In vitro effects of triamcinolone acetonide and in combination with hyaluronan on canine normal and spontaneous osteoarthritis articular cartilage

Euppayo, Thippaporn; Siengdee, Puntita; Buddhachat, Kittisak; Pradit, Waranee; Chomdej, Siriwadee; Ongchai, Siriwan; Nganvongpanit, Korakot

doi:10.1007/s11626-016-0022-4

Cited by 19 publications

(20 citation statements)

References 53 publications

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“…However, in this study, it was found that the combination treatment with CAR with HA (Comb24 and Comb48) did not decrease chondrotoxicity (and did not increase chondrocyte viability). Similar to our previous study involving OA chondrocyte cultures, co-treatment with HA did not decrease chondrotoxicity caused by CAR (Euppayo et al, 2015), triamcinolone acetonide (Euppayo et al, 2016), dexamethasone (Siengdee et al, 2015) and prednisolone (Siengdee et al, 2015). However, some studies have shown that HA could reduce cytotoxicity on chondrocyte viability after cells were exposed to bupivacaine (Onur, Sitron & Dang, 2013), indomethacin (Hashizume & Mihara, 2009), dexamethasone (Hashizume & Mihara, 2009) and celecoxib (Hashizume & Mihara, 2009).…”

Section: Discussionsupporting

confidence: 83%

“…However, HA could lessen the side effects of fluoroquinolones when treatment was given in conjunction with those other drugs (Siengdee et al, 2016). On the contrary, the therapeutic effects of HA could not mitigate the side effects of carprofen (Euppayo et al, 2015), corticosteroid (Siengdee et al, 2015) and triamcinolone acetonide (Euppayo et al, 2016) when subjects were treated with HA at the same time.…”

Section: Introductionmentioning

confidence: 99%

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Post-treatment of hyaluronan to decrease the apoptotic effects of carprofen in canine articular chondrocyte culture

Nganvongpanit

Euppayo

Siengdee

et al. 2020

PeerJ

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A major concern associated with the use of drugs is their adverse side effects. Specific examples of the drugs of concern include antibiotic agents and non-steroidal anti-inflammatory drugs. Despite the presence of a high degree of efficacy for specific conditions, these drugs may deteriorate the surrounding tissues that are exposed to them. Often, carprofen is used for joint inflammation; however, it may stimulate cartilage degradation which can then lead to osteoarthritis progression. In this study, hyaluronan was combined with carprofen treatment in three different applications (pre-treatment, co-treatment and post-treatment) on normal canine chondrocytes to determine whether Hyaluronan (HA) is capable of mitigating the degree of chondrotoxicity of carprofen. Our findings revealed that carprofen at IC20 (0.16 mg/mL) decreased viability and increased nitric oxide (NO) production. Importantly, carprofen induced the apoptosis of canine chondrocytes via the up-regulation of Bax, Casp3, Casp8, Casp9 and NOS2 as compared to the control group. Although the co-treatment of HA and carprofen appeared not to further alleviate the chondrotoxicity of carprofen due to the presence of a high number of apoptotic chondrocytes, post-treatment with HA (carprofen treatment for 24 h and then changed to HA for 24 h) resulted in a decrease in chondrocyte apoptosis by the down-regulation of Bax, Casp3, Casp8, Casp9, NOS2, along with NO production when compared with the treatment of carprofen for 48 h (P < 0.05). These results suggest that HA can be used as a therapeutic agent to mitigate the degree of chondrotoxicity of carprofen.

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Section: Discussionsupporting

confidence: 83%

Section: Introductionmentioning

confidence: 99%

Post-treatment of hyaluronan to decrease the apoptotic effects of carprofen in canine articular chondrocyte culture

Nganvongpanit

Euppayo

Siengdee

et al. 2020

PeerJ

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“…In general, controversy on the effect of corticosteroids on joint cartilage is still considerable. Negative effects of corticosteroids on cartilage integrity have been mainly described in vitro, in monocultures of chondrocytes or cartilage tissue explants (Euppayo et al, ; Suntiparpluacha, Tammachote, & Tammachote, ), although loss of safranin‐O positivity was found upon IA injection of TAA‐delivering MSs in healthy joints (Bodick et al, ). However, we showed that while TAA indeed inhibited proteoglycan content of cartilage explants in monoculture, in co‐cultures of cartilage explants with synovial tissue, the same concentration of TAA enhanced proteoglycan synthesis (Beekhuizen et al, ).…”

Section: Discussionmentioning

confidence: 99%

Local controlled release of corticosteroids extends surgically induced joint instability by inhibiting tissue healing

