Dental and Developmental Anomalies Lecture Notes PDF

Lecture 8: Dental and developmental anomalies Dental anomalies Anomaly Oddity; inconsistency or deviation from the norm Number of teeth ○ Hyperdontia or supernumerary teeth ○ Mes...

Lecture 8: Dental and developmental anomalies Dental anomalies Anomaly Oddity; inconsistency or deviation from the norm Number of teeth ○ Hyperdontia or supernumerary teeth ○ Mesiodent ○ Hypodontia ○ Oligodontia ○ Anodontia Size of teeth ○ Macrodontia ○ Microdontia Eruption or position of teeth ○ Impaction ○ Transposition ○ Ankylosis ○ Ectopia Morphology (form) of teeth ○ Gemination ○ Twinning ○ Fusion ○ Concrescence ○ Taurodontism ○ Dens invagination ○ Dens evagination ○ Dilaceration Congenital A condition that is present at birth by either heredity or environmental influences Acquired Not congenital in that it develops after birth and may be environmental in nature  Number of teeth (anomaly) Hyperdontia or Hyperdontia: too many teeth (premolar: most common in mandible) supernumerary Supernumerary teeth: one extra (i.e: extra premolar) → generalized teeth Mesiodens: most common single supernumerary tooth (commonly found between central incisors) Diseases associated with supernumerary teeth Cleidocranial dysplasia (least serious condition: abnormality of the skull, clavicle and supernumerary teeth) *Gardner’s syndrome: Individuals will have polypoptics in large intestines (a 100% chance of turning malignant) ○ Multiple osteomas (serious component) ○ ALOT OF SUPERNUMERARY TEETH Hypodontia Missing one or a few teeth Most common missing ones: (missing a few) ○ Max. lateral incisors (most common single missing tooth) ○ Third molars ○ 2nd pm in mandible ○ Maxillary lateral ○ Man. central Oligodontia Missing numerous teeth (more than 6) Missing more than 6 Syndromes associated with missing teeth (common with oligodontia) Ectodermal Dysplasia: autosomal dominant disorder where at least two ectodermal structures are missing such as ○ Hair, nails, sweat glands, skin and TEETH Anodontia Missing all of the teeth (generalized) Image of young individual that never had teeth → would need dentures Missing ALL *Size of teeth Rule out: positioning errors (i.e: on panoramic if you’re too far forward) Supernumerary teeth Irradiation to the jaws causing dwarfing of the teeth (i.e: early childhood radiation can affect the size/development of the teeth) Macrodontia Teeth are larger than normal (Usually affects only ONE tooth ) (not a common thing) (larger than normal) May occur with (not common) ○ Vascular abnormalities (hemangioma) ○ Hemihypertrophy of the face ○ Pituitary gigantism (generalized) May cause ○ Crowding ○ Impactions  ○ Malocclusion Could be confused with fusion, gemination and positioning errors *Microdontia A tooth or several teeth that are smaller than normal and may have abnormal form Most common localized Smaller than normal ○ Max. lateral incisors (typical microdontia: peg lateral) teeth ○ Third molars (common) May be syndromic ○ Congenital heart disease ○ Progeria (rapid aging in childhood and failure to grow) ○ Down syndrome → lots of spacing (bc teeth are small or jaw too big) Eruption or position of teeth Impaction: Tooth did not erupt Tooth that “fails” to erupt Evident radiographically Most common ○ Canines and molars Can be bone or soft tissue impaction Transposition:Teeth switch places Transposition: teeth switch places Common in permanent canine and 1st premolar Easily identified Teeth altered prosthetically Usually unilateral (generally not common)  Eruption or position of teeth Ankylosis Common in primary teeth → Not actually a radiographic Fusion to bone caused by diagnosis (it’s a clinical diagnosis) ○ Trauma (avulsion) ○ Infection → loss of periodontal ligament ○ Absence of permanent tooth space Can cause the tooth to look submerged Loss of lamina dura and PDL Difficult to extract → evident clinically Ectopia: abnormal position of tooth/follicle Common in permanent incisors and canines Morphology of teeth: Form Gemination (1 → 2) Clefting or invagination of the crown Single pulp chamber may be enlarged or partially divided “Normal number of teeth when Normal number of teeth counted- (one tooth divide into Most common in primary teeth but also in permanent teeth two)” Most common in incisor and canines, rarely in premolars Gemination (twinning) → complete division of tooth