Effects of silver diamine fluoride on demineralization protection after a secondary acid challenge.

OBJECTIVE: This investigation describes the effects of 5% sodium fluoride varnish and 38% silver diamine fluoride on demineralization protection of human enamel lesions of three different severities after a secondary acid challenge. STUDY DESIGN: Specimens underwent color and enamel surface microhardness change measurements after demineralization and treatment events. Transverse microradiography was conducted following the secondary demineralization. RESULTS: After treatments, enamel surface microhardness change showed that 24-hour lesions treated with fluoride varnish had less rehardening than 24-hour lesions treated with silver diamine fluoride (p<0.05), whereas 144-hour lesions from both treatment groups showed a beneficial decrease in surface microhardness change that was markedly better in samples treated with silver diamine fluoride (p<0.05). After the secondary demineralization, 24- and 144-hour lesions treated with silver diamine fluoride showed a sustained beneficial decrease in enamel surface microhardness change when compared to fluoride varnish-treated samples of the corresponding lesion severity (p<0.05). Transverse microradiography showed no difference between fluoride varnish- and silver diamine fluoride-treated samples of any corresponding lesion severity, indicating that remineralization in both fluoride varnish- and silver diamine fluoride-treated samples was proportional to each other after a secondary acid challenge. CONCLUSIONS: Using silver diamine fluoride may have comparable benefits to fluoride varnish in mineral loss prevention.

Effects of silver diamine fluoride on demineralization protection after a secondary acid challenge

Abstract Objective This investigation describes the effects of 5% sodium fluoride varnish and 38% silver diamine fluoride on demineralization protection of human enamel lesions of three different severities after a secondary acid challenge. Study design Specimens underwent color and enamel surface microhardness change measurements after demineralization and treatment events. Transverse microradiography was conducted following the secondary demineralization. Results After treatments, enamel surface microhardness change showed that 24-hour lesions treated with fluoride varnish had less rehardening than 24-hour lesions treated with silver diamine fluoride (p<0.05), whereas 144-hour lesions from both treatment groups showed a beneficial decrease in surface microhardness change that was markedly better in samples treated with silver diamine fluoride (p<0.05). After the secondary demineralization, 24- and 144-hour lesions treated with silver diamine fluoride showed a sustained beneficial decrease in enamel surface microhardness change when compared to fluoride varnish-treated samples of the corresponding lesion severity (p<0.05). Transverse microradiography showed no difference between fluoride varnish- and silver diamine fluoride-treated samples of any corresponding lesion severity, indicating that remineralization in both fluoride varnish- and silver diamine fluoride-treated samples was proportional to each other after a secondary acid challenge. Conclusions Using silver diamine fluoride may have comparable benefits to fluoride varnish in mineral loss prevention.

Analysis of pain in the rabbit temporomandibular joint after unilateral splint placement.

AIMS: To determine whether behavioral, anatomical, and physiologic endpoints widely used to infer the presence of pain in rodent models of temporomandibular disorders (TMD) were applicable to the rabbit model of TMD associated with altered joint loading. METHODS: Unilateral molar dental splints were used to alter temporomandibular joint (TMJ) loading. Changes in nociceptive threshold were assessed with a mechanical probing of the TMJ region on nine splinted and three control rabbits. Fos-like immunoreacitivty in the trigeminal subnucleus caudalis was assessed with standard immunohistochemical techniques from three splinted and six control animals. Retrogradely labeled TMJ afferents were studied with patch-clamp electrophysiologic techniques from three splinted and three control animals. Remodeling of TMJ condyles was assessed by histologic investigations of three splinted and three control animals. A Student t test or a Mann-Whitney U test was used with significance set at P < .05 to compare splinted to control samples. RESULTS: While variable, there was an increase in mechanical sensitivity in splinted rabbits relative to controls. The increase in Fos+ cells in splinted rabbits was also significant relative to naïve controls (86 ± 8 vs 64 ± 15 cells/section, P < .05). The rheobase (364 ± 80 pA) and action potential threshold (-31.2 ± 2.0 mV) were higher in TMJ afferents from splinted rabbits compared to controls (99 ± 22 pA and -38.0 ± 2.0 mV, P < .05). There was significant remodeling in the condylar fibrocartilage layers as manifested by a change in glycosaminoglycan distribution and a loss of defined cell layers. CONCLUSION: Behavioral and anatomical results were consistent with an increase in nociceptive signaling in concert with condylar remodeling driven by altered TMJ loading. Changes in excitability and action potential waveform were consistent with possible compensatory changes of TMJ afferents for an overall increase in afferent drive associated with joint degeneration. These compensatory changes may reflect pain-adaption processes that many patients with TMJ disorders experience.

Decreased Temporomandibular Joint Range of Motion in a Model of Early Osteoarthritis in the Rabbit.

