## 8 Specific Groups
Screening for low BMD can be performed as stated before (in the section on screening). In PIMD, it is almost without exception impossible to adequately treat the underlying disease. Following this, it is paramount to optimally treat all of the independent factors associated with low BMD. Regarding vitamin D and calcium, the recommendations mentioned in the Section 5 are valid. To adequately treat feeding difficulties, we recommendthe early involvement of a multidisciplinary team, including a pediatric dietician and speech therapist. All anticonvulsants have been, either clinically or preclinically, associated with disturbances in bone metabolism. However, enzyme-inducing anticonvulsants such as phenytoin and carbamazepine have been shown to carry a higher risk, possibly due to inducing vitamin D metabolism [82]. Multiple and prolonged anticonvulsant use (>2 years) is also associated with a higher fracture risk [83]. As in antibiotics, restraint anticonvulsant use should be considered to limit the risk of fragility fractures/low BMD. As gastro-esophageal reflux tends to diminish over time, decreasing or discontinuing proton pump inhibitors could also contribute. Lastly, systemic progestin-only contraceptives should be replaced with alternatives also containing estrogen. Considering immobilization, loading exercises conducted by a physical therapist experienced in children with PIMD are important. Prevention of contractures should also deserve attention to maintain mobility and facilitate imaging options. Aids, such as a standing frame implemented by a pediatric rehabilitation specialist, have also been shown to slightly improve BMD [84]. The Section 7 mentions osteoporosis treatment with bisphosphonate therapy. Neuromuscular disorders  
Children with neuromuscular disorders, including congenital myopathies and (congenital) muscular dystrophies, are at particular risk for reduced bone quality and, consequently, fragility fractures due to a combination of factors. Impaired mobility and altered musculoskeletal interaction reduce cortical thickness and prevent the preservation of the bone structure. Additionally, more myokines are expressed in atrophied muscles, leading to osteoclast differentiation and bone loss induction [85]. Further, children with a neuromuscular disease frequently experience nutritional issues due to swallowing problems and have decreased sun exposure, leading to a deficiency of calcium and vitamin D [86; 87; 88; 89]. Children with Duchenne muscular dystrophy are particularly at risk for decreased bone strength when treated with glucocorticoids [90], as mentioned before. Next, the number of falls increases, and the falling mechanism is altered in patients with neuromuscular diseases. Ambulant patients commonly report problems with walking, poor balance, frequent trips, and falls [91; 92]. Patients with neuromuscular diseases tend to have a different falling mechanism: they fall on their proximal bones because they are not fast enough to reach out their hands in order to break their fall [93]. This results in more frequent long-bone fractures of the long bone that are more proximally located (i.e., humerus, femur). It is essential to prevent long bone fractures in children with neuromuscular diseases as far as possible in order to optimize functional prognosis, quality of life, and survival [94; 95; 96]. There are clues that limb immobilization in patients with neuromuscular disease may cause more loss of muscle mass than in healthy subjects [97]. Fractures of the lower extremities might further lead to permanent loss of ambulance [96; 98]. Low bone strength can impair neuromuscular management and rehabilitation, including surgical treatments for scoliosis or foot deformities [99; 100]. Pain caused by long bone fractures negatively influences rehabilitative care and, consequently, survival [94; 101]. Routine assessment of bone quality in children with neuromuscular diseases is recommended.