Fracture Healing and Mast Cells

Banovac, K; Renfree, Kevin J.; Makowski, Anna Lena; Latta, L.; Altman, Roy D.

doi:10.1097/00005131-199509060-00005

Cited by 34 publications

(34 citation statements)

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“…Taken together, the results indicate that mast cells have a positive impact on bone repair that is mediated in part by recruitment of vascular endothelial cells, as also suggested by the previous work of Boesiger et al (1998) [21], and in part by altered metabolism of newly formed bone. It was proposed more than two decades ago that mast cells are involved in tissue digestion and re-vascularization, which are early and essential steps in the bone healing cascade [9]. Mast cells reside over the long term in connective tissues where they are available locally and for potential trafficking via the vascular and lymphatic systems to sites of tissue injury and repair [22].…”

Section: Discussionmentioning

confidence: 99%

“…An early study of fracture repair in young rats revealed mast cells adjacent to blood vessels in the soft callus at two weeks of healing and distributed throughout the hard callus near osteoclasts at six weeks [9], suggesting these cells played a role in the healing process. A study conducted under steady state on mast cell-deficient mice carrying a mutation in the receptor for stem cell factor Kit ( Kit W/Wv ) revealed alterations in femoral bone mass and geometry leading to decreased mechanical strength [10].…”

Section: Introductionmentioning

confidence: 99%

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Defective bone repair in mast cell-deficient Cpa3Cre/+ mice

et al. 2017

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In the adult skeleton, cells of the immune system interact with those of the skeleton during all phases of bone repair to influence the outcome. Mast cells are immune cells best known for their pathologic role in allergy, and may be involved in chronic inflammatory and fibrotic disorders. Potential roles for mast cells in tissue homeostasis, vascularization and repair remain enigmatic. Previous studies in combined mast cell- and Kit-deficient KitW-sh/W-sh mice (KitW-sh) implicated mast cells in bone repair but KitW-sh mice suffer from additional Kit-dependent hematopoietic and non- hematopoietic deficiencies that could have confounded the outcome. The goal of the current study was to compare bone repair in normal wild type (WT) and Cpa3Cre/+ mice, which lack mast cells in the absence of any other hematopoietic or non- hematopoietic deficiencies. Repair of a femoral window defect was characterized using micro CT imaging and histological analyses from the early inflammatory phase, through soft and hard callus formation, and finally the remodeling phase. The data indicate 1) mast cells appear in healing bone of WT mice but not Cpa3Cre/+ mice, beginning 14 days after surgery; 2) re-vascularization of repair tissue and deposition of mineralized bone was delayed and dis-organised in Cpa3Cre/+ mice compared with WT mice; 3) the defects in Cpa3Cre/+ mice were associated with little change in anabolic activity and biphasic alterations in osteoclast and macrophage activity. The outcome at 56 days postoperative was complete bridging of the defect in most WT mice and fibrous mal-union in most Cpa3Cre/+ mice. The results indicate that mast cells promote bone healing, possibly by recruiting vascular endothelial cells during the inflammatory phase and coordinating anabolic and catabolic activity during tissue remodeling. Taken together the data indicate that mast cells have a positive impact on bone repair.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Defective bone repair in mast cell-deficient Cpa3Cre/+ mice

et al. 2017

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“…Mast cells are connective tissue residents, they have been observed throughout the early inflammatory phases of fracture healing, and mast cell activation has been shown to promote myofibroblast proliferation and increased collagen synthesis [9,13,[27][28][29]. Mast cell hyperplasia has more recently been observed within affected joint capsules GTG TGA GGA AGA GGA CAG CA TAC GTC CAG AGG CAT AGA GG 20 446 55 32 Col I GAT GCG TTC CAG TTC GAG TA GGT CTT CCG GTG GTC TTG TA 20 312 55 22 Col III TTA TAA ACC AAC CTC TTC CT TAT TAT AGC ACC ATT GAG AC 20 255 55 28 TGF-b1 CGG CAG CTG TAC ATT GAC TT AGC GCA CGA TCA TGT TGG AC 20 271 60 32 GAPDH TCA CCA TCT TCC AGG AGC AG CAC AAT GCC GAA GTG GTC GT 20 293 55 harvested from post-traumatic contractures of the human elbow and the rabbit knee [30].…”

Section: Discussionmentioning

confidence: 99%

The mast cell stabilizer ketotifen reduces joint capsule fibrosis in a rabbit model of post-traumatic joint contractures

et al. 2011

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“…Mast cells are known to appear in the fracture callus several weeks after fracture. 51,52 It is interesting that this should occur here by 4 weeks after fracture without regard to whether the bone had reached radiographic union.…”

Section: Discussionmentioning

confidence: 99%

Young, adult, and old rats have similar changes in mRNA expression of many skeletal genes after fracture despite delayed healing with age

Meyer

Desai

Heiner

et al. 2006

Journal Orthopaedic Research

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Genes active in fracture healing are not well understood. Because age slows skeletal repair, the change in gene expression between animals of differing ages may illuminate novel pathways important to this healing response. To explore this, 6-, 26-, and 52-week-old female Sprague-Dawley rats were subjected to mid-diaphyseal femoral fracture with intramedullary fixation. The fracture callus was collected at 0, 0.4 (3 days), 1, 2, 4, or 6 weeks after fracture. RNA was extracted and pooled between two animals for each sample. Three samples were done for each time point for each age for a total of 54 Affymetrix U34A GeneChip microarrays. Of the 8700 genes on each array, 3300 were scored as present. Almost all of these genes were affected by femoral fracture with either upregulation or downregulation in the 6 weeks after fracture. Upregulated genes included markers for matrix genes for both cartilage and bone, osteoblasts, osteocytes, osteoclasts, fibroblasts, and mast cells. Downregulated genes included genes related to blood cell synthesis. Nearly all genes presently associated with bone metabolism showed the same response to fracture healing regardless of the age of the animal. In conclusion, skeletal fracture led to similar changes in RNA expression for most skeletal genes despite the delay in the formation of bone to bridge the fracture gap in old rats. Defects in the healing of skeletal trauma in older rats may lie in systems not normally studied by skeletal biologists. ß

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Fracture Healing and Mast Cells

Cited by 34 publications

References 1 publication

Defective bone repair in mast cell-deficient Cpa3Cre/+ mice

Defective bone repair in mast cell-deficient Cpa3Cre/+ mice

The mast cell stabilizer ketotifen reduces joint capsule fibrosis in a rabbit model of post-traumatic joint contractures

Young, adult, and old rats have similar changes in mRNA expression of many skeletal genes after fracture despite delayed healing with age

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