Effects of Surface Treatments and Cement Types on the Bond Strength of Porcelain‐to‐Porcelain Repair

Purpose The purpose of this in vitro study was to evaluate the effects of four surface treatments and two resin cements on the repair bond strength of a ceramic primer. Materials and Methods Eighty‐eight pairs of disks (10 and 5 mm in diameter, 3 mm thickness) were prepared from heat‐pressed feldspar ceramics (GC Initial IQ). After being stored in mucin‐artificial saliva for 2 weeks, the 10‐mm disks were divided into four surface treatment groups (n = 22) and then treated as follows: (1) no treatment (control); (2) 40% phosphoric acid; (3) 5% hydrofluoric acid + acid neutralizer + 40% phosphoric acid; (4) silica coating (CoJet‐sand) + 40% phosphoric acid. The 5‐mm disks were treated with 5% hydrofluoric acid + 40% phosphoric acid. The two sizes of porcelain disks, excluding the control group, were primed with Clearfil Ceramic Primer. The specimens in each group were further divided into two subgroups of 11 each, and bonded with Clearfil Esthetic Cement (CEC) or Panavia F 2.0 Cement (PFC). The specimens were stored in distilled water at 37°C for 24 hours, thermocycled for 3000 cycles at 5 to 55°C, and stored at 37°C for an additional 7 days. Shear bond strength (SBS) was measured with a universal testing machine at a 0.5 mm/min crosshead speed until fracture. Statistical analysis of the results was carried out with a two‐way ANOVA and Tukey HSD test (α = 0.05). Debonded specimen surfaces were examined under an optical microscope to determine the mode of failure. Results The statistical analysis showed that the SBS was significantly affected by surface treatment and resin cement ( p < 0.05). For treatment groups bonded with CEC, the SBS (MPa) values were (1) 2.64 ± 1.1, (2) 13.31 ± 3.6, (3) 18.88 ± 2.6, (4) 14.27 ± 2.7, while for treatment groups cemented with PFC, the SBS (MPa) values were (1) 3.04 ± 1.1, (2) 16.44 ± 3.3, (3) 20.52 ± 2.2, and (4) 16.24 ± 2.9. All control specimens exhibited adhesive failures, while mixed types of failures were observed in phosphoric acid‐treated groups. The other groups revealed mainly cohesive and mixed failures. Conclusions Combined surface treatment of etching with hydrofluoric acid and phosphoric acid provides the highest bond strengths to porcelain. Also, PFC exhibited higher SBS than CEC did.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/109888/1/jopr12194.pd

Perspective on Dentoalveolar Manifestations Resulting from PHOSPHO1 Loss-of-Function: A Form of Pseudohypophosphatasia?

Mineralization of the skeleton occurs by several physicochemical and biochemical processes and mechanisms that facilitate the deposition of hydroxyapatite (HA) in specific areas of the extracellular matrix (ECM). Two key phosphatases, phosphatase, orphan 1 (PHOSPHO1) and tissue-non-specific alkaline phosphatase (TNAP), play complementary roles in the mineralization process. The actions of PHOSPHO1 on phosphocholine and phosphoethanolamine in matrix vesicles (MVs) produce inorganic phosphate (P(i)) for the initiation of HA mineral formation within MVs. TNAP hydrolyzes adenosine triphosphate (ATP) and the mineralization inhibitor, inorganic pyrophosphate (PP(i)), to generate P(i) that is incorporated into MVs. Genetic mutations in the ALPL gene-encoding TNAP lead to hypophosphatasia (HPP), characterized by low circulating TNAP levels (ALP), rickets in children and/or osteomalacia in adults, and a spectrum of dentoalveolar defects, the most prevalent being lack of acellular cementum leading to premature tooth loss. Given that the skeletal manifestations of genetic ablation of the Phospho1 gene in mice resemble many of the manifestations of HPP, we propose that Phospho1 gene mutations may underlie some cases of “pseudo-HPP” where ALP may be normal to subnormal, but ALPL mutation(s) have not been identified. The goal of this perspective article is to compare and contrast the loss-of-function effects of TNAP and PHOSPHO1 on the dentoalveolar complex to predict the likely dental phenotype in humans that may result from PHOSPHO1 mutations. Potential cases of pseudo-HPP associated with PHOSPHO1 mutations may resist diagnosis, and the dental manifestations could be a key criterion for consideration

Gene therapy using recombinant AAV type 8 vector encoding TNAP-D10 improves the skeletal phenotypes in murine models of osteomalacia

Hypophosphatasia (HPP), caused by loss‐of‐function mutations in the ALPL gene encoding tissue‐nonspecific alkaline phosphatase (TNAP), is characterized by skeletal and dental hypomineralization that can vary in severity from life‐threatening to milder manifestations only in adulthood. PHOSPHO1 deficiency leads to early‐onset scoliosis, osteomalacia, and fractures that mimic pseudo‐HPP. Asfotase alfa, a life‐saving enzyme replacement therapy approved for pediatric‐onset HPP, requires subcutaneous injections 3 to 6 times per week. We recently showed that a single injection of an adeno‐associated virus vector serotype 8 harboring TNAP‐D(10) (AAV8‐TNAP‐D(10)) effectively prevented skeletal disease and prolonged life in Alpl ( −/− ) mice phenocopying infantile HPP. Here, we aimed to determine the efficacy of AAV8‐TNAP‐D(10) in improving the skeletal and dental phenotype in the Alpl ( Prx1/Prx1 ) and Phospho1 (−/−) mouse models of late‐onset (adult) HPP and pseudo‐HPP, respectively. A single dose of 3 × 10(11) vector genomes per body (vg/b) was injected intramuscularly into 8‐week‐old Alpl ( Prx1/Prx1 ) and wild‐type (WT) littermates, or into 3‐day‐old Phospho1 (−/−) and WT mice, and treatment efficacy was evaluated after 60 days for late‐onset HPP mice and after 90 days for Phospho1 (−/−) mice. Biochemical analysis showed sustained serum alkaline phosphatase activity and reduced plasma PP(i) levels, and radiographic images, micro‐computed tomography (micro‐CT) analysis, and hematoxylin and eosin (H&E) staining showed improvements in the long bones in the late‐onset HPP mice and corrected scoliosis in the Phospho1 ( −/− ) mice. Micro‐CT analysis of the dentoalveolar complex did not reveal significant changes in the phenotype of late‐onset HPP and pseudo‐HPP models. Moreover, alizarin red staining analysis showed that AAV8‐TNAP‐D(10) treatment did not promote ectopic calcification of soft organs in adult HPP mice after 60 days of treatment, even after inducing chronic kidney disease. Overall, the AAV8‐TNAP‐D(10) treatment improved the skeletal phenotype in both the adult HPP and pseudo‐HPP mouse models. This preclinical study will contribute to the advancement of gene therapy for the improvement of skeletal disease in patients with heritable forms of osteomalacia. © 2022 The Authors. JBMR Plus published by Wiley Periodicals LLC on behalf of American Society for Bone and Mineral Research