Acts as an antagonist to the effects of PTH and inhibits bone resorption by osteoclasts. Thyroid hormones 4. Insulin 5. Growth hormone, important regulator of calcium absorptionfrom the intestine and renal tubules. Glucocorticoids 8. Bone disorders ofrelevance to an orthodontist 1. Congenital and hereditary disorders 2. Bone infections 3. Metabolic bone diseases 4. Fractures 5. Other non-neoplastic disorders of bone 6.
Bone tumours The condition is most common in children. Treatment: Vitamin D deficiency is treated with supplementation. This relatively common condition is associated with elevated serum and urinary calcium. This disease is associated with continued growth of the bones of the jaw, hands, and feet. Osteoporosis is associated with either a loss of boneor a decrease in bone formation. Complications include fractures, neoplasia, nerve compressionand high output cardiac failure.
There is also a hereditary factor since the disease may appear in more than one family member. Dental features: The maturation of the primary dentition is normal, but permanent teeth are delayed from 1 to 4 years. Most patients have supernumerary permanent teeth. Some of the most prevalent craniosynostosis include Aperts , Crouzon , and Pfeiffer.
Most of these syndromes are due to gain of function mutations in the fibroblast growth factor receptor 2 FGFR2 Inheritance: autosomal dominant trait. There is There may also be evidence of enamel hypermineralisation and hypoplasia. The jaws are composed ofdense bone and the mandible is more frequently affected than the maxilla Inheritance: Autosomal recessive.
This is the most common form of OI and is associated with brittle bones composed ofimmature woven bone. The sclerae are thin and may appear blue due to the visible pigmented choroids. Other abnormalities may include: conductive deafness due to otosclerosis, discoloured teeth due to dentinogenesis imperfecta DI , hypermobility with lax ligaments, Life span is normal and the condition is often mild in severity.
Newborns have soft calvarial bones, distinctive triangular face, bluish sclerae, beaked nose, narrow thorax and short and deformed limbs Type III: Infants born with fractures. Dental related abnormalities may include reduced craniofacial size measurements and a posteriorly inclined maxilla. Treatable with large doses ofvitamin D or its active metabolite calcitriol and oral phosphate.
Embryological primary toothformation In the human embryo, development of the deciduous dentition begins at around 6 weeks with the formation of a continuous horseshoe-shaped band of thickened epithelium around the lateral margins of the primitive oral cavity. The free margin of this band gives rise to two processes, which invaginate into the underlying mesenchyme: 1. The outer process orvestibular lamina is initially continuous, but soon breaks down to form a vestibule that demarcates the cheeks and lips from the tooth-bearing regions.
The inner process ordental lamina gives rise to the enamel organs of the future developing teeth which is called later tooth bud. Stages 1. The dental papilla is formed by localized condensation of neural crest- derived ectomesenchymal cells around the dental lamina. Then the dental papilla extend around the enamel organ to form the dental follicle or tooth bud.
Together, these tissues constitute the tooth germ and will give rise to all structures that make up the mature tooth. This is called bud stage. At the cap stage, the tooth bud folds to demarcate the early morphology of the crown, which is modified by further folding at the bell stage. During the bell stage, the innermost layer of cells within the epithelial component of the tooth organ, the inner enamel epithelium, induce adjacent cells of the dental papilla to differentiate into odontoblasts, responsible for the formation and mineralization of dentine.
Dentine formation is preceded by the formation of predentine. The first layer of predentine acts as a signal to the overlying inner enamel epithelial cells to differentiate into ameloblasts and begin secreting the enamel matrix. At the margins of the enamel organ, cells of the inner enamel epithelium are confluent with the outer enamel epithelial cells at the cervical loop.
Degeneration of this root sheath leads to exposure of the cells of the dental follicle to the newly formed root dentine and differentiation into cementoblasts, which begin to deposit cementum onto the root surface. Surrounding the enamel organ, the cells of the dental follicle producethe alveolar bone and collagen fibres of the periodontium. Successionalteeth form as a result of localized proliferation within the dental lamina associated with each deciduous tooth germ.
In contrast, accessional teeth form as a result of backward extension of the dental lamina into the posterior region of the jaws.
