OD: oral surgery and abnormalities Flashcards
5 signs of inflammation
-rubor (redness)
-callor (heat)
-pallor (pain)
-loss of function
-swelling
What factors affect infection severity
- Virulence of organism – ability to be pathogenic. Commensals v pathogens
- Number of organisms
- Host resistance (disease, drugs, age, immunosuppression)
- Source of infection (can dictate the pathway where it spread) eg. Lingual swelling – increased risk of airway obstruction
What are the stages of odontogenic infection to it becoming an abscess. Timeline
-Initial- no swelling, just pain
-0-3 days: pus breaks through cortices. acute inflammation, mild tender swelling
-3-7 days: pus spreads and causes cellulitis. Warm, painful
-5+ days: abscess formation Undermines skin or mucosa making it compressible, shiny and fluctuant ( can bounce when press it)
-Resolution is either spontaneous (bursts), surgical or antibiotics
What is sepsis and septic shock
-Life threatening organ dysfunction caused by a dysregulated host response to infection.
-Release of mediators due to bacteria and their endotoxins (NO, bradykinin, histamine, prostaglandins)
-Overreaction, vasodilation to bring in immune cells, hypo perfusion, hypotension
-Septic shock- subset of sepsis. Response to dramatic drop in BP and the organs fail to receive sufficient oxygen.
Explain these 4 types of shock: 1) Hypovolaemic 2) Distributive 3) Cardiogenic 4) Obstructive. Which type is due to sepsis. Treatment for each
1) loss of blood volume or extra cellular fluid. eg. due to haemorrhage.
-Control bleeding, replace fluids/blood
2) Vasodilation. eg. sepsis, anaphylaxis, spinal cord injury
-Sepsis 6 /adrenaline, antihistamine, steroid
3) Primary cardiac dysfunction. eg. MI, acute dysrhythmia, cardiomyopathy
4) Blockage of circulation. eg. tension pneumothorax, cardiac temponad, pulmonary embolism
-relieve pressure, thrombolysis, anticoagulation
Signs of sepsis
-purpuric rash
-Respiratory rate >25
-HR >130
-Systolic BP <90
-Lactate >2
-decreased oxygen saturation <90
-decreased consciousness (AVPU assessment)
-pyrexia >38.3 temperature)
-WCC<4, >12
What is the normal body temperature range
36.1 and 37.2 degrees Celsius
Sepsis management (sepsis 6 that you need to do within the hour)
Recognise, ABDCE, resuscitation if unconscious, localise source of infection, manage source of infection
-within the hour
1. Give IV Fluids
2. Give Oxygen (target 94-98% O2 saturation)
3. Give Antibiotics - 1g amoxicillin
4. Take Blood cultures
5. Take Lactate measurement
6. Take Fluid balance
Ways to prevent surgical infection
-prophylactic antibiotics if necessary
-Aseptic technique
-Sterile instruments
-Atraumatic technique (maintains blood supply)
-Elimination of dead space (Close wounds in layers, otherwise space can fill with blood and bacteria can grow)
-debridement
-Drains where appropriate
4 stages of treating infection
- Remove the cause [extract, extirpate, debride]
- Institute drainage [incise, extract, extirpate]
- Prevent spread [drainage, antibiotics]
- Restore function [crown, bridge, denture]
Danger areas of venous spread of infection to brain
- Pterygoid plexus – links up to brain – as it has no valves things can go up
- Angular veins at medial canthus of eye – also has no valves – infection can track up to the cavernous sinus of brain
What areas drain into submental and submandibular nodes. And where these can drain to
-Submental -From FOM, tip of tongue, lower lip and chin
-Submandibular -From face, cheeks, upper lips and anterior two thirds of tongue
-Then these superficial nodes drain to deep cervical lymph nodes along the course of the internal jugular vein.
