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Periarticular bone changes in osteoarthritis.

Weinans H - HSS J (2012)

View Article: PubMed Central - PubMed

Affiliation: Orthopaedic Research Laboratory, Erasmus MC, Room EE-1614, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.

ABSTRACT

The animal models and the imaging tools provide a powerful combination for studying OA. What did we learn from the current approaches? It has been known for some years that subchondral bone is a highly adaptive tissue, and changes in subchondral bone can be accurately visualized and quantified by CT [6] and scintigraphy [5] even in a clinical setting. Animal CT and SPECT have been improved in the last decade to higher resolutions [3, 12], enabling refined in vivo evaluation in small animal research. Besides evaluations of subchondral bone and cartilage with the microimaging modalities, SPECT/CT can image macrophage activation as well [8]. With repetitive imaging of animals, we will learn the precise sequence of events that occur in the various tissues of the diseased joint. The bone scan analyses, with its fast (2 days) response in bone turnover in the MIA OA model, substantiate the often suggested crosstalk between the bone and cartilage compartments. In the different animal models, this sequence of events might be different; in one model, the problems might start in the cartilage, whereas in another model the bone might be triggered first. Each model might expose a different etiological pathway, similar to the differences in OA etiology in humans. Hopefully, these new tools will elucidate concepts and targets that help us in the design of new therapeutic interventions for OA.

No MeSH data available.


Multi pinhole SPECT scan using 99mTc-MDP to visualize bone turnover in MIA-induced OA rat model. At the left, the OA side vs. the contralateral control side at the right. There was a higher signal in the subchondral bone (white arrow) already 2 days after OA induction. The other large signal is from growth plate
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Fig4: Multi pinhole SPECT scan using 99mTc-MDP to visualize bone turnover in MIA-induced OA rat model. At the left, the OA side vs. the contralateral control side at the right. There was a higher signal in the subchondral bone (white arrow) already 2 days after OA induction. The other large signal is from growth plate

Mentions: We attempted to image the higher osteoclast activity (or bone turnover rate) that generates the bone erosion by other more direct means. In a rat model using monoiodoacetate (MIA) to induce OA, a bone scan was made with a novel multi-pinhole SPECT. Methyl diphosphonate labeled with 99m-technetium was used (99mTc-MDP) as a radioactive tracer. As early as 2 days after induction of OA, the SPECT scan showed higher signal intensity (Fig. 4), indicating increased osteoclast activity. Since the growth plate in the rat is not closed, the overall signal intensity around the knee is high. However, the high resolution animal SPECT is able to differentiate the signals from growth plate and subchondral bone. Histology of the same knees 2 days later (i.e., 4 days after MIA injections) could not distinguish the cartilage from the treated knees and the healthy contralateral control knees. At later time points (16 and 44 days after the injections), a clear difference was seen with lower GAG staining, fibrillation, and chondrocyte clustering.Fig. 4


Periarticular bone changes in osteoarthritis.

Weinans H - HSS J (2012)

Multi pinhole SPECT scan using 99mTc-MDP to visualize bone turnover in MIA-induced OA rat model. At the left, the OA side vs. the contralateral control side at the right. There was a higher signal in the subchondral bone (white arrow) already 2 days after OA induction. The other large signal is from growth plate
© Copyright Policy
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC3295953&req=5

Fig4: Multi pinhole SPECT scan using 99mTc-MDP to visualize bone turnover in MIA-induced OA rat model. At the left, the OA side vs. the contralateral control side at the right. There was a higher signal in the subchondral bone (white arrow) already 2 days after OA induction. The other large signal is from growth plate
Mentions: We attempted to image the higher osteoclast activity (or bone turnover rate) that generates the bone erosion by other more direct means. In a rat model using monoiodoacetate (MIA) to induce OA, a bone scan was made with a novel multi-pinhole SPECT. Methyl diphosphonate labeled with 99m-technetium was used (99mTc-MDP) as a radioactive tracer. As early as 2 days after induction of OA, the SPECT scan showed higher signal intensity (Fig. 4), indicating increased osteoclast activity. Since the growth plate in the rat is not closed, the overall signal intensity around the knee is high. However, the high resolution animal SPECT is able to differentiate the signals from growth plate and subchondral bone. Histology of the same knees 2 days later (i.e., 4 days after MIA injections) could not distinguish the cartilage from the treated knees and the healthy contralateral control knees. At later time points (16 and 44 days after the injections), a clear difference was seen with lower GAG staining, fibrillation, and chondrocyte clustering.Fig. 4

View Article: PubMed Central - PubMed

Affiliation: Orthopaedic Research Laboratory, Erasmus MC, Room EE-1614, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands.

ABSTRACT

The animal models and the imaging tools provide a powerful combination for studying OA. What did we learn from the current approaches? It has been known for some years that subchondral bone is a highly adaptive tissue, and changes in subchondral bone can be accurately visualized and quantified by CT [6] and scintigraphy [5] even in a clinical setting. Animal CT and SPECT have been improved in the last decade to higher resolutions [3, 12], enabling refined in vivo evaluation in small animal research. Besides evaluations of subchondral bone and cartilage with the microimaging modalities, SPECT/CT can image macrophage activation as well [8]. With repetitive imaging of animals, we will learn the precise sequence of events that occur in the various tissues of the diseased joint. The bone scan analyses, with its fast (2 days) response in bone turnover in the MIA OA model, substantiate the often suggested crosstalk between the bone and cartilage compartments. In the different animal models, this sequence of events might be different; in one model, the problems might start in the cartilage, whereas in another model the bone might be triggered first. Each model might expose a different etiological pathway, similar to the differences in OA etiology in humans. Hopefully, these new tools will elucidate concepts and targets that help us in the design of new therapeutic interventions for OA.

No MeSH data available.