teriparatide (SBL001 / Kauliv / SBL 001)

Pharmacological effects of PTH1R agonists on jaw bone fracture, periodontitis, orthodontic treatment and MRONJ: a view from dosing regimen settings.

Nakanishi-Kimura Atsuko A, Tsuji Naoki N, Scheller Erica L EL, Iimura Tadahiro T

Parathyroid hormone (PTH) and PTH-related peptide (PTHrP) are endogenous ligands of PTH type I receptor (PTH1R), which are essential for skeletal development and homeostasis. Since the intermittent application of these molecules to organisms exerts bone anabolic effects, they are used pharmacologically to increase bone mass and stimulate bone formation. Teriparatide, an N-terminal 34 amino acid fragment of human PTH, and abaloparatide, a derivative of the N-terminal 34 amino acid of human PTHrP, have been pharmaceutically developed and clinically applied to treat severe osteoporosis and are categorized as PTH1R agonists. An increasing number of clinical and preclinical studies have demonstrated that PTH1R agonists can be used in dental medicine, including jaw bone regeneration and orthodontic treatment, periodontitis, and the management of medication-related osteonecrosis of the jaw (MRONJ). However, it is unclear whether the mandibular bone responds pharmacologically to PTH1R agonists in the same way as other trunk bones, such as the limb and axial bones. Compared with studies using long and vertebral bones, the beneficial effects of PTH1R agonists on the mandibular bone appear to require higher doses and longer treatment durations. Clinical application of PTH1R agonists in dental medicine may result in promising outcomes. However, dosing regimens and the timing of their application should be further investigated with knowledge of the biological uniqueness of the mandibular bone.

Teriparatide Therapy in Children with Hypoparathyroidism: A Systematic Review and Meta-Analysis.

Tantivit Nessa N, Punyawatthananukool Siwakorn S

Hypoparathyroidism in children is conventionally treated with calcium and active vitamin D, however, this approach does not restore parathyroid hormone (PTH) action and may leave hyperphosphatemia unresolved while increasing the risk of hypercalciuria. Teriparatide (PTH 1-34) offers a physiologic replacement, although evidence regarding its role in children remains limited. We systematically reviewed biochemical and skeletal effects of teriparatide in children with hypoparathyroidism. MEDLINE and Embase were searched from inception to January 2026, including studies of patients ≤ 21 years treated with teriparatide for ≥ 4 weeks. Outcomes included calcium and phosphate homeostasis, skeletal outcomes, growth, renal complications, and use of concomitant therapy. Data extraction followed Preferred Reporting Items for Systematic Reviews and Meta-analysis (PRISMA) guidelines by 2 independent reviewers. Meta-analysis using weighted mean differences (WMDs) was performed when feasible. Other outcomes were summarized descriptively. Eighteen studies met the eligibility criteria, and a total of 94 pediatric patients were included. Serum calcium was maintained within target range with teriparatide, with no significant difference compared with conventional therapy (WMD -0.02, 95% CI -0.10 to 0.07). Serum phosphate was lower with teriparatide (WMD -0.28, 95% CI -0.45 to -0.12). Urinary calcium excretion findings were variable, although longer-term studies suggested reductions. Growth and bone mineral density remained within normal ranges. Renal outcomes were heterogeneous. Overall teriparatide maintains serum calcium and may improve phosphate balance in children with hypoparathyroidism. However, given limited and heterogeneous evidence, conventional therapy should remain first-line, with teriparatide considered in selected patients.

Chronic kidney disease: from mineral dysregulation to bone and cardiovascular disease.

Moustaki Melpomeni M, Paschou Stavroula A SA, Palioura Eleni E, Kassi Evanthia E et al.

Chronic kidney disease-mineral bone disorder (CKD-MBD) concerns more than 50% of patients with moderate/severe CKD, increasing their risk for fractures and cardiovascular events. To present its pathogenesis, clinical presentation and management. A Pubmed search for CKD-MBD until December 2025 was conducted using combinations of relevant terms. Total-body positive phosphate balance, increased levels of fibroblast-growth factor 23 (FGF-23) and sclerostin, and bone resistance to parathyroid hormone (PTH) are the earliest detected abnormalities, followed by calcitriol deficiency, secondary hyperparathyroidism, and bone minerals derangement. High bone turnover and adynamic bone disease stem from PTH excess and deficiency/resistance respectively, with the latter being prevalent in early CKD, peritoneal dialysis and post-kidney transplantation. Osteomalacia is rare, while mixed uremic osteodystrophy is rather common. Fracture risk assessment is based on fracture risk assessment tool, bone mineral density testing and vertebral morphometry, while bone biopsy remains the gold standard for renal osteodystrophy evaluation. Cardiovascular manifestations include vascular calcifications and left ventricular hypertrophy induced by mineral stress in the setting of disrupted buffering system, osteoblastic differentiation of vascular smooth cells and direct FGF-23 effects in myocardium. In severe secondary hyperparathyroidism, active vitamin D and analogues, calcimimetics, and, in refractory cases, parathyroidectomy effectively lower PTH. In mild/moderate CKD, the efficacy of all anti-osteoporotic agents is mainly proven in post-menopausal women without biochemical evidence of CKD-MBD. In dialysis patients, denosumab is the best-studied agent, while recent data highlight pronounced therapeutic benefit of romosozumab. Finally, teriparatide has demonstrated utility in treating adynamic bone disease. Fracture risk prevention in CKD-MBD should be prioritized. Dedicated research and validation of CKD-specific bone turnover markers may assist towards this direction.

Letter to the editor regarding "Pre-teriparatide anti-osteoporosis medication therapy and fracture-related hospitalization in patients at very high fracture risk".

Han Xiaotong X, Yang Maowei M