What tissue space is a lower right molar likely to spread to
sublingual
potentially submandibular
Functions of fascia
Fascia is Well defined sheet of connective tissue surrounding organs and other structures
-Support structures – eg. muscle & parotid gland (why mumps is painful)
-Provide pathways for neurovascular structures to pass
-Circulatory function - promote venous drainage through maintaining the shape of structures
-Facilitate movement between structures by acting as a rigid surface for sliding
-Mechanical protection to structures
However fascial planes to provide routes for infection to spread
What are the major fascia that determine routes of infection in the head and neck
-Prevertebral
-Pretracheal
-Deep cervical fascia (enclosing SCM, trapezius)
-Carotid fascia (common carotid artery, IJV, vagus nerve)
-Superficial or subcutaneous fascia
If lower molar abscess breaching below or above buccinator, will infection tract extra or intra orally
-Below= extra oral
-Above= intra oral
[buccinator governs buccal side spread of infection]
If lower molar perforates below or above mylohyoid, what tissue space will it go and will it be intra or extra oral
-Below= extra= submandibular/ submental space
-Above= intra =sublingual, FOM
[mylohyoid governs lingual side spread of infection]
Which spaces will trismus be profound if pus spreads there
lateral pharyngeal or masseteric spaces
Consequences of head and neck spread of infection
-Airway obstruction (Ludwig’s angina)
-Intracranial spread
-Mediastinal infection
-Necrotising fasciitis
-Sepsis
What is Ludwig’s angina. Signs and symptoms
-Bilateral submandibular and sublingual CELLULITIS – spreading of infection through tissue planes
- tracks down to FOM and epiglottis causing oedema and narrowing of glottis – AIRWAY COMPROMISED
-vocal change, stridor, tongue malposition, trismus
needs draining
Signs of airway obstruction
-SOB (dyspnoea)/ stridor
-Drooling/ inability to swallow own saliva
-Difficulty swallowing (not due to pain)
-Decreased SaO2
-Hot potato voice (common in quinsy = PERITONSILLAR cellulitis or abscess)
Signs of intracranial spread of infection such as cavernous sinus thrombosis
-Closure of eye, orbital extension of pus, swelling in infra-orbital ridge
-Proptosis- eye protrusion
- opthalmoplegia - paralysis of muscles within or surrounding the eye (DECREASED EYE MOVEMENT)
-Ptosis (upper eye-lid droops)
-Altered conscious level (GCS)
What does the cavernous sinus contain
-CN III, IV, V1, V2 and ganglion, VI
-Internal carotid artery
=So obstruction in this area not good
Symptoms of mediastinal infection spread
-Pleuritic retrosternal chest pain radiating to neck or between shoulder blades
-Spreading erythema down to sternal notch (top of sterum)
-Crepitus chest or neck (crackling sound during palpation as breaking gas bubbles)
-Hamman sign (crunching sound on auscultation of heart)
-CT showing widening of pre-cervical or retropharyngeal tissues, pre-tracheal tissue
Functions of maxillary sinus
-Respiration -humidifies air before reaching lungs to prevent inflammation of respiratory tract
-Speech – resonance of speech
-Lightening of the skull – skull would be too heavy otherwise
Describe the difference between an OAC and OAF (communication v fistula)
-OAC= hole between oral cavity and sinus.
-If untreated can lead to OAF where the tract epithelises and makes a permanent hole which cannot heal (this takes 7-10 days).
[Usually due to extraction when close to sinus]
How to test for an OAC. Early and late signs
-Get patient to breath through nose. -Snot/ blood comes out into mouth. Bubbling of saliva.
-Swallowing water comes out of nose
-No bone in base of socket, with dark hole
-Maxillary tuberosity damage usually means high chance of OAC
-Sinus lining is like wet tissue
-x-ray
-If missed the OAC to start with pt may come back complaint of reflux of fluid into nose or mouth, bad taste, sinusitis, post-nasal drip, swallowing water comes out nose
How long does it take for OAC to epithelialise over
2 weeks
How to manage OAC. What antibiotics are 1st and 2nd line
-No nose blowing for 2 weeks
-Sneeze with mouth open to decrease sinus pressure
-Ephedrine 0.5% nasal drops 1-2 times daily
-Phenoxymethylpenicillin 500mg 5/7 (doxycycline 2nd line) to prevent sinusitis
If small: <2mm. Closes spontaneously. encourage haemostasis, surgicel. Soft splint for 2 weeks
If large: <5mm. Suture. splint for 2 weeks.
