Accumulation of microdamage in subchondral bone at the femoral head in patients with end-stage osteoarthritis of the hip

Shimamura, Masashi; Iwata, Ken; Mashiba, Tasuku; Miki, Takanori; Yamamoto, Toshiyuki

doi:10.1007/s00774-019-00988-z

Cited by 6 publications

(9 citation statements)

References 24 publications

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“…MDx have been associated with increased osteocyte apoptosis (Noble et al, 2003; Verborgt, Gibson, & Schaffler, 2000) and may disrupt interosteocyte communication via canaliculi (Dooley, Cafferky, Lee, & Taylor, 2014). Regularly, the MDx density is presented as number (Frisch et al, 2001a‐b; Frisch, Bretlau, & Sorensen, 2008b; Frisch et al, 2015) or length per area (Allen & Burr, 2007; Shimamura, Iwata, Mashiba, Miki, & Yamamoto, 2019). However, these methods are essentially semi‐quantitative and measured in a single section plane they may come with an inherent bias.…”

Section: Introductionmentioning

confidence: 99%

Microcrack surface density in the human otic capsule: An unbiased stereological quantification

Hansen

Bloch

Frisch

et al. 2020

The Anatomical Record

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Bone is continuously remodeled to repair and strengthen degenerative bone with accumulating dead osteocytes and microfractures. Inner ear osteoprotegerin (OPG)‐mediated inhibition of otic capsular bone remodeling causes excessive perilabyrinthine bone degeneration. Consequently, microcracks accumulate around the inner ear. Microcracks cause osteocyte apoptosis and may disrupt the canalicular network connecting osteocytes. Despite their linear microscopic appearance, microcracks are three‐dimensional disruption planes and represent surface areas inside a tissue space. With an elevated microcrack burden the number of disconnected osteocytes is expected to increase. This may prove relevant to ongoing research in otic focal pathologies like otosclerosis. Therefore, an unbiased quantification of the microcrack surface density (mm2/mm3) in the human otic capsule is essential. In this study unbiased stereology was applied to undecalcified bulk stained human temporal bones to demonstrate its feasibility in describing the three‐dimensional reality behind two dimensional observations of microcracks. A total of 28 human temporal bones and five ribs were bulk stained in basic fuchsin, serially sectioned and hand‐ground to a thickness of 80–120 μm. Both horizontal and vertical sections were produced and compared. This study showed that surface density of microcracks was significantly higher around the inner ear compared to ribs. Furthermore, no significant difference in microcrack surface density between horizontal and vertical sections in the temporal bone was demonstrated.

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Section: Introductionmentioning

confidence: 99%

Microcrack surface density in the human otic capsule: An unbiased stereological quantification

Hansen

Bloch

Frisch

et al. 2020

The Anatomical Record

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“…Defects of the osteochondral unit were firstly described by Frost in 1960 28 being considered to induce bone remodeling and degenerative changes during OA progression. 29 , 30 , 31 Among those defects, osteochondral cracks constituted the most prominent findings and their presence was associated with abnormal bone remodeling during OA progression. 10 However, the relevance of cracking to demographic characteristics of the population and the degenerative tissue and cellular changes during OA progression remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Sex, but not age and bone mass index positively impact on the development of osteochondral micro‐defects and the accompanying cellular alterations during osteoarthritis progression

