Abstract

Leptin is a non-glycosylated 16 kDa protein synthesized mainly in adipose cells. The main function of leptin is to regulate energy homeostasis and weight control in a central manner. There is increasing evidence that leptin also has systemic effects, acting as a link between innate and acquired immune responses. The expression of leptin and its receptor in human dental pulp and periradicular tissues have already been described, as well as several stimulatory effects of leptin protein expression in dental and periodontal tissues. The aim of this paper was to review and to compile the reported scientific literature on the role and effects of leptin in the dental pulp and periapical tissues. Twelve articles accomplished the inclusion criteria, and a comprehensive narrative review was carried out. Review of the available scientific literature concluded that leptin has the following effects on pulpal and periapical physiology: 1) Stimulates odontogenic differentiation of dental pulp stem cells (DPSCs), 2) Increases the expression of dentin sialophosphoprotein (DSPP) and dentin matrix protein-1 (DMP-1), odontoblastic proteins involved in odontoblastic differentiation and dentin mineralization, 3) Stimulates vascular endothelial growth factor (VEGF) expression in human dental pulp tissue and primary cultured cells of human dental pulp (hDPCs), 4) Stimulates angiogenesis in rat dental pulp cells, and 5) Induces the expression of interleucinas 6 and 8 in human periodontal ligament cells (hPDLCs). There is evidence which suggests that leptin is implicated in the dentin mineralization process and in pulpal and periapical inflammatory and reparative responses.

Highlights

  • At present, the possible association between oral inflammatory processes caused by infection and systemic health is an interesting aspect that the medical and dental community focuses its research on to improve the health of patients [1]

  • Pulpitis and apical periodontitis are oral inflammatory processes caused by infection, and these diseases may help the scientific community as they are ideal models to explore the pathways or mechanisms by which oral local infections can harm systemic health

  • El Karim et al (2009) [47] were the first to report that leptin is synthesized and secreted in vitro by pulp fibroblasts derived from extracted healthy molar teeth (Table 1)

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Summary

Introduction

The possible association between oral inflammatory processes caused by infection and systemic health is an interesting aspect that the medical and dental community focuses its research on to improve the health of patients [1]. When etiological agents invade the dental pulp an immune and inflammatory response is stimulated and pulpitis or dental pulp inflammation appears [10]. If the intensity of the aggressive factors is mild or moderate, a reversible pulpitis will be established and pulp inflammation will be controlled and repaired, maintaining pulp sensitivity. The inflammation of the tissue around the tooth root, usually around the root apex, caused by infection of the dental pulp, is known as apical periodontitis [12]. Apical periodontitis occurs when cariogenic microorganisms or antigenic content that have invaded the dental pulp reach the periapical or periradicular connective tissue, stimulating an inflammatory and immune response. The apical periodontitis can be reversible or irreversible and an acute or chronic inflammation. The aim of this review is to analyze the available scientific evidence about the expression and effects of leptin in dental pulp and periapical tissues in order to clarify and summarize the role of leptin in pulpal and periapical physiology

Literature Search and Scope of The Review
Leptin
Leptin and The Dental Pulp
Leptin and Periradicular Tissues
Highlights
Conclusions
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