Periostin deficiency leads to age-dependent craniofacial, dental, and skeletal morphological alterations in mice

Periostin is an extracellular matrix protein that is highly expressed in hard tissue-associated regions, including the periosteum and periodontal ligament, where it is essential for bone formation and craniofacial development. In this study, the aim was to clarify its functions in skeletal maintenance during aging by comparing periostin-deficient ( Postn −/− ) and wild-type ( Postn +/+ ) mice. Comprehensive micro-computed tomography analyses were performed on Postn −/− and Postn +/+ mice at 18 and 62 weeks of age to assess age-related changes in craniofacial and femoral morphologies. At 18 weeks, there were craniofacial abnormalities in Postn −/− mice, including the absence of the foramen-like structure on the ventral mandible, increased incisor curvature, and a reduction in pulp cavity size. With age, these alterations became more pronounced, with significant differences in the angulation of the upper incisors, vertical height of the mandibular body, progressive enamel defects that expanded across the surface of the maxillary and mandibular incisors, and further narrowing of the pulp cavity. Additionally, in Postn +/+ mice, there was an expected age-dependent reduction in bone volume fraction in the femur, but not in Postn −/− mice at 18 or 62 weeks, suggesting suppression of age-related trabecular deterioration. In contrast, aged Postn −/− mice had ectopic bone formation in the distal femur and around the knee joint, indicating aberrant ossification in the absence of periostin. Periostin deficiency induces alterations in craniofacial, dental, and skeletal morphologies during aging. Periostin is also required for normal trabecular remodeling. These findings underscore its essential role in skeletal integrity and provide insights into bone biology and aging-related tissue remodeling. • Age-dependent craniofacial and dental abnormalities in periostin-deficient mice. • Loss of foramen-like structures on the mandible caused by periostin deficiency. • Suppression of age-related bone loss in the femur of periostin-deficient mice. • Ectopic bone formation around the knee joint in aged periostin-deficient mice.