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      Pre-implantation teriparatide administration improves initial implant stability and accelerates the osseointegration process in osteoporotic rats


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          Osteoporotic individuals who have dental implants usually require a prolonged healing time for osseointegration due to the shortage of bone mass and the lack of initial stability. Although studies have shown that intermittent teriparatide administration can promote osseointegration, there is little data to support the idea that pre-implantation administration is necessary and beneficial.


          Sixty-four titanium implants were placed in the bilateral proximal tibial metaphysis in 32 female SD rats. Bilateral ovariectomy (OVX) was used to induce osteoporosis. Four major groups ( n = 8) were created: PRE (OVX + pre-implantation teriparatide administration), POST (OVX + post-implantation administration), OP (OVX + normal saline (NS)) and SHAM (sham rats + NS). Half of rats ( n = 4) in each group were euthanized respectively at 4 weeks or 8 weeks after implantation surgery, and four major groups were divided into eight subgroups (PRE4 to SHAM8). Tibiae were collected for micro-CT morphometry, biomechanical test and undecalcified sections analysis.


          Compared to OP group, rats in PRE and SHAM groups had a higher value of insertion torque ( p < 0.05). The micro-CT analysis, biomechanical test, and histological data showed that peri-implant trabecular growth, implants fixation and bone-implant contact (BIC) were increased after 4 or 8 weeks of teriparatide treatment ( < 0.05). There was no statistically difference in those parameters between PRE4 and POST8 subgroups ( p > 0.05).


          In osteoporotic rats, post-implantation administration of teriparatide enhanced peri-implant bone formation and this effect was stronger as the medicine was taken longer. Pre-implantation teriparatide treatment improved primary implant stability and accelerated the osseointegration process.

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          Most cited references34

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          Control of osteoblast function and regulation of bone mass.

          The skeleton is an efficient 'servo' (feedback-controlled/steady-state) system that continuously integrates signals and responses which sustain its functions of delivering calcium while maintaining strength. In many individuals, bone mass homeostasis starts failing in midlife, leading to bone loss, osteoporosis and debilitating fractures. Recent advances, spearheaded by genetic information, offer the opportunity to stop or reverse this downhill course.
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            Use of bone turnover markers in postmenopausal osteoporosis

            Bone turnover comprises two processes: the removal of old bone (resorption) and the laying down of new bone (formation). N-terminal propeptide of type I procollagen (PINP) and C-telopeptide of type I collagen (CTX-I) are markers of bone formation and resorption, respectively, that are recommended for clinical use. Bone turnover markers can be measured on several occasions in one individual with good precision. However, these markers are subject to several sources of variability, including feeding (resorption decreases) and recent fracture (all markers increase for several months). Bone turnover markers are not used for diagnosis of osteoporosis and do not improve prediction of bone loss or fracture within an individual. In untreated women, very high bone turnover marker concentrations suggest secondary causes of high bone turnover (eg, bone metastases or multiple myeloma). In people with osteoporosis, bone turnover markers might be useful to assess the response to anabolic and antiresorptive therapies, to assess compliance to therapy, or to indicate possible secondary osteoporosis. Much remains to be learnt about how bone turnover markers can be used to monitor the effect of stopping bisphosphonate therapy (eg, to identify a threshold above which restarting therapy should be considered). More studies are needed to investigate the use of bone turnover markers for assessment of the bone safety of new medications.
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              Molecular and cellular mechanisms of the anabolic effect of intermittent PTH.

              Intermittent administration of parathyroid hormone (PTH) stimulates bone formation by increasing osteoblast number, but the molecular and cellular mechanisms underlying this effect are not completely understood. In vitro and in vivo studies have shown that PTH directly activates survival signaling in osteoblasts; and that delay of osteoblast apoptosis is a major contributor to the increased osteoblast number, at least in mice. This effect requires Runx2-dependent expression of anti-apoptotic genes like Bcl-2. PTH also causes exit of replicating progenitors from the cell cycle by decreasing expression of cyclin D and increasing expression of several cyclin-dependent kinase inhibitors. Exit from the cell cycle may set the stage for pro-differentiating and pro-survival effects of locally produced growth factors and cytokines, the level and/or activity of which are known to be influenced by PTH. Observations from genetically modified mice suggest that the anabolic effect of intermittent PTH requires insulin-like growth factor-I (IGF-I), fibroblast growth factor-2 (FGF-2), and perhaps Wnts. Attenuation of the negative effects of PPAR gamma may also lead to increased osteoblast number. Daily injections of PTH may add to the pro-differentiating and pro-survival effects of locally produced PTH related protein (PTHrP). As a result, osteoblast number increases beyond that needed to replace the bone removed by osteoclasts during bone remodeling. The pleiotropic effects of intermittent PTH, each of which alone may increase osteoblast number, may explain why this therapy reverses bone loss in most osteoporotic individuals regardless of the underlying pathophysiology.

                Author and article information

                Int J Implant Dent
                Int J Implant Dent
                International Journal of Implant Dentistry
                Springer Berlin Heidelberg (Berlin/Heidelberg )
                16 April 2024
                16 April 2024
                December 2024
                : 10
                : 18
                Department of General Dentistry, Peking University School and Hospital of Stomatology, National Center for Stomatology, National Clinical Research Center for Oral Diseases, National Engineering Research Center of Oral Biomaterials and Digital Medical Devices, Central Laboratory, Peking University School and Hospital of Stomatology, Beijing Key Laboratory of Digital Stomatology, NHC Key Laboratory of Digital Stomatology, NMPA Key Laboratory for Dental Materials, ( https://ror.org/02v51f717) Beijing, 100081 China
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                : 9 January 2024
                : 27 March 2024
                Funded by: FundRef http://dx.doi.org/10.13039/501100001809, National Natural Science Foundation of China;
                Award ID: 52111530189
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                © Deutsche Gesellschaft für Implantologie im Zahn‐, Mund‐ und Kieferbereich e.V., Japanese Society of Oral Implantology 2024

                teriparatide,dental implants,osseointegration,osteoporosis


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