Minimum joint space width and tibial cartilage morphology in the knees of healthy individuals: A cross-sectional study

<p>Abstract</p> <p>Background</p> <p>The clinical use of minimum joint space width (mJSW) and cartilage volume and thickness has been limited to the longitudinal measurement of disease progression (i.e. change over time) rather than the diagnosis of OA in which values are compared to a standard. This is primarily due to lack of establishment of normative values of joint space width and cartilage morphometry as has been done with bone density values in diagnosing osteoporosis. Thus, the purpose of this pilot study is to estimate reference values of medial joint space width and cartilage morphometry in healthy individuals of all ages using standard radiography and peripheral magnetic resonance imaging.</p> <p>Design</p> <p>For this cross-sectional study, healthy volunteers underwent a fixed-flexion knee X-ray and a peripheral MR (pMR) scan of the same knee using a 1T machine (ONI OrthOne™, Wilmington, MA). Radiographs were digitized and analyzed for medial mJSW using an automated algorithm. Only knees scoring ≤1 on the Kellgren-Lawrence scale (no radiographic evidence of knee OA) were included in the analyses. All 3D SPGRE fat-sat sagittal pMR scans were analyzed for medial tibial cartilage morphometry using a proprietary software program (Chondrometrics GmbH).</p> <p>Results</p> <p>Of 119 healthy participants, 73 were female and 47 were male; mean (SD) age 38.2 (13.2) years, mean BMI 25.0 (4.4) kg/m². Minimum JSW values were calculated for each sex and decade of life. Analyses revealed mJSW did not significantly decrease with increasing decade (p > 0.05) in either sex. Females had a mean (SD) medial mJSW of 4.8 (0.7) mm compared to males with corresponding larger value of 5.7 (0.8) mm. Cartilage morphometry results showed similar trends with mean (SD) tibial cartilage volume and thickness in females of 1.50 (0.19) μL/mm²and 1.45 (0.19) mm, respectively, and 1.77 (0.24) μL/mm²and 1.71 (0.24) mm, respectively, in males.</p> <p>Conclusion</p> <p>These data suggest that medial mJSW values do not decrease with aging in healthy individuals but remain fairly constant throughout the lifespan with "healthy" values of 4.8 mm for females and 5.7 mm for males. Similar trends were seen for cartilage morphology. Results suggest there may be no need to differentiate a t-score and a z-score in OA diagnosis because cartilage thickness and JSW remain constant throughout life in the absence of OA.</p

Gender-Associated Oral and Periodontal Health Based on Retrospective Panoramic Radiographic Analysis of Alveolar Bone Loss

Gender-based heterogeneity in periodontal disease has been witnessed in the recent past with huge mounting evidence. The composite effect of sex-based genetic structure and the sex steroid hormones runs in line with the corresponding gender-related differences in risk for chronic periodontitis. Since estrogens, the predominant sex hormones in women, show immune protective and anti-inflammatory effects in hormonally active premenopausal women, they show better periodontal status compared to age-matched men. Conversely, after menopause with a weakening estrogen signal, women may show an equal or even more serious periodontal status compared to men. Periodontal status of postmenopausal women may be improved by menopausal hormone therapy. Alveolar bone loss, an irreversible sign of past periodontal disease activity can be easily observed on radiographs in an objective manner. Orthopantomographs provide a fairly accurate assessment of the status of alveolar bone in the whole mouth. A cross-sectional retrospective panoramic radiographic analysis has been carried out in a north Indian dental institute to decipher the gender-based distribution of periodontal bone loss. The current chapter shall provide an update on gender-based differences in oral health, underlying mechanisms, differences in patterns and distribution of alveolar bone loss (case study), and potential gender-specific disease protection and management strategies

Reduction in mesenchymal stem cell numbers in premature aging DNA repair deficient TTD mice

Background: Mice carrying mutations in DNA repair genes often show signs of accelerated ageing and therefore can be used as a model system to study age related diseases like osteoporosis. It has been shown that TTD mice, carrying a mutation in the nucleotide excision repair gene XPD (xeroderma pigmentosa group D), display features of ageing related osteoporosis as well as adipose tissue hypoplasia. Since both cell types involved, osteoblasts as well as adipocytes, arise from the same mesenchymal stem cell population, the aim of the current project was to study the number, proliferation and differentiation potential of these cells in TTD compared to wild type (WT) mice. This might provide us with useful information concerning the mechanism behind age-related osteoporosis and the loss of adipose tissue.Methods: Bone marrow from old TTD and WT mice was cultured under osteogenic or adipogenic conditions and analysed for alkaline phosphatase activity (ALP), mineralisation (osteoblast) and lipid deposition (adipocyte).Results: Under osteogenic conditions the number of ALP-positive colonies after 9 and 14 days of culture was significantly decreased (p=0.02) in TTD compared to WT mice. The rate at which new ALP-positive colonies are formed between day 9 and day 14 of culture has not changed between TTD and WT mice, indicating that the decrease in colony number is not due to a delay in differentiation. Mineralisation of ALP-positive colonies did not seem to be affected, with a borderline significant decrease on day 14 at the onset of mineralisation but no significant changes on day 21 of culture. Lipid deposition was strongly reduced in TTD compared to WT mice (p=0.01) after 35 days of culture.Conclusions: The observed reduction in osteoblast and adipocyte differentiation indicates a reduction of mesenchymal stem cell numbers in TTD mice. This reduction in mesenchymal stem cell numbers and the corresponding decline in osteoblast differentiation could explain the premature osteoporotic features observed in TTD mice. In line with this, the reduction of mesenchymal stem cells and adipocyte differentiation may underlie the adipose tissue hypoplasia observed in TTD mice

Deletion of the ghrelin receptor GHSR corrects the trabecular, but not the cortical bone changes in the femoral head of ob/ob mice

Background: There exists an intriguing and complex relationship between fat and bone cells with respect to aging and osteoporosis, which is mediated in part by leptin. Genetically obese mice (ob/ob), that lack leptin, have aheterogeneous bone phenotype, with differential effects on cortical and trabecular compartments. Besides its role in bone metabolism, leptin is most well known for its anorexigenic properties. Opposed in action to leptin is ghrelin, a potent orexigenic peptide hormone derived from the stomach. Ghrelin and leptin also act as each other’s antagonists in gonadal and immune system function.Objective: To determine if ghrelin opposes leptin action on bone metabolism.Methods: Characterization of femoral micro-architecture in 6 months old male wild type, ob/ob, ghrelin receptor knockout (Ghsr -/-), and ob/ob.Ghsr-/- mice using micro-computed tomography.Results: Deletion of Ghsr alone did not significantly alter bone micro-architecture in wild type mice. Deletion of leptin reduced cortical volume and thickness in the femoral head of wild type mice, while it increased endocortical volume. Tissue volume remained unaffected. Conversely, deletion of leptin increased trabecular bone volume, trabecular number and connectivity in wild type mice. Additional deletion of Ghsr in ob/ob mice restored the changes to wild type levels in trabecular bone, but not in cortical bone (all not significant).Conclusion: We found that leptin deficiency has a negative effect on cortical and a positive effect on trabecular bone micro-architecture, confirming the heterogeneous skeletal effects observed by others in ob/ob mice. Knocking out ghrelin signaling compensates for the effect of leptin deficiency on trabecular bone. These observations demonstrate the positive activity of ghrelin signaling in bone, and suggest that ghrelin and leptin have opposing actions on bone metabolism