bud Fusion ( 2 → 1) Dentin fused together (syndontia) Two pulp chambers No PDL space between one less tooth in arch One teeth will be missing because teeth will fuse \ Concrescence (localized) Teeth fused by cementum Teeth fused by cementum (roots are Maxillary molar most often involved fused) True concrescence: occurs during development by space restriction Acquired concrescence: local trauma, excessive occlusal force, local infection after development On radiograph: No alveolar bone or PDL between teeth Roots connected by cementum PDL and Lamina dura surround roots of both teeth Hypercementosis surrounding roots of both teeth Differential diagnosis Superimposed teeth Fusion Hypercementosis Taurodontism Molars are shaped like a “bull” Large “trunk”-extension of pulp “Head of bull: bifurcation at the Short roots apical ⅓” Normal crown Noted on radiographs only → wide pulp May see with down syndrome or amelogenesis imperfecta ○ Wide pulp chamber, high horns → looks like a bULL Dilaceration → sudden Extreme root or tooth curvature change in direction (localized) Noted radiographically Most common in maxillary premolars and “Developing tooth is affected by incisors trauma” “Curve” Result of mechanical trauma or developmental B/L placed roots appear circular “bull’s eye Dens in dente Invagination, evagination, dilated odontoma Coronal type: folding inward of the enamel organ and is lined by epithelium (most commonly seen in the crown) Looks like a “tooth within a tooth” Radicular type: caused by folding of hertwig’s epithelial root sheath and is lined by cementum (less common in root structure) Enamel inside crown or root ○ Man. 1st PM and 2nd molars (RARE) structure → pulp chamber lined with enamel Communication with oral cavity and pulp → apical inflammation can occur 5% of caucasian and Asian population Possibly hereditary Invagination May result in necrosis and rarefying osteitis- lateral incisors, max central, pm, canines Den evaginatus Folding outward of enamel organ Evagination: enamel covered tubercle may chip resulting in oral (Leong’s premolar) communication Most common in lateral incisors and PM ○ With the PM there’s an extra cusps going thru, so there’s an extra pulp → with occlusion forces it can be a problem Enamel pearl Small globule of enamel that forms on the roots of molars Apical to the CEJ, often in the furcation  Usually NOT clinically detectable “Looks like a pearl bc of the Differential Dx: calculus, pulp stone extra enamel on root” Talon cusp Accessory cusp located on the lingual surface of the maxillary or mandibular incisor “Lingual cusp → incisors” Pathogenesis Developmental anomaly Frequently in cleft palate syndrome Turner’s Hypoplasia → see Local hypoplastic defect in the crown of a permanent tooth in one or few teeth Caused by infectious or mechanical trauma Alteration in normal contours of affected tooth “Issue with baby teeth will Differential diagnosis: high dose of therapeutic radiation, caries affect permanent teeth” Hutchinson’s teeth Back in the day before penicillin, and if babies were born to mother who (congenital syphilis) had syphilis they would have hutchinson’s teeth ○ Central incisors: wider at neck, constricted at incisal ○ Posterior teeth: would have extra cusps (mulberry molar) Congenital anomalies that affect the teeth in general (Both primary and permanent set) Amelogenesis imperfecta: formation of enamel is defective  ○ Hereditary defect of enamel ○ An ectodermal disturbance ○ Enamel hypoplasia due to an incomplete or defective formation of the enamel matrix of primary and permanent teeth ○ Features (color, texture and consistency is off) Tendency toward impaction Normal dentin structure 4 general types Hypoplastic Hypomaturation Hypocalcification Hypomaturation type associated with taurodontism Amelogenesis imperfecta → all teeth (the enamel affected) (4 general types) Hypoplastic (see the crown) Thin piece of enamel that looks whiter than dentin (tissue is okay, size is small, less # Appearance clinically of cells) ○ Can see thru enamel because it’s thinner (color will look brown Can tell better from other types because you can see the dentin) ○ Small tooth → multiple diamitisum On radiograph ○ Small piece (thin) of enamel ○ Calcification is fine ○ Maturation is okay Hypomaturation See teeth (weak enamel crystal → generalized) (crystals don’t mature properly) Eating