Kaspiris

Chronopoulos

Vasiliadis

et al. 2022

Chronic Diseases and Translational Medicine

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Background Osteoarthritis (ΟΑ) is characterized by cartilage breakdown and subchondral sclerosis. Micro‐fractures of the calcified tissues have been, also, detected, but their exact role has not been elucidated yet. This study was to examine the frequency of cracks during OA progression and to correlate them with the underlying cellular modifications and matrix metalloproteinase‐2 (MMP‐2) expression using histological/immunohistological methods. Methods Overall, 20 patients and 3 controls (9 specimens per patient), aged 60–89 years, diagnosed with hip/knee OA were included. The development of cracks was examined in 138 sections, whereas the expression of MMP‐2 was examined in 69 additional sections. Results Based on Mankin score, three groups of OA severity were analyzed: Group I (mild) was constituted of sections with score 1–5 while Groups II (moderate) and III (severe) with score 6–7 and greater or equal to 8, respectively. Demographic characteristics did not reveal any association between the number of microdefects and age or body mass index (BMI). Cartilage micro‐cracks were increased during moderate and severe OA, while bone cracks were increased during mild and severe OA. In knee OA, cartilage cracks were not correlated with Mankin score, whereas in hip OA they appeared association with severity score. Bone cracks were positively correlated with matrix apoptotic osteocytes and osteoblastic cells, but not with osteoclasts. MMP‐2 immunostaining was increasing by OA severity in the osteochondral unit. Similarly, MMP‐2 was expressed on the microcracks’ wall mainly in Group III. Conclusion Our data displayed that bone cracks during primary OA stages, represent an early adaptative mechanism aiming to maintain cartilage integrity. Accumulation of bone defects and concomitant increase of apoptotic osteocytes activated an abnormal remodeling due to osteoblastic activity, in which MMP‐2 played a pivotal role, leading to subchondral sclerosis promoting further osteochondral deformities.

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“…In human SCP (ACC and SCB combined) as a whole, microcracks are found beneath eroded OA cartilage more so than in adjacent healthy regions, and these areas contain higher volumes of osteoid (Shimamura et al, 2019 ). This evidences the role of high‐impact load‐bearing in determining the regions most affected by OA in a given joint—loads result in both soft tissue erosion and hard tissue cracking.…”

Section: Matrixmentioning

confidence: 99%

“…The cell density of the ACC across 2D sections has been reported as 51 cells/mm 2 , significantly fewer than were found in the HAC, 152 cells/mm 2 (Wang et al, 2009 ). However, throughout the TAC, the number of chondrocytes appears to decrease as OA progresses, resulting in overall hypocellularity (Bobacz et al, 2004 ), though not all studies have found that cell density decreases with OARSI grade (Shimamura et al, 2019 ). The chondrocytes within the HAC appear to be equally dense in their distributions throughout the layers between OA and healthier groups (Bobacz et al, 2004 ).…”

Section: Chondrocytes and Chondronsmentioning

confidence: 99%

Structural clues to articular calcified cartilage function: A descriptive review of this crucial interface tissue

Evans

Pitsillides

2022

Journal of Anatomy

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Articular calcified cartilage (ACC) has been dismissed, by some, as a remnant of endochondral ossification without functional relevance to joint articulation or weight‐bearing. Recent research indicates that morphologic and metabolic ACC features may be important, reflecting knee joint osteoarthritis (OA) predisposition. ACC is less investigated than neighbouring joint tissues, with its component chondrocytes and mineralised matrix often being either ignored or integrated into analyses of hyaline articular cartilage and subchondral bone tissue respectively. Anatomical variation in ACC is recognised between species, individuals and age groups, but the selective pressures underlying this variation are unknown. Consequently, optimal ACC biomechanical features are also unknown as are any potential locomotory roles. This review collates descriptions of ACC anatomy and biology in health and disease, with a view to revealing its structure/function relationship and highlighting potential future research avenues. Mouse models of healthy and OA joint ageing have shown disparities in ACC load‐induced deformations at the knee joint. This raises the hypothesis that ACC response to locomotor forces over time may influence, or even underlie, the bony and hyaline cartilage symptoms characteristic of OA. To effectively investigate the ACC, greater resolution of joint imaging and merging of hierarchical scale data will be required. An appreciation of OA as a ‘whole joint disease’ is expanding, as is the possibility that the ACC may be a key player in healthy ageing and in the transition to OA joint pathology.

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Accumulation of microdamage in subchondral bone at the femoral head in patients with end-stage osteoarthritis of the hip

Cited by 6 publications

References 24 publications

Microcrack surface density in the human otic capsule: An unbiased stereological quantification

Microcrack surface density in the human otic capsule: An unbiased stereological quantification

Sex, but not age and bone mass index positively impact on the development of osteochondral micro‐defects and the accompanying cellular alterations during osteoarthritis progression

Structural clues to articular calcified cartilage function: A descriptive review of this crucial interface tissue

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