“…[4] These include skeletal alterations (e.g., radiologic changes, expansion of maxilla and/or mandible, thinning of cortical bone, increased/altered trabecular bone, loss of lamina dura, and radiopaque lesions), hyposalivation and xerostomia, gingival hyperplasia, enamel wear, abnormal dentin accumulation, reduced dental pulp volume, widened PDL, and hypercementosis. [4][5][6][7][8][9]23] Dentin-pulp changes can lead to pulp obliteration and potential effects on tooth vitality, while periodontal changes can contribute to periodontal disease, tooth mobility, malocclusion, and tooth loss. Early-onset forms of CKD due to genetic or environmental disruptions of renal function can disrupt enamel formation in primary and/or secondary dentition (depending on age of onset and severity of renal failure), resulting in enamel hypoplasia and discoloration that have a negative impact on esthetics and quality of life.…”
Section: Journal Of Bone and Mineral Researchmentioning
confidence: 99%
“…[4] Oral defects and abnormalities associated with CKD include bone disturbances (radiologic changes, expansion of maxilla and/or mandible, thinning of cortical bone, increased/ altered trabecular bone, loss of lamina dura, and radiopaque lesions), xerostomia, gingival hyperplasia, abnormal enamel wear, abnormal dentin deposition, reduced dental pulp volume, widened periodontal ligament (PDL), and hypercementosis; altogether these changes can contribute to clinical manifestations of pulp obliteration and periodontal disease. [4][5][6][7][8][9][10][11][12][13][14][15] Early-onset forms of CKD affecting young children can disrupt amelogenesis in primary and/or secondary dentition, resulting in enamel hypoplasia and discoloration, with reduced caries indices but a negative impact on quality of life. [11,12,[16][17][18][19][20][21][22][23] Mechanisms underlying these oral defects remain poorly understood.…”
“…[4] These include skeletal alterations (e.g., radiologic changes, expansion of maxilla and/or mandible, thinning of cortical bone, increased/altered trabecular bone, loss of lamina dura, and radiopaque lesions), hyposalivation and xerostomia, gingival hyperplasia, enamel wear, abnormal dentin accumulation, reduced dental pulp volume, widened PDL, and hypercementosis. [4][5][6][7][8][9]23] Dentin-pulp changes can lead to pulp obliteration and potential effects on tooth vitality, while periodontal changes can contribute to periodontal disease, tooth mobility, malocclusion, and tooth loss. Early-onset forms of CKD due to genetic or environmental disruptions of renal function can disrupt enamel formation in primary and/or secondary dentition (depending on age of onset and severity of renal failure), resulting in enamel hypoplasia and discoloration that have a negative impact on esthetics and quality of life.…”
Section: Journal Of Bone and Mineral Researchmentioning
confidence: 99%
“…[4] Oral defects and abnormalities associated with CKD include bone disturbances (radiologic changes, expansion of maxilla and/or mandible, thinning of cortical bone, increased/ altered trabecular bone, loss of lamina dura, and radiopaque lesions), xerostomia, gingival hyperplasia, abnormal enamel wear, abnormal dentin deposition, reduced dental pulp volume, widened periodontal ligament (PDL), and hypercementosis; altogether these changes can contribute to clinical manifestations of pulp obliteration and periodontal disease. [4][5][6][7][8][9][10][11][12][13][14][15] Early-onset forms of CKD affecting young children can disrupt amelogenesis in primary and/or secondary dentition, resulting in enamel hypoplasia and discoloration, with reduced caries indices but a negative impact on quality of life. [11,12,[16][17][18][19][20][21][22][23] Mechanisms underlying these oral defects remain poorly understood.…”
“…The bone lesions could also affect the orofacial area and result in facial or oral cavity swelling. Both CT and/or MRI would be helpful for diagnosis and management [34, 35]. Fig.…”
Section: Patient Presentation and Imaging Workupmentioning
Brown tumours do not represent neoplastic process, but they are focal bony lesions due to bone remodelling from either primary or secondary hyperparathyroidism. Their incidence is also low. The current literature on brown tumour is mainly in the form of case reports that focus on single affected sites. This pictorial review describes the full imaging workup and pathway of suspected brown tumour in the setting of both primary and secondary hyperparathyroidism. It aims to illustrate the management strategy to aid both clinicians and radiologists in suspected cases of brown tumour. We highlight the complementary roles that different imaging modalities can play in different settings including the importance of parathyroid ultrasound,
99m
Tc-sestamibi scintigraphy and SPECT/CT in the localisation of the parathyroid adenoma. We present cases with full clinical and imaging workup in both the acute and chronic setting and scenarios that require exclusion of primary and secondary bone malignancies.
“…Abnormal levels of calcium/phosphorus and secondary hyperparathyroidism result in bone metabolism disorder in CKD (2,3). Renal osteodystrophy (ROD) is frequently seen at the end stage of renal diseases (4). The decrease in density and strength of bone increased the risk of fracture for patients with CKD (5,6).…”
Background Non-invasive imaging methods are still lacking for evaluating bone changes in chronic kidney diseases (CKD). Purpose To investigate the feasibility of chest CT radiomics in evaluating bone changes caused by CKD. Material and Methods In total, 75 patients with stage 1 CKD (CKD1) and 75 with stage 5 CKD (CKD5) were assessed using the chest CT radiomics method. Radiomics features of bone were obtained using 3D Slicer software and were then compared between CKD1 and CKD5 cases. The methods of maximum correlation minimum redundancy (mRMR) and least absolute shrinkage and selection operator (LASSO) were used to establish a prediction model to determine CKD. The receiver operating characteristic (ROC) curve was used to determine the performance of the model. Results Cases of CKD1 and CKD5 differed in 40 radiomics features ( P <0.05). Using the mRMR and LASSO methods, five features were finally selected to establish a predication model. The area under the receiver operating characteristic curve of the model in the determination of CKD1 and CKD5 was 0.903 and 0.854, respectively, for the training and validation cohorts. Conclusion Chest CT radiomics is feasible in evaluating bone changes caused by CKD.
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