will cause weak enamel to flake away Hypocalcification Can’t tell the difference between enamel and dentin on a radiograph (not enough calcification material ○ Image of bitewing for crystal to form) Weak enamel Enamel not strong enough to withstand occlusal force → brittle enamel → effects primary and permanent dentition Hypomaturation type associated with taurodontism  Dentinogenesis imperfecta: formation of dentin is defective (generalized) ○ “Hereditary opalescent dentin” ○ Hereditary condition affecting primary and permanent dentition where dentin is defective ○ More prevalent than amelogenesis imperfecta ○ Three types: Type 1, 2, 3 (can’t see much pulp) Type 1: associated with osteogenesis imperfecta (genetic collagen disease → lead to brittle bone which is prone to fractures, blue sclera); Type 2: no osteogenesis imperfecta Type 3: white pulp instead of fully obliterated pulps ○ DEJ smooth ○ Bulbous crowns ○ Constricted necks ○ Shortened roots ○ Imperfect formation of dentin Dentinogeneis imperfecta (generalized) → cant see pulp on the radiograph Type 1 (most serious; Patient has intraoral challenges, as well as other challenges to deal with associated with With osteogenesis imperfecta, blue sclera osteogenesis Multiple fractures and scars imperfecta) common Type 2 Does not occur in association with osteogenesis imperfecta Mostly frequently referred to as hereditary opalescent dentin (no osteogenesis Bulbous teeth (wide crown, but constricted at the CEJ) imperfecta) obliterated pulp (no pulp is seen) Clinically: appear: greyish blue Common  Dentin dysplasia: dentin of crown vs root ○ Rare occurrence ○ Rootless teeth ○ Autosomal dominant ○ Two types Type I: radicular- short roots, conical in shape and sometimes known as “rootless teeth” molar will have “W” shape, 20% associated with periapical lesions 4 variations Type II: Coronal- normally shaped roots, normal length, pulp chambers become flame shape with multiple pulp stones Dentin dysplasia (generalized) Dentin dysplasia Look at roots type I: little to no roots (RADICULAR) Dentin dysplasia Look at pulp chamber type II: Normal roots Pulp chamber flame shape (Coronal) → pulp stones can be seen Note: No roots can be from: childhood radiation or Type 1 (radicular)  Regional odontodysplasia: everything is affected: enamel, dentin, cementum ○ Large pulp chambers ○ Thin enamel ○ Hypocalcified, thin dentin ○ Usually restricted to a region such as a single quadrant ○ Also known as “ghost teeth” → not generalized Regional odontodysplasia Enamel is thin Roots not fully developed (not common, not Cant see enamel or dentin generalized) Pulp is very wide (looks like a shell of a teeth) → everything affected: Can’t tell the difference between enamel and dentin dentin, enamel and roots are FUCKED UP!! Acquired abnormalities of teeth (not due to caries or inflammation) Attrition: lost of tooth structure due to Physiologic wearing of the dentition from occlusal occlusion contact between maxilla and mandible Men > women (non-carious lost of tooth structure) Depends on the abrasiveness of the diet, salivary factors, mineralization of teeth, emotional tension Clinical ○ Wear facet on cusps and marginal oblique and transverse bridges, broadening of the incisal edges More pronounced on the lingual cusps of maxillary molars and buccal cusps of mandibular molars Altering the normal curved surfaces into flat planes Reduction in the pulp chamber size, deposition of the secondary dentin Widening of PDL SPACE resulting in tooth mobility Occasionally hypercementosis Abrasions: lost of tooth structure due to Non-physiologic wearing of teeth in contact with foreign object (example: tooth brush) foreign substances as a result of friction Two most common reasons: toothbrush injury, dental floss (non-carious lost of tooth structure) Other reasons: pipe smoking, opening hairpins with tooth improper use of toothpicks, denture clasps, cutting thread with the teeth Toothbrush injury: V-shaped wedge or groove into the cervical area Dental floss injury: frequent on the cervical portion of the proximal surfaces just above the gingiva Radiographic features ○ Toothbrush injury: well defined semicircular radiolucencies ○ Dental floss injury: narrow semilunar radiolucency in the interproximal of cervical area (more on distal surface) Erosion: lost of tooth structure due to Results from a chemical action