Tooth Eruption Process PDF

**Tooth eruption** - **The process of eruptive tooth movement (as distinct from pre-eruptive/post-eruptive tooth movement) and the theories put forward to explain the process** Tooth eruption: - axial/occlusal movement of tooth from dev site in alveolar process -\> functional posi...

**Tooth eruption** - **The process of eruptive tooth movement (as distinct from pre-eruptive/post-eruptive tooth movement) and the theories put forward to explain the process** Tooth eruption: - axial/occlusal movement of tooth from dev site in alveolar process -\> functional position in oral cavity - Continuous process -\> doesn't stop by tooth reaching occlusal plane - Developing teeth can move in 3 dimensions + increase in size in alveolar process before active eruption - Timing is important for healthy development **Phases of tooth eruption:** Active: movement of tooth from dev site in alveolar bone to functional position in oral cavity Pre-eruptive movement: - Tooth germs -\> teeth positioned in jaw for eruptive - Starts from tooth formation initiation -\> root formation initiation - Tooth movement is alongside jaw growth - Tooth movement occurs intra-osseously -\> requires remodelling of bony crypt wall → selective deposition and removal of bone - Starts at the end of bell stage -\> finishes at beginning of root formation Eruptive tooth movement: - Tooth movement here either intraosseous or supraosseous - Begins w onset of root formation and ends by tooth appearance - Moves from dev position -\> occlusal level - Direction of movement axial/occlusal - After emergence, tooth crown keeps moving occlusally unti contact w antagonist in occlusal plane -\> meets tooth on opposite jaw - Crown exposes gradually w apical shift of the dento-gingival junction\*\* - In intraosseous tooth movement: resorption of overlying tissue to make eruptive path + force to push tooth vertically - ↓ blood vessel count + degeneration of nerve fibres & connective tissue on top of tooth germ - Eruptive pathway looks like inverted triangle Post-eruptive tooth movement: - Occurs once tooth reaches functional position in oral cavity - Maintains tooth position in occlusion by wear/erosion -\> occlusal + proximal - Starts when teeth attain occlusion + continues as long as tooth is in oral cavity Passive eruption: - Characterized by apical shift of dento-gingival junction (gum line is lower towards root direction) - Length of clinical crown \^ - Still dunno what is really going on **Eruptive tooth movement:** - Based on type of tooth + time of eruption - Human dentition grouped to primary/deciduous, mixed and secondary/permanent - Primary = 20 teeth + erupts btw 6m and 3y - Mixed dent starts w 1^st^ perm tooth eruption -\> usually lower incisors/1^st^ perm molars @ \~6y -\> finishes w last exfoliation of deciduous tooth Theories of eruptive tooth movement: Pulp theory: - Pulp propels tooth upwards (mandib) or downwards (max) - ↑ thickness of radicular dentine during root formation -\> decrease in pulp cavity size - Growth/constriction of pulp generates force -\> propulsive force in pulpal vasculature - Evidence against this-\> tooth still erupts if pulp is removed Vascular pressure/blood vessel thrust/hydrostatic pressure theory: - Overlap w pulpal theory - Eruption force by pressure from blood vessels within tooth - Tooth movement sync w arterial pressure -\> local volume changes -\> produces lim tooth movement - ↑tissue fluid pressure = tooth movement - Evidence against this -\> pulpless teeth erupt, hypotensive drugs have no effect on eruption, root + local vasculature excision doesn't effect eruption - HOWEVER -\> recently hydrostatic pressure occurs during post-eruptive stage due to dental follicle secreting mediators (vascular endothelial growth factor) -\> angiogenesis -\> ↑ in apical tissue pressure -\> tooth eruption - Injection of vasodilators ↑ tooth eruption AND injection of vasoconstrictors ↓ tooth eruption Root formation/elongation theory: - Tooth propelled towards mouth as root develops - Assumes root hits smth and force is then in the upwards direction - Evidence against this -\> rootless teeth still erupt, some teeth erupt more than root length, doesn't align w root formation Alveolar bone remodelling theory: - Selective resorption and deposition of bone - New bone laid underneath root -\> pushing up - Control of growth via osteoblasts -\> sourced by dental follicle - No dental follicle = no eruptive pathway - Can replace tooth germ w metal/silicone replica -\> retain dental follicle and the replica will erupt - Mutation of PTH receptor 1 = disturbance and primary failure of eruption -\> not bc of defective osteoclasts -\> progressive overbite PDL theory: - PDL tension -\> ligament creates tension that pulls tooth upwards/downwards - PDL cell activity -\> fibroblasts contraction produces eruptive forces - Bone remodelling: alveolar bone responds to erupting tooth by making eruptive pathway - Evidence against: defective fibroblasts have no effect, rate of collagen turnover is