Sequential expressions of MMP‐1, TIMP‐1, IL‐6, and COX‐2 genes in induced periapical lesions in rats

Lin, Sze‐Kwan; Kok, Sang‐Heng; Kuo, Mark Yen‐Ping; Wang, Tzu‐Jou; Wang, Jeng-Tzung; Yeh, Flora Tzu-Chin; Hsiao, Michael; Lan, Wan–Hong; Hong, Chuang‐Ye

doi:10.1034/j.1600-0447.2002.11227.x

Cited by 54 publications

(44 citation statements)

References 36 publications

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“…[40][41][42] Our data clearly indicate that COX-2 is also important in resorption associated with focal, directed remodeling in response to fatigue injury. Ibuprofen also inhibited lamellar bone formation within the resorption spaces along the fracture line.…”

Section: Discussionmentioning

confidence: 62%

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Kidd

Cowling

et al. 2012

Journal Orthopaedic Research

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Anti-inflammatory drugs are widely used to manage pain associated with stress fractures (SFxs), but little is known about their effects on healing of those injuries. We hypothesized that selective and non-selective anti-inflammatory treatments would retard the healing of SFx in the rat ulna. SFxs were created by cyclic loading of the ulna in Wistar rats. Ulnae were harvested 2, 4 or 6 weeks following loading. Rats were treated with non-selective NSAID, ibuprofen (30 mg/kg/day); selective COX-2 inhibition, [5,5-dimethyl-3-3 (3 fluorophenyl)-4-(4 methylsulfonal) phenyl-2 (5H)-furanone] (DFU) (2.0 mg/kg/day); or the novel c5a anatagonist PMX53 (10 mg/kg/ day, 4 and 6 weeks only); with appropriate vehicle as control. Quantitative histomorphometric measurements of SFx healing were undertaken. Treatment with the selective COX-2 inhibitor, DFU, reduced the area of resorption along the fracture line at 2 weeks, without affecting bone formation at later stages. Treatment with the non-selective, NSAID, ibuprofen decreased both bone resorption and bone formation so that there was significantly reduced length and area of remodeling and lamellar bone formation within the remodeling unit at 6 weeks after fracture. The C5a receptor antagonist PMX53 had no effect on SFx healing at 4 or 6 weeks after loading, suggesting that PMX53 would not delay SFx healing. Both selective COX-2 inhibitors and non-selective NSAIDs have the potential to compromise SFx healing, and should be used with caution when SFx is diagnosed or suspected. ß

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Section: Discussionmentioning

confidence: 62%

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Kidd

Cowling

et al. 2012

Journal Orthopaedic Research

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“…Since PMNs are migrating and recruiting cells that are able to penetrate dentinal tubules, MMPs are helpful towards this end. 52 …”

Section: Role Of Mmps In Pulpal Inflammationmentioning

confidence: 99%

Role of matrix metalloproteinases in dental caries, pulp and periapical inflammation: An overview

Jain¹,

Bahuguna²

2015

Journal of Oral Biology and Craniofacial Research

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“…6). Some studies indicate that IL-6 promotes bone resorption and periapical lesion development (43). AAV-sh-Atp6i treatment reduced IL-6 levels in the AAV-sh-Atp6i-treated group compared to IL-6 levels in the periapical lesions of the AAV-sh-Luc-YFP-treated disease model group.…”

Section: Discussionmentioning

confidence: 99%

RNA Interference-Mediated Silencing of Atp6i Prevents Both Periapical Bone Erosion and Inflammation in the Mouse Model of Endodontic Disease

Chen

Zhang³

et al. 2013

Infect Immun

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dDental caries is one of the most prevalent infectious diseases in the United States, affecting approximately 80% of children and the majority of adults. Dental caries may lead to endodontic disease, where the bacterial infection progresses to the root canal system of the tooth, leading to periapical inflammation, bone erosion, severe pain, and tooth loss. Periapical inflammation may also exacerbate inflammation in other parts of the body. Although conventional clinical therapies for this disease are successful in approximately 80% of cases, there is still an urgent need for increased efficacy of treatment. In this study, we applied a novel gene-therapeutic approach using recombinant adeno-associated virus (AAV)-mediated Atp6i RNA interference (RNAi) knockdown of Atp6i/TIRC7 gene expression to simultaneously target periapical bone resorption and periapical inflammation. We found that Atp6i inhibition impaired osteoclast function in vitro and in vivo and decreased the number of T cells in the periapical lesion. Notably, AAV-mediated Atp6i/TIRC7 knockdown gene therapy reduced bacterial infection-stimulated bone resorption by 80% in the mouse model of endodontic disease. Importantly, Atp6i؉/؊ mice with haploinsufficiency of Atp6i exhibited protection similar to that in mice with bacterial infection-stimulated bone erosion and periapical inflammation, which confirms the potential therapeutic effect of AAV-small hairpin RNA (shRNA)-Atp6i/TIRC7. Our results demonstrate that AAV-mediated Atp6i/TIRC7 knockdown in periapical tissues can inhibit endodontic disease development, bone resorption, and inflammation, indicating for the first time that this potential gene therapy may significantly improve the health of those who suffer from endodontic disease.

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Sequential expressions of MMP‐1, TIMP‐1, IL‐6, and COX‐2 genes in induced periapical lesions in rats

Cited by 54 publications

References 36 publications

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Selective and non‐selective cyclooxygenase inhibitors delay stress fracture healing in the rat ulna

Role of matrix metalloproteinases in dental caries, pulp and periapical inflammation: An overview

RNA Interference-Mediated Silencing of Atp6i Prevents Both Periapical Bone Erosion and Inflammation in the Mouse Model of Endodontic Disease

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