogenic mechanisms of the involved muscular degeneration were heterogeneous. As a results of these focally muscular atrophy, the endomysial fatty over growth in the involving muscles could modulate the infiltrating growth of an intramuscular lipoma into the surrounding muscular tissues. In the present study, surgically and histologically proven intramuscular lipomas were analyzed, and only one case was available to evaluate ultrastructurally. Unfortunately, neuromuscular junction or nerve bundles were not included in the ultrastructural specimens, and the involvement of neurogenic factors with the pathogenesis could not be estimated. In a future report, the primary cause of focal muscle involution should be made clearly.