If OAF or >5mm= Surgical management - debride, close with buccal advancement flap
Surgical management of OAF. 1st, 2nd and 3rd line options
- Buccal advancement flap: 3 sided flap stretched over to act as seal. Can sometimes use buccal fat pad
- Palatal advancement flap: mucosa is more keratinised so more robust. Cover plate to allow healing
- Tongue flap= rare. Only indicated in cleft palate or persistent fistula.
Maxillary sinus tumour signs. Which cancer is most common
-SCC
-radiopaque, erodes walls of sinus, cause teeth mobility
-dentures not fitting
-compression of nerves
-deformaties
-Blocked sinuses
-Changes in vision, such as double vision.
-Chronic headaches.
-Generalised pain in upper teeth
What to do if root displaces into maxillary sinus causing OAC
-Normally easiest at the time to retrieve it. Or other option is to leave it
-2 approaches for removal
- Through socket
- Caldwell-Luc – raise flap/ remove bone around sinus and remove tooth- Better to do under GA
Cause, presentation, treatment of sinusitis
-swelling of sinuses usually due to infection or allergy
-due to infected tooth, foreign body (tooth root), reduced drainage (due to inflammation or blockage)
-pain bending forward, congestion, generalised upper tooth ache, bad breath, post-nasal drip, swelling, headache, green mucous from nose
-can be acute or chronic, usually viral
-Tx= if mild rest, fluids, paracetamol and should clear after 4 weeks
- may need steroid nasal drops, surgery to Improve drainage,
-Remove cause (eg. Remove root), antimicrobials
Reasons why LA fails
-Poor operator technique: incorrect site, insufficient solution, not slow enough
-Pharmaceutical reasons: past expiry date, not stored in the dark at room temperature causing oxidation of adrenaline
-infection
-anatomy: dense cortical bone, variations in foramen position, accessory nerve supply
-psychological reasons: anxiety can decrease success
How LA needs to be stored and why
dark, room temperature
otherwise adrenaline oxidises and has decreased effectiveness
How to overcome dense cortical bone or thick zygomatic butters around upper 6s, preventing LA diffusion
-articaine instead
-inject mesial and distal to buttress
-PDL Intraligamentary injections – pass through perforations in socket walls (but mandibular incisors have few so not effective in this region)
Ways of overcoming accessory nerve supply with LA (crossover innervation)
high block, PDL/ intraosseous, articaine infiltrations, intra-pupal (for RCT)
Why LA less effective with an infected tooth. How to overcome
-Alteration in tissue pH: LA is a weak base. Infected tissue is slightly acidic (normal is 7.4) so LA in ionised state outside the cell so less lipid soluble and so it is difficult to penetrate the membrane and into the cell
-Increased vascularity so loss of LA systemically quicker
-Loss of LA via draining sinuses
-Hyperalgesia – already firing lots of action potentials – when trying to anaesthetise it is much more difficult
=Give more LA, inject on either side, articaine for infiltrations, add supplementary techniques, pre-op pain killers
Why articiane diffuses better
-higher concentration (4%)
-contains thiphene ring which folds into smaller molecular position to diffuse better
-therefore better to use over lidocaine for infiltrations. No benefit for blocks to don’t use as increased risk of nerve damage
-Also it has low pKa so is more lipid soluble so effective at crossing membrane so quick onset. And highly protein bond so long lasting
What to do if IDB fails.