PURPOSE: Analysis of mandibular biomechanics could help with understanding the mechanisms of temporomandibular joint (TMJ) disorders (TMJDs), such as osteoarthritis (TMJ-OA), by investigating the effects of injury or disease on TMJ movement. The objective of the present study was to determine the functional kinematic implications of mild TMJ-OA degeneration caused by altered occlusion from unilateral splints in the rabbit. MATERIALS AND METHODS: Altered occlusion of the TMJ was mechanically induced in rabbits by way of a unilateral molar dental splint (n = 3). TMJ motion was assessed using 3-dimensional (3D) skeletal kinematics twice, once before and once after 6 weeks of splint placement with the splints removed, after allowing 3 days of recovery. The relative motion of the condyle to the fossa and the distance between the incisors were tracked. RESULTS: An overall decrease in the range of joint movement was observed at the incisors and in the joint space between the condyle and fossa. The incisor movement decreased from 7.0 ± 0.5 mm to 6.2 ± 0.5 mm right to left, from 5.5 ± 2.2 mm to 4.6 ± 0.8 mm anterior to posterior, and from 13.3 ± 1.8 mm to 11.6 ± 1.4 mm superior to inferior (P < .05). The total magnitude of the maximum distance between the points on the condyle and fossa decreased from 3.6 ± 0.8 mm to 3.1 ± 0.6 mm for the working condyle and 2.8 ± 0.4 mm to 2.5 ± 0.4 mm for the balancing condyle (P < .05). The largest decreases were seen in the anteroposterior direction for both condyles. CONCLUSION: Determining the changes in condylar movement might lead to a better understanding of the early predictors in the development of TMJ-OA and determining when the symptoms become a chronic, irreversible problem.

Temporomandibular joint fibrocartilage degeneration from unilateral dental splints.

OBJECTIVE: The objective of this study was to determine the extent to which altered loading in the temporomandibular joint (TMJ), as might be associated with a malocclusion, drives degeneration of articulating surfaces in the TMJ. We therefore sought to quantify the effects of altered joint loading on the mechanical properties and biochemical content and distribution of TMJ fibrocartilage in the rabbit. DESIGN: Altered TMJ loading was induced with a 1mm splint placed unilaterally over the maxillary and mandibular molars for 6 weeks. At that time, TMJ fibrocartilage was assessed by compression testing, biochemical content (collagen, glycosaminoglycan (GAG), DNA) and distribution (histology), for both the TMJ disc and the condylar fibrocartilage. RESULTS: There were no changes in the TMJ disc for any of the parameters tested. The condylar fibrocartilage from the splinted animals was significantly stiffer and the DNA content was significantly lower than that in control animals. There was significant remodeling in the condylar fibrocartilage layers as manifested by a change in GAG and collagen II distribution and a loss of defined cell layers. CONCLUSIONS: A connection between the compressive properties of TMJ condylar fibrocartilage after 6 weeks of splinting and the changes in histology was observed. These results suggest a change in joint loading leads to condylar damage, which may contribute to pain associated with at least some forms of TMJ disease.

Poly (glycerol sebacate) elastomer supports osteogenic phenotype for bone engineering applications.

For bone engineering, the optimal scaffolding material and composition has yet to be elucidated. In this study, we investigated poly (glycerol sebacate) (PGS), an elastomer known primarily for its soft tissue regeneration ability, as a suitable substrate to support osteo-precursor cell attachment and function. We synthesized PGS in the form of sheets where MC3T3-E1 cells were seeded in three different densities of 25,000, 50,000 and 100,000 cells mm(-3) and we investigated the cells/scaffold constructs for their cellular proliferation, matrix deposition, maturation, mineralization and their mechanical compression strength at 24 h and two and four weeks. MC3T3-E1 cells proliferated, synthesized a collagenous matrix and expressed osteogenic markers Runx2, bone sialoprotein and osteocalcin according to their initial seeding density on PGS. We conclude that PGS can support the osteoblastic phenotype in vitro and is a promising osteoconductive substrate for bone regeneration research and for future clinical translation.

The effect of magnesium ion concentration on the fibrocartilage regeneration potential of goat costal chondrocytes.

Magnesium has recently been explored as a potential biomaterial for degradable orthopedic implants but its effect on fibrocartilage remains unknown. The objective of this study was to assess the effect of high concentrations of magnesium ions on the matrix production of goat costal fibrochondrocytes in vitro. Cells were cultured using a scaffoldless approach with media containing magnesium chloride (MgCl(2)) or magnesium sulfate (MgSO(4)) at concentrations of 20, 50, and 100 mM in addition to the baseline magnesium concentration of 0.8 mM MgSO(4). At 4 weeks, there were no significant differences in compressive tangent modulus and total matrix production between constructs cultured in 20 mM Mg(2+) and the 0.8 mM Mg(2+) control (435 ± 47 kPa). There was a significant decrease in compressive tangent modulus compared to the 0.8 mM Mg(2+) constructs in the 50 mM MgCl(2) and MgSO(4) groups, while the 100 mM groups were not mechanically testable (p < 0.05). The collagen and glycosaminoglycan (GAG) content of the 50 and 100 mM MgCl(2) and MgSO(4) constructs was significantly lower than the control (6.9 ± 0.5% and 16.5 ± 1.3% per dry weight, respectively) (p < 0.05). The results show that goat costal fibrochondrocytes exhibit a high degree of resiliency to magnesium ion concentrations up to 20 mM in vitro.

Sjögren's syndrome: an old tale with a new twist.

Sjögren's syndrome (SjS) is chronic autoimmune disease manifested by the loss of saliva and/or tear secretion by salivary and/or lacrimal glands, respectively. The pathogenesis of the disease remains elusive, perhaps due to the multiple triggers of the disease. However, substantial advances have been made in attempting to resolve the complexity of SjS using both animal models and human subjects. The primary objectives of this review are to provide a better understanding of the disease processes with major emphasis on the use of mouse models, how genetic predisposition plays a role in the natural history of the disease, as well as a presentation of new findings pertaining to the role of T(H)1, T(H)2, and T(H)17 cells in the pathogenesis of SjS.