Combat Lesion in Triceratops: Histological and Chemical Diagnosis

In the collective imagination derived from scientific and popular literature, Triceratops often faced each other in combat. Thus, from the second half of the twentieth century, these ceratopsids were described as pugnacious animals. This arises primarily from the interpretation of extracranial fenestrae in ceratopsids being the result of combat trauma. However, the diagnosis of the traumatic nature of these anatomical variants of their neck frill requires evidence of bone healing and remodelling by microscopy analysis. Here, we present the case of the Triceratops horridus known as Big John, which is one of the largest specimens discovered in the Hell Creek Formation (Upper Cretaceous; MT, USA). Its right squamosal bone shows an extrafenestra with irregular margins and signs of inflammation. Microscopy analysis revealed newly formed and healing bone, with histological signs typical of the bone remodelling phase. Chemical analysis revealed sulphur that was derived from glucosaminoglycans and sulphated glycoproteins of the preosseous osteoid substance present in the healing phases of a bone trauma. Histological and microanalytical analyses confirm that the squamosal fenestra of Big John is the result of a traumatic event, which might indeed have occurred during combat with another Triceratops.

Flavonoids: Classification, Function, and Molecular Mechanisms Involved in Bone Remodelling

Flavonoids are polyphenolic compounds spotted in various fruits, vegetables, barks, tea plants, and stems and many more natural commodities. They have a multitude of applications through their anti-inflammatory, anti-oxidative, anti-carcinogenic properties, along with the ability to assist in the stimulation of bone formation. Bone, a rigid connective body tissue made up of cells embedded in a mineralised matrix is maintained by an assemblage of pathways assisting osteoblastogenesis and osteoclastogenesis. These have a significant impact on a plethora of bone diseases. The homeostasis between osteoblast and osteoclast formation decides the integrity and structure of the bone. The flavonoids discussed here are quercetin, kaempferol, icariin, myricetin, naringin, daidzein, luteolin, genistein, hesperidin, apigenin and several other flavonoids. The effects these flavonoids have on the mitogen activated protein kinase (MAPK), nuclear factor kappa β (NF-kβ), Wnt/β-catenin and bone morphogenetic protein 2/SMAD (BMP2/SMAD) signalling pathways, and apoptotic pathways lead to impacts on bone remodelling. In addition, these polyphenols regulate angiogenesis, decrease the levels of inflammatory cytokines and play a crucial role in scavenging reactive oxygen species (ROS). Considering these important effects of flavonoids, they may be regarded as a promising agent in treating bone-related ailments in the future.

Generalised S-System-Type Equation: Sensitivity of the Deterministic and Stochastic Models for Bone Mechanotransduction

The formalism of a bone cell population model is generalised to be of the form of an S-System. This is a system of nonlinear coupled ordinary differential equations (ODEs), each with the same structure: the change in a variable is equal to a difference in the product of a power-law functions with a specific variable. The variables are the densities of a variety of biological populations involved in bone remodelling. They will be specified concretely in the cases of a specific periodically forced system to describe the osteocyte mechanotransduction activities. Previously, such models have only been deterministically simulated causing the populations to form a continuum. Thus, very little is known about how sensitive the model of mechanotransduction is to perturbations in parameters and noise. Here, we revisit this assumption using a Stochastic Simulation Algorithm (SSA), which allows us to directly simulate the discrete nature of the problem and encapsulate the noisy features of individual cell division and death. Critically, these stochastic features are able to cause unforeseen dynamics in the system, as well as completely change the viable parameter region, which produces biologically realistic results.