-repeat if asymptomatic tooth. Don’t if symptomatic (eg. irreversible pulpits)
-then do buccal and lingual infiltrations with articaine
-then supplementary techniques (intra-osseous, intraligamentary lidocaine/ articaine)
-then high block as foramen is higher
What to do if buccal infiltration fails
repeat buccal with articaine
then palatal
then supplementary technique (intra-osseous, intraligamentary lidocaine/ articaine)
then superior alveolar nerve block in maxilla
Explain Gow gates and Akinosi-vairani high mandibular blocks. Which nerves will they anaesthetise
-will anaesthetise IAN, lingual, long buccal, mylohioid, auriculotemporal nerves if worried about accessory nerve supply
1. higher success rate. Region of palatal cusps of upper 7s
2. easier. Closed mouth technique, loosely bite together. Maxillary mucogingival junction distal to 7
What is Crestal (aka intraseptal) anaesthesia
-Similar to intra-ligamentary-relies on tiny perforations
-Insert needle into papilla = intraosseous anaesthesia
-Don’t have to insert needle into PDL membrane space
-Usually if not extracting the tooth
-Inject mesial and distal to the tooth until BLANCHING occurs. Similar amount to infiltrations
Common teeth affected in hypodontia. How many teeth are missing. Genes responsible
-1-6 missing teeth (oligodontia is missing 6+ teeth), excluding wisdom
-8s, then upper 2s, then lower 5s
-30% have missing 8s
-MSX1 and PAX9
Hypodontia can be managed with a combination of orthotic and restorative. For missing laterals, what factors affect the decision to either close the spaces, or open space for a prosthesis
-Closing space: natural teeth at front of smile. But canines may look contrasting to centrals as darker and pointy.
-Opening space and fill gaps: More tx required. corrects axial inclinations
Depends on:
-Skeletal relationships (class III, class II div 1)- space closing more preferable
-Extent of Crowding or spacing
-Colour and form of adjacent teeth – if very contrasting then likely to open spaces
-Inclination of teeth
-Desired occlusion of posterior teeth
-Wishes and cooperation of patient
Difference between supernumerary and supplementary types of hyperdontia. Explain mesiodens, paramolar, distomolar
1-Supplemental: extra teeth have normal form
2-Supernumerary: extra tooth with atypical form. Can cause failed eruption or displacement.; smaller and conical. Types: tuberculate (barrel shape) or conical.
-Mesiodens (between the 2 centrals)
-Paramolar (tooth lying buccal/palatal)
-Distomolar (another tooth behind a tooth)
What guidelines to follow when managing supernumeraries. How to manage failed eruption of upper 1s due to supernumeraries
RCS
-extract supernumerary, +/- gold chain exposure of unerupted central if remains high to encourage it down
-Can cause crowding and cause displacement of permanent tooth.
- Removing tooth depends on risk-benefit
Syndromes associated with hypodontia and hyperdontia
-Hypodontia= hypohidrotic ectodermal dysplasia, cleft lip and palate, Down’s syndrome, crouzon, oro-facial digital syndrome
-Hyperdontia= cleidocranial dysplasia, cleft lip and palate, gardner’s syndrome, oro-facial digital syndrome
General and dental features of hypohidrotic ectodermal dysplasia
Genetic
-hypodontia or anodontia
-delayed eruption
-deformed teeth, conical crowns
-dry skin, sparse hair
-partial/ total absence of sweat glands
-nail abnormalities
General and oral features of cleido-cranial dysplasia
-absent /hypoplastic clabicles
-skull sutures persist= helmet-like skull
-hypoplastic maxilla= high narrow palate
-retained deciduous teeth
-supernumerary teeth with abnormal form
-delayed/ failed eruption (supernumeraries prevent permanent teeth coming down and resorbing the primary teeth)
-hypocementosis
Types of developmental abnormalities in tooth size and form
-supernumerary (extra small conical teeth)
-microdontia
-macrodontia
-peg-shaped laterals
-double teeth (fused, or not divided)
-concerescence (roots of teeth have fused)
-taurodontism (pulp chamber larger height than normal)
-dilaceration (bend in crown or tooth)
Syndromes associated with microdontia
-Ehlers danlos syndrome
-Down’s syndrome
-Congenital heart disease
List causes of developmental abnormalities in structure of enamel
1-local causes: trauma, infection, idiopathic enamel opacity
2- Amelogenesis imperfecta
-causes usually unknown
– infections (rubella, syphilis)
-low birth weight, premature birth
-diabetes
-hypoparathyroidism
-vit D deficiency
-chemotherapy
4. Fluorosis: >2ppm.
5. Tetracycline
What is amelogenesis imperfecta. Explain the different types
-genetic defect in enamel. Autosomal dominant
-type depends on when during development the mother’s illness etc. occured.