not involving bacteria chemicals Etiology: contact acid with teeth Involving multiple teeth Thinner enamel with glossy surface Loss of enamel, a pink spot shows through the enamel Radiographic: dished out or V-shaped defect, well defined or diffuse Edges are usually rounded off than those caused by abrasion Internal: palatal of maxillary teeth (common) Internal and external resorption: The removal of tooth structure by osteoclasts External or internal type → based on the surface being absorbed External type (outside) Localized inflammatory lesions Root resorption Reimplanted tooth Tumors and cysts 2 TYPES: ( treating them is different) Excessive mechanical and occlusal forces - APEX: external apical resorption Impacted teeth - Cervical: external cervical resorption Characteristics: Short roots, blunted, square shape Irregular, ragged border The canal can be followed Canal straight Internal type (resorption) → Localized Acute trauma (affecting one tooth) Direct and indirect pulp capping Pulpotomy Dense invagination (WITHIN PULP CHAMBER) Characteristics: Enlarged root canal system Sharp, smooth clearly defined margins Canal is NOT PRESENT Enlarged canal Pulp stones Foci of calcification in the dental pulp Unknown cause Radiograph: radiopaque structures in the pulp chamber or root canals (any shape) Pulp tissue is calcified Hypercementosis Deposition of cementum on the tooth root surfaces Unknown etiology, however supraerupted teeth after loss of the opposing teeth Inflammation Patients with Paget’s disease and with hypopituitarism (gigantism, acromegaly) Radiograph: ○ excessive buildup of cementum around the all or part of a root, ○ Bulbous enlargement of the root ○ Uniform lamina dura and PDL space around the root Developmental and congenital anomalies (NONODONTOGENIC ANOMALIES) Nonodontogenic anomalies of the jaws Stafne bone defect Exostosis/enostosis TMJ abnormalities Cleft palate Maxillary sinus anomalies Craniofacial developmental disturbances of the face and skull Definition Hypertrophy: enlargement of an organ or tissue due to an increase in the size of the cells, non tumorous growth Hyperplasia: an enlargement of an organ or tissue due to an abnormal increase in the number of cells Hypoplasia: incomplete of underdevelopment of an organ tissue Brachycephalic: someone who has a short, broad head Hypertelorism: abnormal increase between two organs/parts of the body - eyes (eyes too far apart) Wormian bones: extra small, irregular pieces of bone that occur within a suture of the cranium Synostosis: abnormal fusion of neighboring skeletal bones making one larger bone Oxycephaly: congenital abnormality of the skull that leads to a cone shape appearance of the head. Caused by premature closure of the lambdoid and coronal suture Trigonocephaly: congenital abnormality of the skull that leads to triangular appearance of the head due to premature fusion of the cranial bones Stafne bone defect (don't need to do Group of concavities on mandibular lingual surface- anything) submandibular gland fossa most common Described by stafne in 1942 Lingual salivary gland depression Caused by growth of salivary gland Rarely-medial surface of ascending ramus from parotid gland Unknown etiology- pressure resorption and fatty tissue growth Typical below IAN: has a thick white area around it Location and shape is typical Exostoses/enostoses/tori Limited bone hyperplasia Maxillary tori are most common (%20) Exostoses: extra bone coming out of lingual cortex (i.e: tori) Man tori (lingual tori) (%8) > exostoses Enostoses: inward growth Exostoses seen mostly in maxilla ○ Usually along the facial/buccal surfaces Composed of compact bone Enostoses= internal counterparts to exostoses Mandibular tori TMJ abnormalities Condylar agenesis → non formation of condyle Condylar Hyperplasia → one bigger than the other Bifid condyle (2 heads) Cleft palate Palate does not fuse → communication between nasal and oral cavity treatment starts early for these patients Will typically have a class III appearance; affecting growth of maxilla Sutures: a baby's brain grows 70% of its adult size by age one Premature closure makes the head shape irregular and can lead to mental retardation, blindness and hearing loss Craniofacial developmental disturbances Cleidocranial dysplasia A congenital hereditary conditions Abnormalities of skull, teeth, jaws, clavicle and long