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Bone Health in Children with Rheumatic Disorders: Focus on Molecular Mechanisms, Diagnosis, and Management
Francesca Di Marcello1, Giulia Di Donato1, Debora Mariarita d'Angelo1
1Department of Pediatrics, University of Chieti, 66100 Chieti, Italy.
Insights
Bone health is influenced by genetics, nutrition, and activity, impacting peak bone mass. Chronic diseases like juvenile arthritis can cause secondary osteoporosis in children, increasing fracture risk.
Area of Science:
- Bone biology and metabolism
- Skeletal homeostasis
- Pediatric bone health
Background:
- Bone is a dynamic tissue influenced by hormonal, mechanical, nutritional, immunological, and pharmacological factors.
- Genetic factors and lifestyle (nutrition, physical activity) are critical for achieving peak bone mass, which influences adult bone health and fracture risk.
- Secondary osteoporosis is a significant concern in children with chronic diseases, particularly autoimmune disorders like juvenile idiopathic arthritis.
Purpose of the Study:
- To discuss molecular mechanisms of skeletal homeostasis.
- To explore the impact of inflammation and chronic disease on bone metabolism in children.
- To highlight the importance of a standardized diagnostic and management approach for at-risk children.
Main Methods:
- Review of molecular mechanisms governing skeletal homeostasis.
- Analysis of factors contributing to reduced bone strength in chronic pediatric diseases.
- Discussion of clinical observations in juvenile arthritis patients regarding bone density and fracture patterns.
Main Results:
- Systemic inflammation, nutritional deficiencies, medication side effects (e.g., glucocorticoids), and delayed puberty contribute to reduced bone strength in children with chronic diseases.
- Osteoporosis in juvenile arthritis often affects the femoral neck and radius, but vertebral fractures are also a concern, especially with glucocorticoid use.
- A standardized approach to musculoskeletal assessment, prophylaxis, therapy, and follow-up is crucial for at-risk children.
Conclusions:
- Inflammation and chronic diseases significantly disrupt bone metabolism and homeostasis in children.
- Early identification and management of secondary osteoporosis in pediatric patients are essential for preventing long-term skeletal complications.
- Understanding the interplay between systemic disease and bone health is vital for optimizing pediatric skeletal care.
Abstract:
Bone is an extremely dynamic and adaptive tissue, whose metabolism and homeostasis is influenced by many different hormonal, mechanical, nutritional, immunological and pharmacological stimuli. Genetic factors significantly affect bone health, through their influence on bone cells function, cartilage quality, calcium and vitamin D homeostasis, sex hormone metabolism and pubertal timing. In addition, optimal nutrition and physical activity contribute to bone mass acquisition in the growing age. All these factors influence the attainment of peak bone mass, a critical determinant of bone health and fracture risk in adulthood. Secondary osteoporosis is an important issue of clinical care in children with acute and chronic diseases. Systemic autoimmune disorders, like juvenile idiopathic arthritis, can affect the skeletal system, causing reduced bone mineral density and high risk of fragility fractures during childhood. In these patients, multiple factors contribute to reduce bone strength, including systemic inflammation with elevated cytokines, reduced physical activity, malabsorption and nutritional deficiency, inadequate daily calcium and vitamin D intake, use of glucocorticoids, poor growth and pubertal delay. In juvenile arthritis, osteoporosis is more prominent at the femoral neck and radius compared to the lumbar spine. Nevertheless, vertebral fractures are an important, often asymptomatic manifestation, especially in glucocorticoid-treated patients. A standardized diagnostic approach to the musculoskeletal system, including prophylaxis, therapy and follow up, is therefore mandatory in at risk children. Here we discuss the molecular mechanisms involved in skeletal homeostasis and the influence of inflammation and chronic disease on bone metabolism.
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