-can affect primary and permanent
-involves all the teeth
1- hypoplastic: less enamel, grooves, pits, smaller, abnormal cusp morphology. Matrix not laid down
2- hypomineralised: soft, chalky, white or brown, chipping. Qualitative defect
What is Turner tooth
-An enamel defect in the permanent teeth
-Due to trauma or infection to overlying primary tooth. This affects the tooth germ of developing successor
= hypoplasia
Is fluorosis a hypoplastic or hypominerlaised defect. Does it affect all teeth. Appearance
-Hypoplastic or hypomineralised enamel
-depends on dosage, duration and timing
-doesn’t involve all teeth
-usually permanent dentition. Usually molars are spared
-white patches
-can get yellow/brown discolouration
List causes of developmental abnormalities in structure of dentine
-Local causes = trauma / Infection
-Dentinogenesis imperfecta
-Dentinal dysplasia
-Environmental
o Rickets (Vitamin D deficiency)
o Hypophosphatasia (metabolic defect in calcium formation)
o Juvenile hypoparathyroidism (issue with Ca and mineralisation)
What are the different type of dentinogenesis imperfecta. Appearance
-Type I: associated with osteogenesis imperfecta
-Type II: bones not affected, only dentine
-Type III Brandywine isolate
-discoloured, grey/ brown tint, bulbous crowns, rapid attrition, enamel chipping, reduced and irregular dentine tubules, pulp chamber becomes obliterated
What are the 2 types of dentinal dysplasia and their appearance
-Type I: Radicular dentine dysplasia (Rootless teeth, normal crowns)
-Type II: Coronal dentine dysplasia
pulp obliterated, short roots, disorganised tubules, calcified globules of abnormal dentine
What is osteogenesis imperfecta. How teeth are affected
-Brittle bone disease
-Autosomal dominant
-Chest deformities may lead to respiratory compromise – implications for GA/IV sedation
-Skeletal deformities – bowing of legs
-Muscle weakness, hearing loss-genetic, present at birth
-lax ligaments, thin translucent skin
-blue sclera
-more than often have dentinogenesis imperfects (aka type I)
What is rickets (causes, presentation) Dental abnormalities
-Lack of Vit D, affecting calcification
-Due to not enough in Diet, Decreased GI absorption, Lack of UV, Renal disease, Phenytoin (affects its uptake)
-Short stature, Bow-legs, Bone deformity and fractures
-Delayed tooth eruption, Enamel hypoplasia, Dentine abnormalities
What is regional odontodysplasia
-aka ghost teeth
-rare and idiopathic
-Very Hypoplastic teeth, very fragile, Abnormal form, Delayed eruption
-Deciduous and permanent
Hypercementosis/ankylosis causes
-Idiopathic
-Infection
-Overloaded teeth
-Functionless / unerupted teeth
-Feature of Paget’s disease
(hard to extract)
Disorders with Hypocementosis
-Cleidocranial dysplasia
-Hypophosphatasia (Defect of mineralisation causing Skeletal and dental defects)
=Mobile and Premature tooth loss
Causes of delayed eruption
-Localised
* Retention of deciduous teeth
* Hypodontia
* Abnormal crypt position
* Reduced space
*. eruption cyst
* Supernumerary teeth
crowding, ectopic tooth,
Generalised
* Hypothyroidism (Cretinism) -everything is delayed within body
* Rickets
* Cleidocranial dysplasia (hyperdontia)
* Downs syndrome (hyperdontia)
* hypohidrotic ectodermal dysplasia (hyperdontia)
What are natal and neonatal teeth and their problems. Management
-Natal tooth – tooth at birth
-Neonatal tooth – tooth that erupts within 30 days of birth
Usually Mandibular incisors
Tooth germs develop in superficial position
=Usually Hypoplastic enamel / Rootless
=Mobile – risk to airway
=Interfere with feeding. Can ulcerate tongue
-Only consider extracting if causing huge problem (with feeding etc.). But they are part of normal dentition so child would be without these teeth
List causes of impacted teeth, unable to erupt correctly
-Lack of space: overcrowding, small arch or jaw, space closure due to early tooth loss, supernumerary teeth, delayed eruption, irregular positioning of adjacent teeth
-cysts, odontomes, tumours, infection
-delayed growth of jaw (malnutrition, radiation, anaemia etc.)