bones Skulls has a flat appearance Partially or totally missing clavicle Retention of deciduous teeth Delay in eruption of permanent teeth Supernumerary teeth → delayed eruption Multiple impactions Dentigerous cysts may develop Craniofacial dysplasia Large head with front and parietal bossing (crouzan’s syndrome) High arched palate Small sinuses-maxillary Skull has a problem and midface Micrognathia has a problem Hearing loss Crouzan’s syndrome Early closure of all cranial sutures (radiographic absence of sutures) “Frontal bossing”- bulging of frontal bone Hypertelorism (eyes are wide apart) Beaten metal appearance: cranial markings which look like digital impressions seen in the cranial vault Normal mental capacity Maxilla is underdeveloped Skull has multiple lined patterns (looks like a piece of metal that has been beaten) What’s going on: brain doesn't know that the suture has closed, so the brain is still growing (exerting pressure on inner plate of the skull) Mandibulo-facial dysplasia Underdevelopment of the midfacial region (treacher-collins syndrome) ○ Coloboma of the eyes ○ Malformation of the external ear ○ Atypical hair grown Midface is affected and mandible is ○ Macrostomia → BIG MOUTH affected Radiographic findings ○ Hypoplasia of the facial bones (especially the zygoma) NO METAL BEATEN APPEARANCE ○ Facial cleft and other skeletal deformities OF SKULL In this image you see that the midface is affected  Lecture 9: infectious and inflammatory diseases of the jaws Periodontal ligament fibers: holds the tooth within the bone (the socket) The tooth root is outline with alveolar bone The alveolar bone is more mineralized than the surrounding bone (this is known as lamina dura) ○ Lamina dura appears thicker than surrounding bone because it has more calcium content Mental foramen is located → Between premolars or periapical of premolar How does caries start? 1. Caries: involving enamel, dentin and pulp horn a. If caries happen only in enamel/dentin you just need to restore that tooth b. If caries reach pulp → do a root canal treatment (endodontic treatment is required) i. When caries reach the pulp, it can lead to a necrosis of pulp (the pulp is important because its the neurovascular supply to the tooth) 1a. Trauma of tooth: can also lead to necrosis of pulp 2. Showing necrotic pulp 3. Image is showing how infection can progress down to the periapical area (you would see a radiolucency near periapical region) 4. If the infection stays for a long period of time it can become osteomyelitis (inflammation of cortical and marrow bone) Osteo: cortical bone Myel: marrow bone Itis: inflammation What are the two things leading to the necrosis of pulp? Caries Trauma Necrotic pulp can lead to → apical periodontitis (acute or chronic) Acute (few days)→ periapical abscess/ granuloma / periapical cysts → osteomyelitis Chronic → periapical granuloma/ periapical abscess → periapical cyst Any infection in the body that is long standing can lead to osteomyelitis Note: Using the term apical periodontitis instead of radiographic radiolucency Radiographically we don't say periapical radiolucency (this is the finding), i.e: when you see the tooth on an x ray- you found a periapical radiolucency due to trauma or caries Basically: Trauma or caries (which involves enamel/dentin/pulp) → infection from the pulp can travel to the periapical area You’ll see a periapical radiolucency on radiograph (THIS IS YOUR FINDING) Differential diagnosis Early radiographic features of inflammatory disease Widening of PDL (periodontal ligament) includes: space → this is the shit that hold tooth in socket (There’s a uniform widening) Pushing up of the tooth because of the inflammatory exudate (fluid that move to site in response to inflammation → this fluid will slightly push the tooth up) Loss of the lamina dura and trabecular bone (lamina dura is broken down due to the infection) Very early lesions may not show any radiographic features Synonyms for Periapical inflammatory Apical periodontitis disease Periapical abscess/granuloma Cysts Rarefying osteitis The preferred radiologic term for an inflammatory process in bone associated with bone destruction at the apex Rarefying: loss of bone mineralization Osteitis: refers to inflammation of bone Appearance: increased radiolucency Sclerosing osteitis Inflammation process in bone associated with bone