To the editor, A 39-year-old female achondroplastic patient was admitted to our outpatient clinic for her back and lower extremity pain. Her height and weight were 125 cm and 38 kg, respectively (Fig. 1). She had a body mass index of 24.3 kg/m. She had undergone leg lengthening on bilateral tibias when she was 12. On physical examination, she had bilateral paravertebral muscle spasm at her back. She also had painful hip internal rotation and knee flexion on both sides with bilateral positive Clarke’s sign. Her physical examination was otherwise noncontributory. X-ray examination revealed early degenerative changes, especially at the hip joints and strikingly osteopenia. On detailed questioning, it was understood that she had been advised to receive 300,000 IU vitamin D3 (the form of vitamin D available in our country) once a year and to exercise regularly for low bone density 2 years ago. The past two bone mineral density (BMD) measurements, performed by a single technician using dual-energy X-ray absorptiometry (DEXA) on a Lunar DPX-IQ scanner in our center, were analyzed, and a new BMD measurement was performed under similar conditions with the ones referred above (Table 1, Fig. 2). The laboratory tests was as follows: serum total calcium, 9.3 mg/dl (8.2–10.6); inorganic phosphate, 3.2 mg/dl (2.5–4.5); alkaline phosphatase (ALP), 47 U/l (30–126); type 1 collagen C terminal telopeptide (CTX), 0.253 (25–573); osteocalcin, 3.46 ng/ml (3.1–13.7); parathormone, 34.23 pg/ml (15–65), and vitamin D3, 20.1 ng/ml (>30). Risk factor examination for low bone density yielded no results. Low bone density was considered as a consequence of altered bone metabolism due to achondroplasia. She was prescribed 300,000 IU oral vitamin D3 and recommended to continue on her exercises. She was also included in a physical therapy program for her symptoms due to degenerative changes. Achondroplasia is the most common form of skeletal dysplasias. A spontan or inherited mutation in the fibroblast growth factor receptor 3 (FGFR3) gene on the fourth chromosome brings out the disease [1]. The primary defect is abnormal endochondral ossification [2]. It has a number of wellknown neuromusculoskeletal manifestations [3]. Recently, Arita et al. reported low bone density, diagnosed with spinal BMD analysis and panoramic radiographic measurements, in 5 of 11 achondroplastic patients for the first time in the literature [4]. To the best of our knowledge, our report is the second one referring the relationship between