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Tissueand MolecularInteractions The genes that participate in different stages of tooth formation: Pax; Msx; Barx , Shh; FGF and BMPs signalling protein Tissue RecombinationExperiments important Mohammed A series of highly informative recombination experiments carried out by Andrew Lumsden at Guys Dental Hospital in the 's demonstrated for the first time that not only does cranial neural crest participate in mammalian odontogenesis, it only expresses its odontogenic potential when combined with oral epithelium. When limb epithelium was combined with mandibular arch ectomesenchyme, no teeth formed.
After the bud stage, the recombination of molar epithelium with incisor dental papilla results in the formation of an incisiform tooth. Similarly, at the same stage the recombination of incisor epithelium with molar dental papilla produces a molariform tooth. Therefore, after the tooth has reached the bud stage, the ectomesenchyme of the dental papilla is responsible for dictating what type of tooth will develop. Infection 2. Trauma Systemic factors 1. Endocrine disorders 2.
Infections 3. Drugs 4. Nutritional deficiency 5. Haematological disorders 6. Neonatal illness 7. Postnatal illness 8. Fluoride ingestion Dentine defects Localized factors 1. Trauma Systemicfactors 1. Rickets 2. Ehlers-Danlos syndrome 3. Hypophosphatasia 4. Dentinogenesisimperfecta DGI represents the most common group of inherited dentine disorders and there are three essential subgroups: 1.
Type I is associated with osteogenesis imperfecta with type I collagen abnormaility. The deciduous and permanent teeth are affected by discolouration, attrition and pulp canal obliteration. The crowns are bulbous and the pulp canals also becomeobliterated. Removable appliances should be used where possible; 2. Care needs to be taken if direct bonding is undertaken becausebracket failure or removal can lead to enamel fracture; 3.
Orthodontic bands can be used where possible; and 4. Oral hygiene and diet control must be carefully monitored during treatment. Questions and answers From your knowledge of the functions of osteoblasts and osteoclasts whydo osteoblasts have prominentendoplasmic reticulum ER whereas osteoclasts have few ER Osteoblasts have prominent endoplasmic reticulum ER because their role is to actively producelarge amounts of protein, particularly type I collagen and other bone matrix proteins.
In contrast, osteoclasts do not require active ER as they The main function of the osteoclast is to resorb bone by acid and enzymic hydrolysis. Which structures in the mature tooth are formed from the enamelorgan, dental papilla and dentalfollicle? The enamel organ is derived from epithelium and forms the ameloblasts, which producethe enamel of the tooth crown. The dental papilla and dental follicle are derived from neural crest cells and form the remainder of the tooth. The papilla forms the odontoblasts, which producedentine and the pulp. The follicle produces the periodontium, consisting of the odontoblasts that form root dentine, cementoblasts that producecementum and cells that producethe periodontal ligament.
Give an outline of the early mechanismsinvolved during hard tissue formation in the developing tooth. Hard tissue formation in the tooth relies upon inductive interactions between the internal enamel epithelium and adjacent ectomesenchymal cells of the dental papilla. Morphological changes in the cells of the internal enamel epithelium precede cues from these cells to the adjacent dental papilla cells to differentiate into odontoblasts. Odontoblasts begin secreting predentine, which itself seves as a cue for the internal enamel epithelium to differentiate into ameloblasts. Odontoblasts and ameloblasts migrate away from each other and producethe enamel and dentine of the tooth crown.
Why are ectomesenchymal cells so importantduring early tooth development? Ectomesenchymal cells are essentially a specialised form of embryonic connective tissue. They are derived from the neural crest, which are really a form of embryonic stem cells. They can therefore be induced to differentiate into a variety of cell types. In the caseof the developing tooth, this includes odontoblasts, pulp cells and cementoblasts.
In other words, the connective tissue components of the tooth. You just clipped your first slide! Clipping is a handy way to collect important slides you want to go back to later. For example, Tu et al. However, Morse et al. Recent studies showed that the activity of osteocytes during bone remodeling is under tight control of hormones secreted by other endocrine glands, such as the parathyroid hormone PTH of the parathyroid gland, a regulator of bone resorption and formation, or gonadal estrogen, an inhibitor of osteocyte apoptosis Khosla et al.