deposition around tooth root Sclerosis: refers to a “hardening” of bone Appearance: radiopacity of bone Radiographic features of periapical inflammatory lesions Location Within the periodontal ligament space around the apex Periphery ill-defined → not able to trace margin of periapical region ○ Bc too much infection (refers to outline shape) Well-defined → can trace margin of periapical region I.e: well defined outline Internal structure Loss of bone density Sclerotic bone formation → more radiopaque Effects on 1. Bone resorption surrounding 2. Sclerotic bone formation structure 3. External root resorption a. (if infection stays for a long time, it might eat up tooth structure) 4. Destruction of adjacent cortical bones a. (infection goes from marrow bone to cortical bone) 5. Inflammatory periosteal bone reaction (periostitis) a. infection from cortical bone to periosteum. b. Periosteum contains pluripotent cells (when infection reach these cells they will form osteoblasts → osteoblast forms new layers of bone called periosteal reaction) c. If the infection doesn’t stop it will come out thru the gingiva (prulis) → skin  Caries → (infection enamel, dentin pulp) apical periodontitis → rarefying osteitis → sclerosing osteitis *if infection spreads for a long period of time it becomes (marrow → cortical bone) osteomyelitis → periosteal will differentiate pluripotent cells → forms new bone → (infection still spreading → gingiva → skin) Apical periodontitis → Rarefying osteitis → Sclerosing osteitis Periapical space (PDL) widening due to See radiolucent around periapical region Surrounding bone is more radiopaque trauma or caries Rarefying → radiolucent Sclerosing → Sceloritic bone which is more -When you see widening of periapical Osteitis → inflammation of the bone radiopaque space you have to do a vitality check Osteitis → inflammation If infection started to spread, use the term What is a vitality check? osteomyelitis - There’s certain instruments: it → body will start reacting because body doesn’t can be with electric or it can be want infection to spread, by forming sclerotic with ice bone - Put the instrument near the cervical region because the This is host dependent: your body might be able enamel is thin there to develop the sclerotic bone faster (stop spread - There’s a certain value and if of infection) than other individuals (spread of tooth responds within that value infection → osteomyelitis) it means vital Inflammatory periosteal bone reaction (periostitis) (KNOW THIS) Periosteum: dense and irregular thick layer of connective tissue that lines the floors of air cavities and covers the surface of the jaw bones Extension of collagen from the bone: SHARPEY’S Fibers: anchor the periosteum to bone Periosteum consists of two discrete cell layers ○ Inner osteogenic layer: has pluripotent mesenchymal stem cells ○ Outer fibrous layer: contains fibroblasts and collagen Under the right conditions, the stem cells within the osteogenic layer can produce osteoblasts → newbone Floor of maxillary sinus: ribbon-like radiopacity follow the shape of the floor of the sinus) Other cortices: buccal and lingual surface of alveolar process Inflammatory periosteal bone reaction Parulis= when periosteum infection spread to gingiva 1st image Showing new layers of cortical bone Onion ring like formation 2nd image (periosteum bone formation at maxillary sinus) → Infection going into maxillary sinus, causing the stimulation of periosteum layer Periostitis: (inflammation of periosteum) layers of new bone formation Periostitis Starts off as a layers of bone There’s gap between the layers If infection continues, the gap will be filled by more bone  Changes in the maxillary sinus Displacement of the floor of the sinus Perforation of the floor of the maxillary sinus ○ Infection will drain into sinus and spread (will have odontogenic sinusitis) cold like symptoms 3 things with respect to sinus 1. Lead to stimulation of periosteum layer at floor of sinus (leads to periostitis) 2. Leads to superior displacement of floor of sinus 3. Lead to perforation of sinus floor Odontogenic sinusitis: caused by dental infection Normal structures that mimic periapical lesions Mental foramen Present at the apex of premolar → mimic a periapical radiolucent (rarefying osteitis) The presence of uniform periodontal ligament space and intact lamina dura Inferior alveolar