-greater density of overlying bone or soft tissue. Fibrosis of mucosa
-supernumerary teeth causing delayed eruption (aka in cleidocranial dysplasia, Gardner’s syndrome, cleft lip and palate)
-ectodermal dysplasia (delayed eruption)
Which teeth are most commonly impacted
8s
upper 3s (palatal more common)
upper 1s
lower 4s and 5s
supernumerary teeth
Complications of impacted teeth
-Pericoronitis (most common with 8s)
-Resorption = unerupted impacted permanents accelerate resorption of overlying primary teeth
-Dentigerous cyst formation in follicle over unerupted tooth, leading to destruction of bone in local area – if perforates buccal cortex get infection there also
-Infection (hard to clean)
-Caries -Food trap and difficulty cleaning
-Mandibular fracture
Signs and symptoms of impacted teeth
-Retention of deciduous tooth
-Tooth appears missing
-Swelling
-Mobility or tilting of adjacent tooth (resorption of roots)
-Loss of vitality of adjacent tooth
-Pericoronitis
-Trismus
Radiographic signs that indicate increased risk of IAN nerve damage with XLA of lower molar
-Darkening of the root
-Diversion of the canal
-Interruption of the cortical outline
-Narrowing of the canal or root
-Deflected roots
Imaging required for ectopic tooth
-Parallax view using 2 PAs or Occlusal + DPT
(2 different views to check where the ectopic tooth is)
-CBCT may be indicated but unnecessary high dose
2 PAs are used to image an ectopic tooth. Is the tooth positioned buccally or lingually if the tooth moves in the same direction as the tube/ viewer
-The further away object always moves in the same direction as the tube / viewer
-SLOB: same way, lingual, opposite way, buccal
-so if tube shifts left to right and the tooth also moves right then it is lingual/ palatal
Also if palatal then further away so less magnified /smaller
What are the NICE guidelines for when removing 8s are necessary. Is pericoronitis an indication for XLA
-don’t remove pathology free impacted wisdom teeth
-consider removal when such pathology includes unrestorable caries, non-treatable pulpal/ periapical pathology, cellulitis, abscess, osteomyelitis, resorption of the tooth or adjacent teeth, fracture of tooth, cyst/tumour
-remove if impeding reconstructive jaw surgery, or involved in or within the field of tumour resection.
-consider to remove if repeated pericoronitis, or 1 severe bout of pericoronitis
Guidelines for managing ectopic palatal upper canines (Royal college of surgeons)
- Interceptive tx: XLA upper C at 10-13 years old, if not severely displaced. +/- space maintenance. If no improvement in position then alternative tx.
