The authors report a case of a late repair of a missed, large, osteochondral fracture of the femoral trochlea in a 14-year-old boy due to lateral patellar dislocation after a twisting injury of the knee a year ago. The late—1 year after the knee injury—imaging assessment of the patient regarding radiograph images, CT scan, and MRI was misleading, misinterpreted, and failed to reveal this osteochondral fracture. The free osteochondral fragment was detected during diagnostic arthroscopy. Open reduction and fixation of the osteochondral fragment with bioabsorbable pins were done, and healing was achieved within an acceptable time. The patient's clinical and imaging examination with knee MRI, a year after the surgical treatment, was highly satisfactory. Fixation with bioabsorbable pins showed to be a worthwhile option in this case. The technique used was straightforward, with excellent short- and long-term results. Bioabsorbable pins may be used to restore successfully even an old, large osteochondral fracture in the immature skeleton.

We report the case of an 11-year-old immunocompetent patient presenting with a 2-week history of upper back pain, diagnosed with thoracic vertebral osteomyelitis and a paraspinal abscess caused by Bartonella henselae. He was treated with gentamicin and doxycycline followed by oral rifampicin and doxycycline with favorable outcome.

A boy and his father with severe short stature, progressively evolving body asymmetry, and skeletal abnormalities are presented. A next-generation sequencing exome study was performed, and the patient was found heterozygous for the c.1609G>A (p.Gly537Ser) mutation in the <i>COL2A1</i> gene. This mutation is considered a pathogenic variant and has been previously registered in the Human Gene Mutation Database (HGMD) in association with spondyloepiphyseal dysplasia (accession: CM052184). It has been described in a patient as a sporadic case and resulted in a severe phenotype. Segregation studies, in order to determine the inheritance pattern, identified the same mutation in our patient's father. The variant was transmitted in an autosomal dominant pattern. In conclusion, we describe a patient with hereditary spondyloepiphyseal dysplasia congenita, caused by a c.1609G_A (p.Gly537Ser) mutation in the <i>COL2A1</i> gene, which resulted in a milder phenotype.

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