The current patient s case highlights the intricate relationship between systemic health and dental pathology. Delayed supplementation and complex clinical presentations both posed a challenge to achieving complete healing of the patient s lesions. Monitoring of patient progression and metabolic parameters was recommended to the patient s endocrinologist (the evaluation of treatment utilized since 2018 for this condition) to gain insights into the impact of vitamin deficiency on healing outcomes. Burosumab, a monoclonal antibody targeting the FGF23 receptor, blocks its overexpression to normalize the concentrations of calcium, vitamin D, and phosphorus 1617.

As mentioned at the beginning of this case report, there are other forms of rickets, which are summarized in Table 2 and Table 3. These include vitamin D-dependent rickets (Table 2), which are characterized by disorders in the biosynthesis of vitamin D or its receptor activity, resulting in vitamin D deficiency (type 1A (VDDR1A) and type 1B (VDDR1B)) or resistance (type 2A (VDDR2A) and type 2B (VDDR2B)). All vitamin D dependent rickets present with similar clinical and biochemical manifestations, including findings related to hypocalcemia (irritability, fatigue, muscle cramps, and seizures) and rickets (craniotabes, delayed closure of fontanelles, frontal bossing, enlarged wrists, bowed legs, short stature, and bone pain) 1. Additionally, hypophosphatemic rickets (Table 3) can be categorized as FGF23-dependent (linked to a mutation in FGF23) or FGF23- independent (linked to a mutation in another protein involved in phosphate reabsorption in the kidneys) 1.