- Surgical exposure
and ortho alignment of the ectopic canine if appropriate degree of malposition - Surgical removal: if radiographic evidence of early root resorption of adjacent incisors [12.5% chance] Also if very crowded, severely displaced, unhappy with appearance
- ^although if severe root resorption of incisor, then extract incisor, then expose and align canine
- Transplantation: only considered if other tx failed, unwilling to wear ortho, or degree of malpossition is too great for ortho. Needs sufficient space and bone
- leaving if no risk of resorption or patient accepts the risk
Why upper 3s are commonly displaced
-Eruption starts high in maxilla. Forward and mesial migration to lie buccal and mesial to apex of deciduous canine before erupting down. Commonly displacement due to this long path of eruption
-Displacement of the crypt
-Short rooted or absent upper lateral incisor,
-Crowding- causes buccal displacement
-Palatal displaced usually have sufficient space, they just miss their eruption pathway
-3s rarely missing (0.2%) so if unerupted then likely ectopic
How to assess positioning of ectopic upper canine
-palpate for position at 9 years old. Feel for buccal bulge - Presence of hallowing is worrying so needs radiograph at 10 years old
-horizontal parallax or vertical parallax for 2 angles
-canine buccal if moved in opposite direction of tube shift. If goes with tube shift then palatal
Treatment for aligning 1) buccal displaced canine and 2) palatally displaced canine
1) more likely to erupt than palatal so best managed by reliving crowding with XLAs and ortho to encourage tooth to come through. Closed exposure to preserve gingival architecture =apically repositioned flap, bone removal, attach gold chain to tooth and brace, close flap back over
2) Palatal mucosa thicker and canine is less likely to erupt on its own. Open exposure more preferable- cut hole in gum to allow canine to come through. Could also do closed exposure and gold chain
Options for managing ectopic teeth
-leave and monitor
-surgical removal (MOS)
-expose and align with ortho bracket or chain
-transplant (risky, rare. Donor tooth into extracted impacted tooth socket, 2 week splint, composite camouflage. ANKYLOSIS risk)
-coronectomy
-interceptive orthodontics during mixed dentition stage (planned XLA of deciduous teeth to create space for permanent successors)
Indication for coronectomy. Complications afterwards.
-May be indicated with lower 8s with high risk of IAN injury
-remove crown and leave roots
-this reduces risk of damaging IAN during extraction
-Complications: dry socket, infection, eruption of roots
Difference between open and closed exposure procedures for helping align ectopic teeth
- Open= keratinised tissue (eg. on palate, sometimes buccally)
- Closed= non-keratinised tissue
Mucoperiosteal flap raised, bone removal to expose crown only, chain/bracket/magnet applied, soft tissue flap closed over top
-Usually of buccally displaced teeth that are superior to keratinised tissue, insufficient attached mucosa
[Tooth must erupt through keratinised gingiva in order to establish a MGJ, otherwise perio and aesthetic problems]
Process of exposing ectopic palatal canine. Is it an open or closed exposure
-open exposure (keratinised)
-remove palatal gingiva to expose crown, remove bone with chisels rather than drill as risk damaging successors
-Need to maintain hole in palate to allow tooth to come through. Zinc oxide eugenol dressing to prevent healing/ re-epithelialising.
cover plate for 2 weeks
What is an odontome
-amorphous collection of tooth tissue. Unrecognisable tooth due to weird differentiation of mesenchymal and epithelial cells into dentine and enamel
-can deflect eruption pathway or can displace teeth out of line of arch
Reasons for labial fraenectomy for high frenum
-Facilitate closure of diastema/ reduce chance of the diastema relapse
- Eliminate tension on the gingiva to solve tongue tie and perio problems
-resolve recession issues
-improve movement of the lip
-Aid tooth brushing
-Lip lengthening
How many teeth are missing in hypodontia, oligodontia, anodontia
Hypo 1-6 missing
Oligo >6 missing
Ano= no teeth present
What is a polyp and torus
-Polyp= Fibroepithelial, pink, red or white knob-like growth, due to trauma, cheek sucking overextended denture
-Torus= bony lump on midline of palate or lingual to premolars. No treatment needed
What cells make up radicular cysts. Is the pulp vital or non-vital. What cells line it
-Rests of mallesez proliferation
-residue from root sheath of hertwig
-mostly due to trauma
-non-vital tooth
-usually an incidental finding
-lined by stratified squamous epithelium
Most common tooth to be submerged. Management
-Primary molars. Retained as missing permanent successor. Starts to ‘sink’ as adult teeth continue to erupt around it
-Important to retain these teeth in hypodontia cases to maintain position for later ortho and implant tx
-if teeth start to disappear below the gingiva or is below the contact point then removal likely needed
-can build up with composite to build up the occlusion
What is transposition
Interchange of position between 2 teeth. 2 types:
1. pseudo transposition
2. True transposition – completely switched position
