Association of Quantified Costal Cartilage Calcification and Long-Term Cumulative Blood Glucose Exposure: The Multi-Ethnic Study of Atherosclerosis.

Aims: Anecdotal reports have suggested increased soft tissue calcification in individuals with long-term exposures to high blood glucose. The association of costal cartilage calcification (CCC), a reliably quantifiable marker obtainable from non-contrast cardiac computed tomography (CT) with cumulative fasting blood glucose (FBG) exposure, is unknown. In this study, we aimed to determine the association between quantified CCC and cumulative glucose exposure using non-contrast coronary artery calcium (CAC) scoring computed tomography (CT) images in the Multi-Ethnic Study of Atherosclerosis (MESA). Methods: The volume of bilateral CCC was quantified in high-density pixels (threshold of Hounsfield Unit>180) using the CAC scoring CT images acquired in the 5th MESA exam. Prior long-term cumulative exposure to FBG was calculated by area under the FBG-time curve over ten years before the time of the CT exam. Results: A total of 2,305 participants (mean age: 69, female/male: 1.3) were included in this study. The median CCC volume was lower in females than males (1158 mm3 [IQR: 1751] vs. 3054 mm3 [3851], p<0.001). In cross-sectional analysis, quantified CCC was associated with FBG (9% increase per SD) and HbA1c (7% increase per SD) at the CT exam only in female participants after adjustment for age, race, BMI, and glomerular filtration rate. Only in female participants, quantified CCC was also associated with prior cumulative FBG (3% increase per decile change). In the subgroup of females with zero CAC scores, the adjusted CCC was still associated with FBG (13% increase per SD) at the time of CT exam and with prior cumulative FBG exposure (4% increase per decile change) before the CT exam. Conclusions: The CCC, a reliably quantified marker in non-contrast cardiac CT, is associated with 10-year cumulative FBG exposure only in female participants, even those with zero CAC.

Control of optical transparency and infrared laser heating of costal cartilage via injection of iohexol.

Infrared (IR) laser impact has no analogues for rapid and safe cartilage reshaping. For better penetration of radiation optical clearing agents (OCAs) can be applied. In present work, the effect of low-osmolality agent iohexol on costal cartilage is studied. Specifically, it is shown that ½ of total increase of optical transparency occurs in 20 minutes of immersion. Maximally, cartilage transparency on 1560 nm can be increased in 1.5 times. Injection of iohexol results in increased tissue hygroscopicity, lower drying rate and higher percentage of bound water. Effective diffusion coefficients of water liberation at 21°C are (5.3 ± 0.4) × 10-7 and (3.3 ± 0.1) × 10-7 cm2 /s for untreated and iohexol-modified tissue, respectively. Raman spectroscopy of irradiated iohexol solution reveals its photo and thermo-stability under clinically used IR laser energies up to 350 W/cm2 for exposure times of several seconds. At energies higher than 500 W/cm2 [Correction added on 5 September 2018, after first online publication: This unit has been changed] decomposition of iohexol occurs rapidly through formation of molecular iodine and fluorescent residue.

Cell yield, chondrogenic potential, and regenerated cartilage type of chondrocytes derived from ear, nasoseptal, and costal cartilage.

Functional reconstruction of large cartilage defects in subcutaneous sites remains clinically challenging because of limited donor cartilage. Tissue engineering is a promising and widely accepted strategy for cartilage regeneration. To date, however, this strategy has not achieved a significant breakthrough in clinical translation owing to a lack of detailed preclinical data on cell yield and functionality of clinically applicable chondrocytes. To address this issue, the current study investigated the initial cell yield, proliferative potential, chondrogenic capacity, and regenerated cartilage type of human chondrocytes derived from auricular, nasoseptal, and costal cartilage using a scaffold-free cartilage regeneration model (cartilage sheet). Chondrocytes from all sources exhibited high sensitivity to basic fibroblast growth factor within 8 passages. Nasoseptal chondrocytes presented the strongest proliferation rate, whereas auricular chondrocytes obtained the highest total cell amount using comparable cartilage sample weights. Importantly, all chondrocytes at fifth passage showed strong chondrogenic capacity both in vitro and in the subcutaneous environment of nude mice. Although some significant differences in histological structure, cartilage matrix content and cartilage type specific proteins were observed between the in vitro engineered cartilage and original tissue; the in vivo regenerated cartilage showed mature cartilage features with high similarity to their original native tissue, except for minor matrix changes influenced by the in vivo environment. The current study provides detailed preclinical data for choice of chondrocyte source and thus promotes the clinical translation of cartilage regeneration approach.

