ISSN: 2165-7890
Short Communication - (2025)Volume 15, Issue 4
Autism Spectrum Disorder (ASD) is increasingly recognized not only as a neurodevelopmental condition but also as one associated with unique systemic health comorbidities. Among these comorbidities, bone health is often overlooked and undertreated. Multiple studies have reported that individuals with ASD exhibit reduced Bone Mineral Density (BMD), a higher prevalence of osteoporosis, and increased fracture risk compared to neurotypical peers [1-4]. Management of bone health becomes particularly important when considering the risk of vertebral compression fractures, including Vertebra Plana Fractures (VPF), that often present with pain, deformity, and functional decline.
In our recent study on vertebra plana fractures, we highlighted the clinical nuances of identifying and managing these severe vertebral injuries [5]. Within the context of ASD, the implications of VPF are significant; diminished bone strength increases susceptibility to vertebral collapse, and communication or sensory processing differences may obscure recognition and timely diagnosis of fracture-related pain.
Several contributing factors compound the risk of delayed diagnosis and treatment of VPF in ASD populations.
Reduced physical activity
Many individuals with ASD engage in reduced levels of weightbearing exercise due to motor coordination difficulties, sensory sensitivities, or restricted interests. This limits optimal bone mineralization during critical growth periods [1,2,6].
Nutritional challenges
Feeding difficulties, food selectivity, and gastrointestinal comorbidities predispose this patient population to calcium, vitamin D, and protein deficiencies. These deficiencies compound the risk of low BMD [1,2].
Medication effects
Long-term use of anticonvulsants, antipsychotics, and selective serotonin reuptake inhibitors (SSRIs) can negatively impact osteogenesis, either through direct effects on bone remodeling or by inducing weight gain and reduced mobility [3,7].
Motor and sensory impairments
Altered gait mechanics, balance deficits, and proprioceptive challenges increase fall risk. Even minor falls in individuals with low BMD may precipitate vertebral or long bone fractures [4,6,8].
Communication barriers
Perhaps the most detrimental barrier is under-reporting of pain. Even high-functioning individuals with ASD may have atypical pain perception or limited ability to articulate discomfort. Pain may manifest as behavioral changes, irritability, or functional regression. These communication barriers contribute to delayed recognition of fractures and suboptimal pain management [9-11].
These factors culminate to create a clinical scenario in which patients with ASD are at higher risk for severe vertebral injury, including VPF, and may not receive timely evaluation or treatment. For clinicians treating patients with ASD, awareness of these unique comorbidities and unique diagnostic challenges is critical. Vertebral fractures in ASD may present as behavioral changes, decline in mobility, or nonspecific discomfort rather than overt pain complaints.
Moving forward, a multidisciplinary approach is required. Preventative strategies should include bone health screening, attention to diet and supplementation, promotion of safe physical activity, and close monitoring of medication side effects on BMD. Clinicians must also adopt a high index of suspicion for vertebral fractures in ASD patients presenting with unexplained pain, behavioral regression, or changes in posture.
The findings of our study underscore the need to bridge the fields of autism research, bone health, and pain medicine. By recognizing the heightened risk of VPF and other fractures in this population, we can improve diagnostic accuracy and timeliness, enhance quality of life, and tailor pain management strategies to a vulnerable patient population that often faces unique diagnostic challenges.
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Citation: Komachkov Z, Javed S (2025). Bone Health, Vertebral Fractures and Pain in Autism: An Overlooked Intersection. Autism-Open Access. 15:439.
Received: 07-Oct-2025, Manuscript No. AUO-25-38818 ; Editor assigned: 09-Oct-2025, Pre QC No. AUO-25-38818 (PQ); Reviewed: 23-Oct-2025, QC No. AUO-25-38818; Revised: 30-Oct-2025, Manuscript No. AUO-25-38818 (R); Published: 06-Nov-2025 , DOI: 10.35248/2165-7890.25.15.439
Copyright: © 2025 Komachkov Z, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.