Molecular and Cellular Biology of Bone, Part A, Volume 5
Osteocytes were shown to communicate with osteoblasts in a paracrine manner. The ability of osteocytes to modulate osteoblast function is associated with the synthesis of previously mentioned SOST Neve et al. As a result of this interaction, the rate of bone formation slows down Fig. Similar effects on bone formation can be observed in the presence of Dickkopf-1 DKK1 protein Li et al. Figure 2 Download Figure Download figure as PowerPoint slide Interaction of bone cells: osteocytes, osteoblasts, and osteoclasts during the bone remodeling. Bone-lining cells support the process of bone turnover.
Original artwork, data from Kular et al.
Li et al. Moreover, osteocytes modulate function of osteoclasts, either stimulating them to bone resorption or inhibiting their resorptive activity. Whereas some of the molecules synthesized by osteocytes, such as the macrophage colony stimulating factor and RANKL, promote osteoclast differentiation, the other, e. Studies by Nakashima et al. The knowledge on the bone cell interaction that is affected during the process of bone remodeling may help with the understanding of the bone pathophysiology at the tissue level and generate novel strategies targeting bone diseases.
Furthermore, recent findings point to an important role of osteocyte apoptosis in the regulation of bone turnover. Local skeletal microinjuries, e. Cardoso et al. Activation of osteoclasts and osteoblasts may also result from the osteocyte necrosis caused by a mechanical stress and resultant inflammation Heino et al. Torreggiani et al. This may happen whenever regeneration of an injury requires massive migration of osteoblasts and proliferation thereof. The ability of osteocytes to dedifferentiate was documented in a murine model, both in vitro and in vivo.
According to Torreggiani et al. The external environment is an important source of various signals that may induce a transformation of osteocytes into proliferating osteoblasts, thus enabling healing of large bone defects. However, identification of the exact molecular mechanisms involved in the process of osteocyte dedifferentiation requires further research.
Explanation of this phenomenon would undoubtedly have serious implications for novel strategies of regenerative medicine, based on an easy access to proliferating osteoblasts originating from terminally differentiated osteocytes. This is especially promising if the dedifferentiated cells could be obtained in an in vitro culture. Bone remodeling is a complex process modulated by a number of factors taking place simultaneously at many sites. Not only various substances released in an auto-, para- or endocrine manner control the activity of cells involved in the remodeling process; nowadays we know that also the CNS plays a vital role in this process acting, e.
Rich vascularization and innervation of the skeleton constitute the main source of various growth factors, neurotransmitters, and hormones regulating function of the bone also through the cooperation with other organs and tissues. Bone metabolism and remodeling are to a large extent controlled by, e. Synthesis of these factors is in turn under strong influence of hormones, e. Bone is a richly innervated tissue. The topography of nerve fibers within the bone, especially those containing neuropeptides, is presently a subject of extensive research. Neuropeptides released from the bone nerve fibers were identified as enzymes, sensory, sympathetic, and glutaminergic peptides Elefteriou , Masi These neuropeptides play the roles of neurotransmitters and immunomodulators, acting in a paracrine manner, i.
This constitutes an indirect proof for involvement of the CNS in the control of all of the biological processes, including those taking place in the bones, such as bone remodeling. The results published by Ma et al. Moreover, they were shown to promote the activity of ALP and synthesis of osteocalcin in osteoblasts, additionally facilitating communication between these cells via gap junctions.
Mei et al. Also the work by Fu et al. Furthermore, the findings reported recently by Baldock et al. In their murine model-based study, these authors showed that NPY can directly regulate central and peripheral noradrenergic neurons, activating their receptors Y2, and thus preventing the release of noradrenaline.
This mechanism likely protects us against the bone loss resulting from a stress-induced release of catecholamines. The hypothalamus and its semipermeable blood—brain barrier turned out to be one of the most potent intrinsic regulators that integrate not only the signals from peripheral tissues but also the internal signaling pathways of the brain. One of the most important extra-skeletal biologically active compounds regulating bone remodeling is serotonin 5-hydroxytryptamine ; serotonin receptors are expressed on the plasma membranes of osteoblasts, osteoclasts, and osteocytes de Vernejoul et al.
Mammalian serotonin is synthesized in the CNS and peripheral nervous system, whereby it acts as a neurotransmitter and hormone respectively Goodrich et al. As serotonin does not penetrate across the blood—brain barrier, these two pools act independently from each other. Binding to the 5-hydroxytryptamine 2c HTR2c receptors on the plasma membrane of hypothalamic neurons, serotonin inhibits the transmission of sympathetic stimulation and inactivates type 2 beta adrenoreceptors present in osteoblast membranes Fig.
