Idiopathic osteosclerosis in the jaws is often detected incidentally on dental radiographic examination and may resemble other radiopaque lesions or normal anatomical structures. This study aimed to evaluate the imaging characteristics of osteosclerosis on panoramic radiographs and cone-beam computed tomography (CBCT) to improve differential diagnosis. Fifty-nine lesions from 55 patients(32 male, 23 female, mean age 29yrs±15) were retrospectively analyzed for location, shape, border, and internal structure on panoramic images, and for external contour, size, radiodensity, and cortical bone relationship on CBCT images. Most lesions were smaller than 10 mm, lacked a radiolucent border, and showed variable internal patterns. The cases where the internal structure appeared as mixed radiolucent and radiopaque on panoramic radiographs were found to show more uniform radiopacity on CBCT compared to panoramic radiographs. These findings may help clinicians distinguish osteosclerosis from other radiopaque entities and support more accurate diagnosis in daily dental practice.
Cysteine-rich intestinal protein 1 (CRIP1) has recently emerged as a potential regulator of inflammatory responses, yet its role in metabolic disease remains poorly understood. Given the critical contribution of inflammation to diabetes mellitus and its established link with chronic inflammatory conditions such as periodontitis, we investigated the role of CRIP1 in the pathogenesis of diabetes mellitus using a streptozotocin (STZ)-induced mouse model. STZ administration induced pancreatic dysfunction in both wild-type (WT) and CRIP1 knockout (KO) mice. However, KO mice displayed delayed body weight recovery and impaired metabolic adaptation compared to WT controls. Unexpectedly, histological analysis revealed that CRIP1 deficiency preserved pancreatic islet architecture, with KO mice displaying a greater number of intact islets and reduced atrophy following STZ exposure. This preservation was associated with significantly reduced circulating TNF-α levels, suggesting attenuated inflammatory responses. Despite improved structural preservation of pancreatic islets, CRIP1-deficient mice showed no improvement in metabolic outcomes. Instead, they exhibited lower insulin levels, higher fasting glucose, and a trend toward increased insulin resistance. These findings indicate a dissociation between β-cell structural integrity and systemic metabolic function. Mechanistically, CRIP1 deficiency appears to dampen inflammation-mediated tissue damage while simultaneously impairing inflammation-dependent adaptive responses required for metabolic recovery. Collectively, our results identify CRIP1 as a key modulator of the balance between inflammatory damage and metabolic adaptation in diabetes mellitus. These findings further suggest that CRIP1 may serve as a molecular link connecting chronic inflammatory conditions, such as periodontitis, with systemic metabolic dysfunction.