Avascular necrosis with non-union of the scaphoid managed with a dorsal pedicled vascularised bone graft of the distal radius – a case report

Avascular necrosis (AVN) of the scaphoid is common following proximal pole fractures due to an arduous retrograde arterial vascular supply and it is a challenge to the hand surgeon. The treatment for scaphoid non-union with avascular necrosis is vascularized or non-vascularized bone grafts. Non vascularised bone grafts (NVBGs) can be categorized as autograft or allograft and cancellous or cortical bone grafts. Vascularised bone grafts promote biological healing and revascularizes ischaemic bone and they are free or pedicled grafts. Pedicled vascularised bone grafts maintain the vascular supply of the donor bone graft and this leads to better bone remodelling, less osteopenia, faster incorporation and better maintenance of bone mass compared to the non-vascularised graft with good clinical and radiological outcomes. In this paper, we have treated avascular necrosis of scaphoid with a pedicled vascularised bone graft based on the 1, 2 intercompartmental supraretinacular artery (1, 2-ICSRA) that resulted in a favourable outcome.

Rethinking Fragility Fractures in Type 2 Diabetes: The Link between Hyperinsulinaemia and Osteofragilitas

Patients with type 2 diabetes mellitus (T2DM) and/or cardiovascular disease (CVD), conditions of hyperinsulinaemia, have lower levels of osteocalcin and bone remodelling, and increased rates of fragility fractures. Unlike osteoporosis with lower bone mineral density (BMD), T2DM bone fragility “hyperinsulinaemia-osteofragilitas” phenotype presents with normal to increased BMD. Hyperinsulinaemia and insulin resistance positively associate with increased BMD and fragility fractures. Hyperinsulinaemia enforces glucose fuelling, which decreases NAD+-dependent antioxidant activity. This increases reactive oxygen species and mitochondrial fission, and decreases oxidative phosphorylation high-energy production capacity, required for osteoblasto/cytogenesis. Osteocytes directly mineralise and resorb bone, and inhibit mineralisation of their lacunocanalicular space via pyrophosphate. Hyperinsulinaemia decreases vitamin D availability via adipocyte sequestration, reducing dendrite connectivity, and compromising osteocyte viability. Decreased bone remodelling and micropetrosis ensues. Trapped/entombed magnesium within micropetrosis fossilisation spaces propagates magnesium deficiency (MgD), potentiating hyperinsulinaemia and decreases vitamin D transport. Vitamin D deficiency reduces osteocalcin synthesis and favours osteocyte apoptosis. Carbohydrate restriction/fasting/ketosis increases beta-oxidation, ketolysis, NAD+-dependent antioxidant activity, osteocyte viability and osteocalcin, and decreases excess insulin exposure. Osteocalcin is required for hydroxyapatite alignment, conferring bone structural integrity, decreasing fracture risk and improving metabolic/endocrine homeodynamics. Patients presenting with fracture and normal BMD should be investigated for T2DM and hyperinsulinaemia.

Bone remodelling patterns around orthodontic mini-implants migrating in bone: an experimental study in rat vertebrae

Summary Background Orthodontic implant migration has been clinically observed in presence of continuous loading forces. Recent studies indicate that osteocytes play a crucial role in this phenomenon. Objectives Aim of this study was to investigate local osteocytic gene expression, protein expression, and bone micro-structure in peri-implant regions of pressure and tension. Material and methods The present work reports a complementary analysis to a previous micro-computed tomography study. Two customized mini-implants were placed in one caudal rat vertebra and connected by a nickel–titanium contraction spring generating different forces (i.e. 0, 0.5, 1.0, and 1.5 N). Either at 2 or 8 weeks, the vertebrae were harvested and utilized for 1. osteocytic gene expression using laser capture micro-dissection on frozen sections coupled with qPCR, 2. haematoxylin–eosin staining for qualitative and quantitative analyses, 3. immunofluorescence staining and analysis, and 4. bone-to-implant contact on undecalcified samples. Results At the two time points for all the performed analyses no significant differences were observed with respect to the applied force magnitudes and cell harvesting localization. However, descriptive histological analysis revealed remarkable bone remodelling at 2 weeks of loading. At 8 weeks the implants were osseointegrated and, especially in 1.0 and 1.5 N groups, newly formed bone presented a characteristic load bearing architecture with trabecula oriented in the direction of the loading. Conclusions The present study confirmed that stress-induced bone remodelling is the biological mechanism of orthodontic implant migration. Bone apposition was found at ‘tension’ and ‘pressure’ sites thus limiting implant migration over time.