In turn, the intestinal equivalent of cerebral serotonin, synthesized by the enterochromaffin cells and representing ca. According to Cui et al. It stimulates osteoblast activity indirectly through the hypothalamus.
Production of BDS remains under control of leptin—adipocytes-derived hormones. Leptin indirectly inhibits BDS synthesis, causing a decreased osteoblast differentiation. As mentioned previously, there is a tight association between the activity of serotonin and leptin, a hormone of adipocytes, during the control of the bone remodeling process. Cerebral synthesis of serotonin is believed to be regulated by leptin, a hormone of adipocytes.
Apart from the bone remodeling, leptin is also involved in a number of other processes, e. Leptin prevents enhanced osteogenesis resulting from the overproduction of serotonin in the brain stem in a mechanism of negative feedback loop D'Amelio et al.
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The role of leptin in the control of bone formation is indirectly associated with the activity of hypothalamic neurons. The inhibitory effect of leptin on the synthesis of serotonin is associated with the activation of leptin receptors on serotoninergic neurons of the brain stem. Another factor contributing to the inhibitory effect of leptin on the process of bone growth is a protein, neuromedin U, a peptide synthesized by hypothalamic neurons and small intestinal cells, that plays an important role in the transmission of leptin signaling, acting downstream of leptin and inhibiting bone growth Yadav et al.
Impaired synthesis of leptin results in serious structural skeletal disorders, e. Moreover, leptin prevents excessive resorption of the bone, acting via a precursor protein of cocaine- and amphetamine-regulated transcript CART neuropeptide. Elefteriou et al. A study of patients with depression treated with selective serotonin reuptake inhibitors showed that binding serotonin extracellularly not only within a synaptic space but also in the gut may exert a negative effect on bone mass An et al.
Data published by Gustafsson et al. This may point to another potential cellular regulatory mechanism of bone growth. As mentioned previously, contrary to its cerebral equivalent, the serotonin of intestinal origin inhibits bone formation. Recent studies documented tight association between the activity of intestinal enterochromaffin cells and osteoblasts in the regulation of bone growth; however, the exact nature of this interaction is still not completely understood and there are many unsolved controversies around this issue.
According to one theory, osteoblasts may inhibit the synthesis of intestinal serotonin acting via the LRP5 protein present in the plasma membrane of the enterochromaffin cells Fig. Deletion of the LRP5-encoding gene in enterochromaffin cells was reflected by the overexpression of Tph1 , release of intestinal serotonin into circulation and inhibition of bone growth Yadav et al.
The postulated ability of osteoblasts to affect the synthesis of serotonin points to a significant cellular mechanism of bone growth control.
Building strong bones: molecular regulation of the osteoblast lineage
However, Cui et al. These authors rather suggest that osteoblasts activity is under control of LRP5, present in their plasma membrane, which is directly associated with the Wnt signaling pathway. It is the so-called autonomous-osteoblast control of the bone mass accrual. Thus, according to Cui et al. Serotonin may also regulate the activity of osteoclasts. Chabbi-Achengli et al. All of this evidence points to the crucial role of serotonin in the regulation of both bone formation and bone resorption.
The results of recent studies suggest that these proteins may also play a role in the development of some neoplasms Sharma et al. A total of 19 members of the Wnt family were described to date. In particular, Wnt7b and Wnt10b are postulated to play the significant important roles in the process of bone mass control Kubota et al.
Mice with mutations of the Wnt7b and Wnt10b genes presented with impaired osteogenesis and slower bone growth rate respectively Bennett et al. However, it also is worth mentioning two other members of the Wnt superfamily, namely Wnt1 and Wnt16, which have recently been revealed to play an important role in either the bone formation or repression of osteoclastogenesis and the prevention of cortical bone fragility fractures respectively Laine et al.
The Wnt proteins can activate at least three independent signaling pathways that are crucial for bone remodeling. Another pathway, the so-called non-canonical Wnt pathway, involves two distinct mechanisms: planar cell polarity important during embryogenesis and the regulation of calcium ion concentration within the bone cells Wang et al.
The canonical Wnt pathway Fig. Minear et al. The liposome-based delivery of Wnt3a enhances its activity and results in faster bone regeneration, i. These data suggest that Wnt signaling can be amplified successfully at the injury site, being an alternative for bone morphogenetic proteins BMPs -based bone therapies.