Classification
The common type is sIBM; it strikes individuals apparently at random. There is a type that has been observed in multiple siblings in the same generation in several families, termed familial inflammatory sIBM, but it is not passed on from generation to generation. There are also several very rare forms of hereditary inclusion body myopathy (hIBM) that are linked to specific genetic defects and that are passed on from generation to generation, each inherited in different ways. Management
There is no standard course of treatment to slow or stop the progression of the disease as of 2019. sIBM patients do not reliably respond to anti-inflammatory, immunosuppressant, or  immunomodulatory medications. Most of disease management is supportive care. Prevention of falls is an important consideration. There is no consensus on exercise guidelines; however, physical therapy is recommended to teach the patient a home exercise program, to teach how to compensate during mobility-gait training with an assistive device, transfers and bed mobility. An exercise regimen preferentially minimizes a patients risk of injury and corresponds to the patients goals. Other related disorders
When sIBM was originally described, the major feature noted was muscle inflammation. Two other disorders were also known to display muscle inflammation, and sIBM was classified along with them.
sIBM is a challenge to the pathologist and even with a biopsy, diagnosis can be ambiguous.A diagnosis of inclusion body myositis was historically dependent on muscle biopsy results. Antibodies to cytoplasmic 5-nucleotidase (cN1A; NT5C1A) have been strongly associated with the condition. However, other inflammatory conditions, such as lupus, can have a positive anti-NT5C1A. As of 2019, it remains to be established whether a positive anti-NT5C1A antibody test can make muscle biopsy unneeded. Muscle imaging can help establish the pattern of muscle involvement and selection of a biopsy site. Differential diagnosis
IBM is often initially misdiagnosed as polymyositis. A course of prednisone is typically completed with no improvement and eventually, sIBM is confirmed. sIBM weakness comes on over months or years and progresses steadily, whereas polymyositis has an onset of weeks or months. Muscular dystrophy (e.g. limb girdle muscular dystrophy) must be considered as well. sIBM can be mistaken for physical deconditioning.Hereditary myopathies can mimic sIBM, both in signs and symptoms and in the appearance of muscle biopsies. A small percentage of those initially diagnosed with sIBM are later found to have pathogenic mutations in the genes VCP and SQSTM1, which are known to cause hIBM.IBM has a distinctive pattern of muscle involvement that distinguishes it among inflammatory myopathies. Characteristic of IBM is weakness of finger flexion, knee extension, and ankle dorsiflexion. Other inflammatory myopathies cause a proximal muscle weakness pattern, such as weakness of hip flexion, abduction, and extension, as well as shoulder abduction. IBM and other inflammatory myopathies both cause bicep/tricep weakness.