While the definitive etiology is unknown, RMH is believed to be derived from aberrant embryonic migration of mesodermal tissue and the presence of a disorganization gene found in mouse models [2,5]. The striated muscle component is believed to be comprised of superficial muscular aspects originating from the second branchial arch which underwent erroneous migration, resulting in characteristic striated muscle bundles just below the epidermis [3,7]. More recently, elongation hyperplasia of striated muscles has been described as a potential etiology of adult-onset RMH.

RMH usually presents as a flesh-colored, pedunculated lesion or nodule, but can also be seen as a papule that may be subcutaneous or sessile. Most (88.2 %) of the reported lesions have been localized to areas with immediately underlying striated muscle on the head and neck region [7]. At least 14 cases in the literature have specified RMH to have occurred on the chin specifically, as observed in our patient [3,6]. The proximity of the mentalis and platysma muscles in the mandible to the subcutaneous tissue, leading to direct confluence with the dermis likely offers anatomical predisposition to the development of RMH [3,6]. Other lesions in the literature have been detected on the sacral area, hallux, digits, orbit, anus, chest, back, and vagina [1,2,4,8]. 

More recently, the literature has made efforts to classify RMH according to age demographics; congenital type (in those under 18 years of age) or acquired type (in those above 18 years of age). A nodular-type lesion morphology predominates in congenital RMH (74%), while plaque-type composition (43.8%) is more common in acquired RMH [3]. Among reported cases in the literature, it is becoming evident that the chin is a common location for acquired RMH (43.8%) [3].

In addition to distinguishing clinical morphologies in congenital and acquired RMH, more recently, differentiating histopathologic patterns have also been recognized. All RMH tumors display a histologically normal epithelium and papillary dermis, with a disorganized reticular dermis. In congenital RMH, the reticular dermis and subcutaneous layers often (80%) contain a predominance of highly differentiated skeletal muscle, mesenchymal elements (adipose tissue, sclerotic collagen bundles, elastic fibers, and blood vessels), and occasional neural elements. Acquired plaque type usually features solely skeletal muscle fiber dermal proliferation, with no other mesenchymal tissue propagation.³ A minority (33%) of acquired RMHs have been observed to display hamartomatous proliferation with alternative mesenchymal elements in addition to striated skeletal muscle [3]. However, hamartomatous proliferation of multiple types of mesenchymal elements has only been observed in acquired nodular RMH (75%) [3]. Therefore, our case represents a unique variant of acquired plaque type RMH with hamartomas proliferation of multiple mesenchymal elements in addition to skeletal muscle fibers. This is notable, as the acquired plaque type is expected to solely comprise striated skeletal muscle on histology, and a heterogenous mesenchymal composition is also less commonly observed in adult-onset RMH [3,6].

RMH has a favorable prognosis in adults and no risks for complications following treatment in these patients. Although treatment is not necessary unless lesions become symptomatic, surgery is the main treatment for RMH, though laser treatments have been described [9]. Some RMH lesions spontaneously regress, and treated lesions show no recurrence [2]. It is recommended to observe subcutaneous and plaque‐type variants where removal is not easily executed [6].