Rudnik-Jansen

Tellegen

Pouran

et al. 2019

British J Pharmacology

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Background and PurposeCorticosteroids are intra‐articularly injected to relieve pain in joints with osteoarthritis (OA) or acute tissue damage such as ligament or tendon tears, despite its unverified contraindication in unstable joints. Biomaterial‐based sustained delivery may prolong reduction of inflammatory pain, while avoiding harmful peak drug concentrations.Experimental ApproachThe applicability of prolonged corticosteroid exposure was examined in a rat model of anterior cruciate ligament and medial meniscus transection (ACLT + pMMx) with ensuing degenerative changes.Key ResultsIntra‐articular injection of a bolus of the corticosteroid triamcinolone acetonide (TAA) resulted in enhanced joint instability in 50% of the joints, but neither instability‐induced OA cartilage degeneration, synovitis, nor the OA‐related bone phenotype was affected. However, biomaterial microsphere‐based extended TAA release enhanced instability in 94% of the animals and induced dystrophic calcification and exacerbation of cartilage degeneration. In healthy joints, injection with TAA releasing microspheres had no effect at all. In vitro, TAA inhibited cell migration out of joint tissue explants, suggesting inhibited tissue healing in vivo as mechanisms for enhanced instability and subsequent cartilage degeneration.Conclusions and ImplicationsWe conclude that short‐term TAA exposure has minor effects on surgically induced unstable joints, but its extended presence is detrimental by extending instability and associated joint degeneration through compromised healing. This supports a contraindication of prolonged corticosteroid exposure in tissue damage‐associated joint instability, but not of brief exposure.

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“…Part III, in vitro studies — There were five studies [ 22 , 23 , 38 – 40 ], including anabolic gene ( ACAN and COL2A1 ) expression, catabolic gene ( ADAMTS5 , COX-2 , IL-1β , MMP2 , MMP3 , and MMP13 ) expression, and GAG remaining in chondrocyte pellets or cartilage explants.…”

Section: Resultsmentioning

confidence: 99%

Effects of hyaluronic acid combined with anti-inflammatory drugs compared with hyaluronic acid alone, in clinical trials and experiments in osteoarthritis: a systematic review and meta-analysis

Euppayo¹,

Punyapornwithaya²,

Chomdej³

et al. 2017

BMC Musculoskelet Disord

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BackgroundThe objectives are to compare the efficacy of intra-articular hyaluronic acid (IA-HA) alone and in combination with anti-inflammatory drugs (IA-HA + AI), corticosteroids (CS) or non-steroidal anti-inflammatory drugs (NSAIDs) in clinical trials and in vivo and in vitro studies of osteoarthritis (OA).MethodsData in the BIOSIS, CINAHL, Cochrane Library, EMBASE and Medline databases were collected and analyzed. Random effects models were used to compute the effect size (ES) of the mean difference in pain reduction scores from baseline and the relative risk (RR) of adverse events. The ES of histological scores in vivo and cartilage metabolism in vitro were also calculated. We conducted sensitivity analysis of blinding and intention-to-treat (ITT), compared IA-HA combined with CS vs. IA-HA alone in trials, and compared the effects of HA + AI vs. AI alone in vitro, including anabolic and catabolic gene expression.ResultsThirteen out of 382 papers were included for data analysis. In clinical trials, the ES of pain reduction scores within the 1st month was −4.24 (−6.19, −2.29); 2nd–12th month, −1.39 (−1.95, −0.82); and within one year, −1.63 (−2.19, −1.08), favoring IA-HA + AI (P < 0.001). The ES of RR was 1.08 (0.59, 1.98), and histological scores was 1.38 (−0.55, 3.31). The ES of anabolic gene expression was 1.22 (0.18, 2.25), favoring HA alone (P < 0.05); catabolic gene expression was 0.74 (−0.44, 1.53), favoring HA alone; and glycosaminoglycans remaining was −2.45 (−5.94, 1.03).ConclusionsIA-HA + AI had greater efficacy for pain relief than IA-HA alone within a one-year period. However, HA + AI down-regulated the ACAN gene when compared with HA alone in vitro.

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In vitro effects of triamcinolone acetonide and in combination with hyaluronan on canine normal and spontaneous osteoarthritis articular cartilage

Cited by 19 publications

References 53 publications

Post-treatment of hyaluronan to decrease the apoptotic effects of carprofen in canine articular chondrocyte culture

Post-treatment of hyaluronan to decrease the apoptotic effects of carprofen in canine articular chondrocyte culture

Local controlled release of corticosteroids extends surgically induced joint instability by inhibiting tissue healing

Effects of hyaluronic acid combined with anti-inflammatory drugs compared with hyaluronic acid alone, in clinical trials and experiments in osteoarthritis: a systematic review and meta-analysis

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