The complications of classic celiac disease listed on pages 839 and 843 of the article include osteoporosis (1). This is correct only if it refers to the symptom of a reduction in bone minerals confirmed by densitometry, not the symptoms of osteoporosis. In adult medicine, this differentiation is important (2– 4). In my experiences in bone histology, active, untreated celiac disease leads to clear vitamin D and calcium deficiencies, as a result of malabsorption. According to the extent of this deficiency, what follows is a bone mineralization disorder in the sense of volume osteoidosis. However, this is not associated with a volume deficit of the entire bone tissue. Osteoidosis alone usually heals without causing further complications, in tandem with the celiac disease. Patients with severe, long-term calcium deficiency will experience, in addition to osteoidosis, reactive fibro-osteoclasia as a feature of secondary hyperparathyroidism. Both bone changes lead to the clinical picture of mixed intestinal osteopathy. This can ultimately result in sustained volume deficits of the bones. In older patients with mixed intestinal osteopathy who have been treated for celiac disease and in whom the celiac disease has become inactive, a structural deficit corresponding to osteoporosis can be interpreted as “residual bone damage” if mineralization levels are normal. Osteoporosis is a pathogenetically different disease entity and can be linked to celiac disease only in terms of a differential diagnosis. Osteoporosis and osteomalacia should always be distinguished from one another, since they require completely different therapeutic strategies. For this reason, the term that should be used in connection with the complications of active celiac disease is that of osteomalacia, which is pathogenetically appropriate, and not osteoporosis.