Periosteal Pathologic Conditions: Imaging Findings and Pathophysiology.

The periosteum plays a key role in bone health and is a primary means by which the skeleton responds to a wide range of insults, both benign and malignant. Developmental and histologic features of normal periosteum explain some of the characteristic imaging findings seen in the setting of bone abnormalities. Patterns of periosteal reaction, both in morphology and distribution, are key to distinguishing benign or physiologic periosteal reaction from types of periosteal reaction that warrant further evaluation. The authors review the histologic features, distribution, and development of normal periosteum. Nonaggressive and aggressive types of periosteal reaction are presented with key associations for each. The presence of nonaggressive types of periosteal reaction implies that the underlying process affecting the bone is slow enough that the periosteum is able to heal it or contain it in an organized manner. In contrast, aggressive types of periosteal reaction are seen when the underlying bone insult outpaces the ability of the periosteum to contain it. Image-guided biopsies of lesions with periosteal reaction should be used to sample the site of the most aggressive pattern, as this approach can aid in accurate histologic grading and in detection of tumor cells and bone matrix. The distribution of periosteal abnormalities is as important as the morphology, with a diffuse periosteal reaction favoring systemic causes such as rheumatologic, metabolic, and hematologic conditions compared with a more localized periosteal reaction. Important causes of localized and diffuse periosteal reaction are discussed in a systems-based format, with an emphasis on clinically important causes. © RSNA, 2022.

Dynamic epigenetic mechanisms regulate age-dependent SOX9 expression in mouse articular cartilage.

While the developmental role of the SOX9 transcription factor in chondrocyte differentiation and cartilage formation is well documented, age-dependent SOX9 expression in articular chondrocytes (ACs) and its regulatory mechanisms remain unclear. This study aimed to explore epigenetic regulatory mechanisms for age-related changes in SOX9 expression in ACs of mice, spanning from the developmental stage to 18 months of age. Sox9 mRNA and protein were highly expressed in ACs during joint development but significantly decreased after 2 months of age. Histopathological features of osteoarthritis were not observed in examined hip and shoulder joints by 18 months of age. Epigenetic studies revealed that DNA methylation levels were increased at specific CpG islands of the Sox9 gene at 6 and 12 months; treatment of cultured ACs from 6-month-old mice with 5-azacytidine (an inhibitor of DNA methylation) elevated the level of Sox9 expression in ACs by lowering DNA methylation levels in the Sox9 promoter region. Histone 3 lysine 4 dimethylation (H3K4me2, a histone modification for transcriptional activation) in the Sox9 promoter region was decreased with age, which was associated with the age-dependent decrease in SOX9 expression in ACs. Knockdown of lysine-specific demethylase-1 up-regulated SOX9 expression in ACs of adult mice through increased recruitment of H3K4me2 in the Sox9 promoter region. Our results suggest that SOX9 expression in mouse ACs is significantly decreased after the completion of joint development. These age-dependent changes in SOX9 expression are dynamically regulated by DNA methylation and histone methylation.