higher than rate of eruption, no diff btw metabolism of erupting and mature teeth - Rootless teeth erupt on schedule anyways -\> PDL not necessary Dental follicle theory: - Force comes from dent follicle -\> induces bone resorption -\> forms eruptive pathway - Eruption reg by inductive signals - Osteoclastogenesis (resorption) -\> coronal dent follicle - Osteogenesis (formation) -\> basal dent follicle - Removal of follicle -\> eruption failure - Follicle thought to have lots of cytokines + growth factors -\> communication btw dental epithelium + dental mesenchyme Neuromuscular theory: - aka unification theory - muscles around face contract apply forces to teeth to help the erupt - nerve signals to muscles and erupting teeth to guide them the right place at the right time - functional adaptation to make sure the erupting teeth are guided to align w opposing teeth Factors affecting tooth eruption: - downsyndrome - delayed/failure eruption - cleidocranialdysostosis - hypothyroidism - hypopituitarism - achondroplastic dwarfism - supernumerary teeth - crowding - arch length deficiency - cysts/tumors - enamel pearls - gingival hyperplasia - premature loss of primary teeth - ankylosis - digit sucking - tongue thrusting - fibrous developmental malformations - **The process of physiological tooth movement and that this takes place throughout life and is a key tool in the way the dentition adapts to functional stresses** - Post-eruptive tooth movements happen after erupted tooth reaches functional position in mouth - Movements keep tooth in place as jaw grows + compensates for any occlusal + proximal wear - Dentition reacting to stresses 3 types: - Movements help accommodate jaw growth - Movements that compensate for occlusal wear - Movements that accommodate interproximal tooth wear **BONE HEALING** - **Describe different types of bone fractures** Closed (simple fracture) -- broken bone has not pierced skin Open (compound) fracture -- broken bone juts out through skin/wound leads to fracture site -\> infection + external bleeding ↑ chance Greenstick fracture -- small, slender crack -\> children bc their bones are more flexible Hairline fracture -- common form of stress fracture, common in foot/lower leg -\> repeated stress from activity Complicated fracture -- structures surrounding fracture are injured -\> dmg to blood vessels/nerves + injury to bone lining (periosteum) Comminuted fracture -- bone shattered to small pieces -\> slow healing Avulsion fracture -- muscles contraction pulls tendon that also pull pieces of bone out -\> common w knee and shoulder joints Compression (impacted fracture) -- when 2 bones forced together -\> vertebrae -\> old ppl esp w osteoporosis vulnerable - **Describe bone healing in terms of primary and secondary fracture repair** **PRIMARY** Direct: - Accurate reduction + rigid internal fixation performed - Cutting cones -\> spearhead of osteoclasts cut space in bone - In this space -\> central blood vessel + cavity walls line w osteoblasts -\> creates new bone - Multiple cutting cones across fracture gap looks like giant microcrack -\> fracture line obliterated and replaced by new bone Gap healing: - Modified form of primary bone repair - Occurs if fracture is rigidly fixed and fracture gap is few hundred microns - Immature bone initially laid down along fracture surface of each end so gap becomes small enough for cutting cones to be transverse to allow primary bone healing **SECONDARY** - Response from periosteum + endosteum -\> formation of callus - Callus = immature bone - Bone ends not in position or rigidly fixed - Some degree of mobility (mechanical stimulation) enhances secondary healing - 5 stages: hematoma, inflam, soft callus, hard callus, remodelling Hematoma: - Occurs right after fracture -\> bleeding from bone surface + surrounding soft tissue - Blood clot rich in factors such as VEGF - Important in initiating inflam response + recruiting cells and blood vessels -\> macrophage + neutrophils - No hematoma = delayed fracture healing/impaired healing Inflam phase: - Infiltration of neutrophils + macrophage - Macrophage engulf fibrin + RBC - Other inflam cells (T + B cells + mast cells) - Inflam cytokines (list\*\*) recruit inflam cells + stim angiogenesis - IL-1 -\> osteoblasts -\> makes IL-6 -\> stim angiogenesis at fracture sity + diff of osteoblasts and osteoclasts Soft callus: - Organisation of blood clot -- invasion of capillaries + fibroblasts - Fibroblasts + chondrocytes lay fibrocartilaginous matrix btw fracture ends - Bridge of soft callus forms - Muscle + periosteum contribute to external callus - Medullary tissue + bone ends contribute to internal callus - MSC attracted from periosteum, endosteum + bone marrow - TNF-α recruit osteoprogenitor stem cells -\> stim apoptosis of hypertrophic chondrocytes + enhancing recruitment of osteoclasts to callus (calcified) Hard callus: - Matrix becomes mineralised -\> Ca containing granules accumulate in cytoplasm -\> transported to ECM -\> combine w P -\> precipitate -\> become nidus for