Impaired periodontium and temporomandibular joints in tumour necrosis factor‐α transgenic mice

Dobsak, Toni; Heimel, Patrick; Tangl, Stefan; Schwarze, Uwe Yacine; Schett, Georg; Gruber, Reinhard

doi:10.1111/jcpe.12799

Cited by 10 publications

(9 citation statements)

References 45 publications

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“…There is strong but indirect evidence for the presence of endochondral bone formation, similar to the formation of cartilage upon sinus augmentation [45]. It is the characteristic morphology, in combination with the typical strong staining of cartilage by the Levai-Laczko [46], together with the shift in the mineral distribution that points towards the formation of a hypertrophic mineralized cartilage inside the VSCM. Moreover, considering that also endochondral bone formation during development and fracture healing is a continuous process, we observed a gradient where the mineralized hypertrophic chondrocytes are adjacent to the new bone, further supporting the impression of an endochondral bone formation.…”

Section: Discussionmentioning

confidence: 99%

Osteoconductive Properties of a Volume-Stable Collagen Matrix in Rat Calvaria Defects: A Pilot Study

et al. 2021

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Volume-stable collagen matrices (VSCM) are conductive for the connective tissue upon soft tissue augmentation. Considering that collagen has osteoconductive properties, we have investigated the possibility that the VSCM also consolidates with the newly formed bone. To this end, we covered nine rat calvaria circular defects with a VSCM. After four weeks, histology, histomorphometry, quantitative backscattered electron imaging, and microcomputed tomography were performed. We report that the overall pattern of mineralization inside the VSCM was heterogeneous. Histology revealed, apart from the characteristic woven bone formation, areas of round-shaped hypertrophic chondrocyte-like cells surrounded by a mineralized extracellular matrix. Quantitative backscattered electron imaging confirmed the heterogenous mineralization occurring within the VSCM. Histomorphometry found new bone to be 0.7 mm2 (0.01 min; 2.4 max), similar to the chondrogenic mineralized extracellular matrix with 0.7 mm2 (0.0 min; 4.2 max). Microcomputed tomography showed the overall mineralized tissue in the defect to be 1.6 mm3 (min 0.0; max 13.3). These findings suggest that in a rat cranial defect, VSCM has a limited and heterogeneous capacity to support intramembranous bone formation but may allow the formation of bone via the endochondral route.

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Section: Discussionmentioning

confidence: 99%

Osteoconductive Properties of a Volume-Stable Collagen Matrix in Rat Calvaria Defects: A Pilot Study

et al. 2021

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“…Nitric oxide (NO) induced by iNOS inhibits mitochondrial respiration and leads to chondrocyte apoptosis through the release of cytochrome C (Cyt C) and caspase‐9 43 . Furthermore, tumour necrosis factor (TNF) and FGFR1 are crucial cytokines that can facilitate chondrocyte apoptosis by acting on the death receptor pathway 44,45 …”

Section: The Canonical Pathological Changes During the Tmj Osteoarthritismentioning

confidence: 99%

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Guan

et al. 2021

J Cellular Molecular Medi

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Temporomandibular joint (TMJ) osteoarthritis is a common chronic degenerative disease of the TMJ. In order to explore its aetiology and pathological mechanism, many animal models and cell models have been constructed to simulate the pathological process of TMJ osteoarthritis. The main pathological features of TMJ osteoarthritis include chondrocyte death, extracellular matrix (ECM) degradation and subchondral bone remodelling. Chondrocyte apoptosis accelerates the destruction of cartilage. However, autophagy has a protective effect on condylar chondrocytes. Degradation of ECM not only changes the properties of cartilage but also affects the phenotype of chondrocytes. The loss of subchondral bone in the early stages of TMJ osteoarthritis plays an aetiological role in the onset of osteoarthritis. In recent years, increasing evidence has suggested that chondrocyte hypertrophy and endochondral angiogenesis promote TMJ osteoarthritis. Hypertrophic chondrocytes secrete many factors that promote cartilage degeneration. These chondrocytes can further differentiate into osteoblasts and osteocytes and accelerate cartilage ossification. Intrachondral angiogenesis and neoneurogenesis are considered to be important triggers of arthralgia in TMJ osteoarthritis. Many molecular signalling pathways in endochondral osteogenesis are responsible for TMJ osteoarthritis. These latest discoveries in TMJ osteoarthritis have further enhanced the understanding of this disease and contributed to the development of molecular therapies. This paper summarizes recent cognition on the pathogenesis of TMJ osteoarthritis, focusing on the role of chondrocyte hypertrophy degeneration and cartilage angiogenesis.

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“…Periodontium, the complex tissue supporting the teeth, comprises the gingiva, alveolar bone, periodontal ligament, and cementum . The integrity of the periodontium is crucial for the proper functioning of teeth.…”

Section: Introductionmentioning

confidence: 99%

Effects of oleanolic acid acetate on bone formation in an experimental periodontitis model in mice

Adhikari

Neupane

Aryal

et al. 2019

J of Periodontal Research

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Objective We evaluated the role of oleanolic acid acetate (OAA), a triterpenoid commonly used in the treatment of liver disorders, inflammatory diseases, and metastasis, in bone formation after tooth loss by periodontitis. Background Periodontitis causes the sequential degradation of the alveolar bone and associated structures, resulting in tooth loss. Several studies have attempted to regenerate the bone for implantation following tooth loss. Methods Maxillary left second molar was extracted from 8‐week‐old male mice following induction of periodontitis by ligature for 5 days. The extraction socket was treated with 50 ng/µL OAA for 1, 2, and 3 weeks. Detailed morphological changes were examined using Masson's trichrome staining, and the precise localization patterns of various signaling molecules, including CD31, F4/80, interleukin (IL)‐6, and osteocalcin, were observed. The volume of bone formation was examined by Micro‐CT. Osteoclasts were enumerated using tartrate‐resistant acid phosphatase (TRAP) staining. For molecular dissection of signaling molecules, we employed the hanging‐drop in vitro cultivation method at E14 for 1 day and examined the expression pattern of transforming growth factor (TGF)‐β superfamily and Wnt signaling genes. Results Histomorphometrical examinations showed facilitated bone formation in the extraction socket following OAA treatment. In addition, OAA‐treated specimens showed the altered localization patterns of inflammatory and bone formation‐related signaling molecules including CD31, F4/80, IL‐6, and osteocalcin. Also, embryonic tooth germ mesenchymal tissue cultivation with OAA treatment showed the significant altered expression patterns of signaling molecules such as transforming growth factor (TGF)‐β superfamily and Wnt signaling. Conclusions Oleanolic acid acetate induces bone formation and remodeling through proper modulation of osteoblast, osteoclast, and inflammation with regulations of TGF‐β and Wnt signaling.

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Impaired periodontium and temporomandibular joints in tumour necrosis factor‐α transgenic mice

Abstract: Our findings suggest that chronic inflammation in hTNFtg mice causes destructive changes of the periodontium and the TMJ.

Cited by 10 publications

References 45 publications

Osteoconductive Properties of a Volume-Stable Collagen Matrix in Rat Calvaria Defects: A Pilot Study

Osteoconductive Properties of a Volume-Stable Collagen Matrix in Rat Calvaria Defects: A Pilot Study

Pathological mechanism of chondrocytes and the surrounding environment during osteoarthritis of temporomandibular joint

Effects of oleanolic acid acetate on bone formation in an experimental periodontitis model in mice

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