Influence of Aging on Biological Properties of Periodontal Ligament Cells

Benatti, Bruno Braga; Silvério, Karina Gonzáles; Casati, Márcio Zaffalon; Sallum, Enílson Antônio; Nociti, Francisco Humberto

doi:10.1080/03008200802171159

Cited by 36 publications

(39 citation statements)

References 46 publications

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“…1). However, a dramatic reduction in Col3 mRNA expression occurs in aged mice, consistent with the decreased Col3 described in other tissues during aging [28-32]. Mice of both genotypes were found to have Col3 mRNA expression at levels of <10% of that seen in young wild-type mice.…”

Section: Resultssupporting

confidence: 66%

Type III Collagen Regulates Osteoblastogenesis and the Quantity of Trabecular Bone

et al. 2014

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Type III Collagen (Col3), a fibril-forming collagen, is a major extracellular matrix component in a variety of internal organs and skin. It is also expressed at high levels during embryonic skeletal development and is expressed by osteoblasts in mature bone. Loss of function mutations in the gene encoding Col3 (Col3a1) are associated with vascular Ehlers Danlos Syndrome (EDS). Although the most significant clinical consequences of this syndrome are associated with catastrophic failure and impaired healing of soft tissue structures, several studies have documented skeletal abnormalities in vascular EDS patients. However, there are no reports of the role of Col3 deficiency on the murine skeleton. We compared craniofacial and skeletal phenotypes in young (6-8 weeks) and middle-aged (>1 year) control (Col3+/+) and haploinsufficient (Col3+/−) mice, as well as young null (Col3−/−) mice using microcomputed tomography (μCT). Although Col3+/− mice did not have significant craniofacial abnormalities based upon cranial morphometrics, microCT analysis of distal femur trabecular bone demonstrated significant reductions in bone volume (BV), bone fraction volume (BV/TV), connectivity density (ConnD), structure model index (SMI) and trabecular thickness (TbTh) in young adult, female Col3+/− mice relative to wild-type littermates. The reduction in BV/TV persisted in female mice at one year of age. Next we evaluated the role of Col3 in vitro. Osteogenesis assays revealed that cultures of mesenchymal progenitors harvested from Col3−/− embryos display decreased alkaline phosphatase activity and reduced capacity to undergo mineralization. Consistent with this data, a reduction in osteogenic markers (type I collagen, osteocalcin and bone sialoprotein) correlates with reduced bone Col3 expression in Col+/− mice and with age in vivo. A small but significant reduction in osteoclast numbers was found in Col3+/− compared to Col3+/+ bones. Taken together, these findings indicate that Col3 plays a role in development of trabecular bone through its effects on osteoblast differentiation.

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Section: Resultssupporting

confidence: 66%

Type III Collagen Regulates Osteoblastogenesis and the Quantity of Trabecular Bone

et al. 2014

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“…Aging causes a delay in the regeneration of periodontal tissues (Benatti et al, 2006), probably due to modifications in cell phenotype (Lossdörfer et al, 2010), defects in cell proliferation, and changes in the regulation of inflammatory cytokines (Benatti et al, 2009). In addition, aging may decrease the synthesis of collagen types I and III (Benatti et al, 2008). All these studies have made important contributions to our understanding of the effects of aging on periodontal tissues.…”

mentioning

confidence: 99%

Defective Wound-healing in Aging Gingival Tissue

Cáceres

Oyarzún

2014

J Dent Res

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Aging may negatively affect gingival wound-healing. However, little is known about the mechanisms underlying this phenomenon. The present study examined the cellular responses associated with gingival wound-healing in aging. Primary cultures of human gingival fibroblasts were obtained from healthy young and aged donors for the analysis of cell proliferation, cell invasion, myofibroblastic differentiation, and collagen gel remodeling. Serum from young and old rats was used to stimulate cell migration. Gingival repair was evaluated in SpragueDawley rats of different ages. Data were analyzed by the Mann-Whitney and Kruskal-Wallis tests, with a p value of .05. Fibroblasts from aged donors showed a significant decrease in cell proliferation, migration, Rac activation, and collagen remodeling when compared with young fibroblasts. Serum from young rats induced higher cell migration when compared with serum from old rats. After TGF-beta1 stimulation, both young and old fibroblasts demonstrated increased levels of alpha-SMA. However, alpha-SMA was incorporated into actin stress fibers in young but not in old fibroblasts. After 7 days of repair, a significant delay in gingival wound-healing was observed in old rats. The present study suggests that cell migration, myofibroblastic differentiation, collagen gel remodeling, and proliferation are decreased in aged fibroblasts. In addition, altered cell migration in wound-healing may be attributable not only to cellular defects but also to changes in serum factors associated with the senescence process.

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“…Recent studies have evaluated the role of aging on the proliferative potential of periodontal cells. Concerning gingival and periodontal wound healing, Benatti et al (2008) described that primary cultures of human periodontal ligament fibroblasts derived from aged donors displayed a reduction in cell proliferation compared with cells obtained from young individuals. These results were also confirmed in our recent study that evaluated cell proliferation in human gingival fibroblasts derived from young and aged donors (Cáceres et al 2014).…”

Section: Cell Proliferationmentioning

confidence: 99%

“…Matrix metalloproteinases (MMPs) also have been involved in the remodeling of ECM components that are necessary to adjust the amount of newly formed tissue during gingival wound healing (Ravanti et al 1999). Increased levels of MMPs and tissue inhibitors of MMPs (TIMPs) have been identified in aged periodontal ligament cells compared with cells derived from young donors (Benatti et al 2008). Therefore, it is possible that tissue remodeling and maturation develop with an increased level of proteolytic enzymes in aged subjects, which might degrade and eventually weaken the newly formed tissue.…”

Section: Tissue Remodelingmentioning

confidence: 99%

Gingival Wound Healing

Cáceres

Martínez

et al. 2014

J Dent Res

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Gingival wound healing comprises a series of sequential responses that allow the closure of breaches in the masticatory mucosa. This process is of critical importance to prevent the invasion of microbes or other agents into tissues, avoiding the establishment of a chronic infection. Wound healing may also play an important role during cell and tissue reaction to long-term injury, as it may occur during inflammatory responses and cancer. Recent experimental data have shown that gingival wound healing is severely affected by the aging process. These defects may alter distinct phases of the wound-healing process, including epithelial migration, granulation tissue formation, and tissue remodeling. The cellular and molecular defects that may explain these deficiencies include several biological responses such as an increased inflammatory response, altered integrin signaling, reduced growth factor activity, decreased cell proliferation, diminished angiogenesis, reduced collagen synthesis, augmented collagen remodeling, and deterioration of the proliferative and differentiation potential of stem cells. In this review, we explore the cellular and molecular basis of these defects and their possible clinical implications.

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Influence of Aging on Biological Properties of Periodontal Ligament Cells

Cited by 36 publications

References 46 publications

Type III Collagen Regulates Osteoblastogenesis and the Quantity of Trabecular Bone

Type III Collagen Regulates Osteoblastogenesis and the Quantity of Trabecular Bone

Defective Wound-healing in Aging Gingival Tissue

Gingival Wound Healing

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