apatite crystal formation - Soft callus becomes stiffer -\> osteoblasts ossify tissue - Hard mineralised bridge of callus is formed when callus experiences mechanical stress (\~2%) - If excessive movement present -\> hypertrophic non-union -\> excessive bone formation but stabilisation is not achieved - Hard callus initially repair form of bone -\> woven bone -\> type III + I collagen Remodelling - Woven bone gradually replaced w lamellar bone -\> cutting cones - Laid along stress lines responding to the mechanical movements/requirements of the bone - **Detail the process and timeline of healing of bone in the context of physiological processes** 12hrs -- blood clot + fibrous exudate collects inbtw bone fragments 24hrs -- inflam -\> sequential infiltration of neutrophils + macrophages 48hrs -- granulation tissue formation 5 days -- start of bone formation 3 weeks -- fibrous union + primary callus 6 weeks -- fibrous shell of external callus w bone ends joined w woven bone 6 weeks-6months -- formation of secondary callus + remodelling - **Identify the main healing phases of bone** **1. Inflammatory Phase:** **Duration**: A few days to about a week. **What happens**: This is the initial response to the fracture, where blood vessels are damaged, leading to the formation of a **hematoma** (blood clot) at the fracture site. Inflammatory cells, such as macrophages and neutrophils, arrive to clean up debris and trigger the healing process. This phase sets the stage for new tissue formation. **2. Repair Phase:** **Duration**: Several weeks. **What happens**: New tissue begins to form. During this phase: A **soft callus** made of collagen and cartilage forms around the fracture site within the first 2-3 weeks. Later, the soft callus is replaced by a **hard callus** (woven bone), providing more stability to the fracture. This phase bridges the fracture with new bone tissue, but the bone is still weaker than its original state. **3. Remodeling Phase:** **Duration**: Several months to years. **What happens**: The woven bone laid down in the repair phase is gradually replaced by stronger, more organized **lamellar bone**. The bone shape and structure are refined as the excess callus is removed, and the bone regains its normal strength and function. - **To identify the main cells involved in healing** 1\. Osteoclasts: - Function: Bone-resorbing cells. - Role in healing: During the remodeling phase, osteoclasts break down and remove damaged or excess bone tissue, clearing the way for new bone formation. They help reshape the bone and remove the soft callus as new bone forms. 2\. Osteoblasts: - Function: Bone-forming cells. - Role in healing: Osteoblasts produce new bone matrix, laying down collagen and minerals (calcium and phosphate) to form new bone tissue. They are active during the repair and remodeling phases, helping to build the hard callus and convert it into strong lamellar bone. 3\. Chondroblasts: - Function: Cartilage-forming cells. - Role in healing: These cells are responsible for producing the cartilaginous soft callus during the early repair phase. This callus stabilizes the fracture and acts as a scaffold for future bone formation. 4\. Fibroblasts: - Function: Connective tissue-forming cells. - Role in healing: Fibroblasts produce collagen and other extracellular matrix components that form the early connective tissue (soft callus) that bridges the fracture. This happens early in the repair phase before the formation of hard bone. 5\. Osteocytes: - Function: Mature bone cells. - Role in healing: Osteocytes, derived from osteoblasts, maintain bone tissue and regulate the bone remodeling process. They sense mechanical stress and coordinate the activity of osteoclasts and osteoblasts to adapt the bone\'s structure. 6\. Macrophages: - Function: Immune cells involved in tissue repair. - Role in healing: During the inflammatory phase, macrophages help clear out dead cells and debris at the fracture site. They also release signaling molecules (cytokines) that recruit other cells like fibroblasts and osteoblasts to initiate tissue repair. 7\. Endothelial cells: - Function: Blood vessel-forming cells. - Role in healing: Endothelial cells are responsible for forming new blood vessels during the healing process, ensuring that the injured area gets sufficient blood supply to support healing. - **Discuss the main themes of pathophysiology of bone fractures** Factors affecting bone healing: Injury variables: - Open fractures - Severity - Intra-articular fracture - Segmental fracture - Soft tissue interposition - Damage to blood supply Patient variables: - Age - Nutrition - Systemic hormones Tissue variables: - Form of bone -\> cortical or cancellous - Bone necrosis - Bone disease - Infection Treatment variables: - Decreasing fracture gap - Stabilising fracture - Restoring fracture segments - **Be aware of different types of healing (1º vs. 2º)** Primary: - No movement (normally through pins/plates) - Absolute stability - Direct healing of bone - Bone ends directly in contact/small gap - Less common Secondary: - Movement present - Relative stability - Healing through intermediate stages - Big gap btw bone ends - common **DENTAL TISSUE HEALING** - **Discuss the healing processes in dental soft tissues** 3 kinds of cells: - Labile cells -\> unstable, proliferative, divide -\> skin, oral mucosa -\> killed by chemo - Stable cells -\> divide under conditions (injury) -\> liver, pancreas - Permanent cells -\> don't divide -\> brain, heart -\> die after injury Wound healing stages: haemostasis -\> inflam -\> proliferative -\> remodelling Oral Mucosa: - Heal w minimal scarring - Tongue heals quick w little inflam -\> altered TGF-B Possible reasons ↑: - Distinct fibroblast phenotype - Bacteria there stims wound healing - Moist environment + saliva (↑ epidermal growth factor) - Rapid but transient inflam response - Rapid remodelling - **Consider the process of wound healing with special reference to the periodontal complex and the periapical regions  ** Chronic gingivitis: - Bacterial plaque in gingival sulcus - Hyperplasia of junctional epithelium (more tissue) - Superficial dilated capillaries Pathogenesis of perio: - Bacterial plaque collects in gingival crevice - Bacterial metabolism waste (protease, hyaluronidase, collagenase) gets to gingival connective tissue - Dmg provokes inflam reaction - Chronic inflam starts - Dmg to junctional epithelium increases permeability to plaque + other bacteria - Bacterial metabolism waste attracts neutrophils -\> increase in gingival crevice -\> phagocytosis of plaque bacteria - Neutrophils die -\> release lysosomal enzymes -\> destroys junctional epithelium \_ connective tissue - Endotoxin -\> complement pathway -\> vaso-active + chemotactic factors -\> cell death - Bc gingival connective tissue turnover is high but not high enough for dmg caused - Tissue dmg remains localised -\> balanced altered = burst of tissue destruction Objective of perio treatment: - Eliminate factors causing PD - Smooth root surfaces - Guided tissue regeneration Healing periodontium: - Cells first attached to root likely to proliferate more - **Contextualise this to situations encountered in periodontology and endodontics** F DOWN SYNDROME - Overview of Down's Syndrome and other disabilities. - 1/1800 - Trisomy 21 -\> 21^st^ chromosome has 3 pairs - 3 varients -\> 92% = extra chromosome in all cells, 2-4% in some cells, 3-4% material from once chromosome 21 translocated onto a diff chromosome Unknown cause: - 2 copies of C21 fail to separate in egg formation -\> egg w 2 copies -\> sperm fertilises -\> 3 copies - Increased chance w age - No link to race, nationality, SE, religion or preg behaviours Key facial characteristics: - Small folded ears - Brushfield spots - Flattened nasal bridge - Short neck - Epicanthal fold - Positive canthal tilt Physical characteristics: - Short - Mid-face hypoplasia - Widely spaced eyes - Ext and int ear dysmorphia -\> high risk hearing loss - Short + broad neck - Clinodactyly (curved finger) - Simian palmar creases - Health challenges faced by people with Down's Syndrome. - 50% have congenital heart defects (mitral valve prolapse, ↑ risk of arrhythmias, emboli + infective endocarditis) - Early onset pulmonary hypertension -\> low number of alveoli + impaired endothelial function - 5-13% w seizure - 3% w cataracts - Hearing loss - Immune defects - Gastric reflux -\> erosion, tube feeding = less saliva - Obesity Dent problems: - Macroglossia - Thick, dry, fissured lips - ↑ rate of candida infections - Aphthous ulceration - Malocclusions common - Protrusive mandible, class 3, small molars, high + short palate - Cleft palate - Delayed eruption Tooth development abnormalities - Missing prim and perm teeth common - Smaller crown and root - Unusual shape - Hypoplasia -\> pitted enamel -\> plaque retention + staining - ↓ caries risk but ↑ perio risk - bruxism - Strategies for providing oral care. - Early intervention - Cardiac issues - Habit forming - Know support network - Reward + praise - Patience - Teach them to do it themselves rather than do it for them - Don't overload them w info - Don't think they cant learn smth - More frequent visits CHILD DEV Motor dev: 5-11m -\> crawl 10-14m -\> stand + walk 18-30m -\> run, jump, climb, tip toes 3y -\> holding crayon 4-5y -\> write name Adverse childhood event = poorer health + immunosuppression 4 or more ACE: - Alcohol + drug misuse - Violence - Offence - Depression + suicide - Poor health -\>smoking and obesity Piaget: - Assimilation -\> treat new objects, people + events as familiar - Accommodate -\> modify/change way of thinking Sensorimotor: birth -- 2y -\> thought based on senses and action -\> here and now Pre-operational: 2-7y -\> can solve concrete problems, symbols, egocentric, animism. Lack of logic, focus on one factor Concrete operations: 7-11y -\> reasoning + logic Formal operations: adolescence -\> abstract reasoning, manipulate variables, hypothesis Calgary-Cambridge Guide initiation Prep -\> greet -\> engage -\> est reason -\> whats gonna happen -\> consent