[Costal cartilage structural and functional changes in children with a funnel or keeled chest]. / Strukturnye i funktsional'nye izmeneniia rebernykh khriashchei pri voronkovidnoi i kilevidnoi deformatsii grudnoi kletki u detei.

Congenital chest wall deformities (CCWDs) in children are severe diseases leading to cosmetic defects and diseases of the respiratory and cardiovascular systems. The most common of these deformities are funnel-shaped (pectus excavatum, FD) and keeled (pectus carinatum, KD) ones. The pathogenesis of CCWDs and the role of costal cartilage structural and functional changes in their pathogenesis have now been not well studied, which makes it difficult to elaborate pathogenetic approaches to correcting these diseases. Analysis of the literature has shown that structural and functional changes occur in the matrix and chondrocytes from the costal cartilage in FD. Similar costal cartilage changes are observed in KD. It is still unknown exactly which pathological processes are present in the costal cartilage and how they result in the development of one or other type of CCWDs. The role of amianthoid transformation (AT) of costal cartilages in these processes is also unknown. It is not improbable that it is AT drastically changing the native cartilage matrix, which is one of the key mechanisms leading to changes in its properties and to the subsequent development of FD or KD.

Deletion of IFT80 Impairs Epiphyseal and Articular Cartilage Formation Due to Disruption of Chondrocyte Differentiation.

Intraflagellar transport proteins (IFT) play important roles in cilia formation and organ development. Partial loss of IFT80 function leads Jeune asphyxiating thoracic dystrophy (JATD) or short-rib polydactyly (SRP) syndrome type III, displaying narrow thoracic cavity and multiple cartilage anomalies. However, it is unknown how IFT80 regulates cartilage formation. To define the role and mechanism of IFT80 in chondrocyte function and cartilage formation, we generated a Col2α1; IFT80f/f mouse model by crossing IFT80f/f mice with inducible Col2α1-CreER mice, and deleted IFT80 in chondrocyte lineage by injection of tamoxifen into the mice in embryonic or postnatal stage. Loss of IFT80 in the embryonic stage resulted in short limbs at birth. Histological studies showed that IFT80-deficient mice have shortened cartilage with marked changes in cellular morphology and organization in the resting, proliferative, pre-hypertrophic, and hypertrophic zones. Moreover, deletion of IFT80 in the postnatal stage led to mouse stunted growth with shortened growth plate but thickened articular cartilage. Defects of ciliogenesis were found in the cartilage of IFT80-deficient mice and primary IFT80-deficient chondrocytes. Further study showed that chondrogenic differentiation was significantly inhibited in IFT80-deficient mice due to reduced hedgehog (Hh) signaling and increased Wnt signaling activities. These findings demonstrate that loss of IFT80 blocks chondrocyte differentiation by disruption of ciliogenesis and alteration of Hh and Wnt signaling transduction, which in turn alters epiphyseal and articular cartilage formation.

Chronological assessment of airway lesions in relapsing polychondritis by positron emission tomography.

A 40-year old woman presented with pyrexia, productive cough, and bilateral precordial pain. Positron emission tomography (PET)-computed tomography (CT) showed high, diffuse F-18 deoxyglucose accumulation in the tracheal, peribronchial, and bilateral costal cartilage. We diagnosed her with relapsing polychondritis (RP) based on McAdam's criteria. Airway lesions are a major prognostic indicator of RP, and so chronological assessment and control is essential. In this patient, PET-CT accurately reflected both the location and severity of the inflammation and helped to guide treatment decision-making and facilitated early detection of recurrence. However, its high cost is prohibitive to frequent use, making it necessary to comprehensively evaluate serum C-reactive protein levels, bronchoscopy, spirometry, and 3D-CT.