canal extending from the foramen Another radiograph with different angulation Mental foramen vs rarefying osteitis Can look at lamina dura (if intact, then it’s mental foramen) Do a vitality test SLOB technique (if moved to opposite direction → its mental foramen bc present buccally) Nasopalatine foramen/duct With a nasopalatine foramen → there’s a big radiolucent between the central incisors and the surrounding borders are corticated (well-defined: trace all borders) (incisive foramen) Enlarged foramen vs Cysts (radiographically) More than 10mm (a cysts) At the end of the canal Less than 10 mm (enlarged foramen) there’s nasopalatine foramen Foramen vs periapical lesion Look at lamina dura Vitality test Within canal there can be a cysts formation Cysts formation can mimic periapical radiolucency Enlarged foramen vs cysts: this radiograph showed the size of stayed the same size throughout the years so it's an enlarged foramen *Request for another periapical and see if dimension differ Submandibular gland fossa  Large marrow space Lamina dura space- intact and well defined ○ If it was an infection it would break down lamina dura Maxillary sinus Floor of maxillary sinus dips Continues to expand because sinus is filled with air (pneumontatization is a continuous process, sinus will continue to pneumatized surround structure) Summary: Structures that mimic periapical lesions Mental foramen Nasopalatine foramen/duct Submandibular gland/fossa Large marrow space Maxillary sinus  Differential diagnosis for periapical inflammatory lesions *Dense bone island Localized growth of compact bone within cancellous bone (natural process) Note: would look *Radiographic features: (KNOW THIS) radiopaque → mimic ○ more common in the mandible sclerotic osteitis ○ Well-defined ○ Uniformly radiopaque ○ No radiolucent rim Don't need to worry No effects on the surrounding structures (sometimes can cause external root resorption) Synonyms of dense bone ○ Enosteous (formation of cortical bone inside the marrow) ○ Idiopathic (no effects on surrounding structure) ○ Osteosclerosis (new bone formation) Dense bone island (left) Sclerosing osteitis (right) No caries See caries More radiopaque Less radiopaque compared to dense bone island → nothing to worry about On a 3D radiograph: can see a dense bone island that is attached to the cortex (buccal and lingual of cortical bone)  Dense bone island Condensing osteitis Uniforma periodontal ligament Caries space Everything is diffused (diffusing Well defined (no blending) with surrounding bone) Non-problematic Ill defined outline Can trace edges ○ Can't trace edges Dense bone island Cementoblastoma No radiolucent rim Radiolucent rim “looks like a Non-problematic wheel” Root resorption is less likely Root resorption is more likely  Periapical scar tissue Replacement of bone with dense fibrous tissue after apical surgery or endodontic treatment Tooth is endodontically Clinical signs and symptoms treated → now there’s a Radiating, spoke-like pattern of the new bone at the periphery radiolucent lesion (in the process of healing) With a healing scar, the bone start healing at the periphery first, then it goes internally Periapical Localized changed in normal bone metabolism that results in the cemento-osseous ○ resorption of normal cancellous bone dysplasia ○ replacement with fibrous tissue & amorphous bone ○ Abnormal bone trabeculae Cells coming from cementoblasts and → teeth are whiter (because it’s not caused by infection) osteoblasts - but not organized 3 different stages 1. Radiolucent 2. Mixed: radiolucent/radiopaque Doesn’t require treatment 3. Mature → more radiopaque (bc forming cemento & osteo structure) Radiographic features of Periapical cemento-osseous dysplasia Location: periapical region of the teeth Internal structure, depending on the maturity of the lesion ○ Early stage: normal bone is replaced by fibrous tissue radiolucent ○ Mixed stage: radiopaque center in the radiolucent region ○ Mature stage: totally radiopaque with a thin radiolucent rim Early Mixed Mature - Radiolucent Radiolucent → Completely radiopaque with - is it dysplasia or becomes radiopaque radiolucent ring rarefying osteitis? → Do a vitality test to → see a radiopaque mature stage vs cementoblastoma? determine center → both have radiolucent ring → If vital, wait a couple of months to see if it Mature cementoblastoma progress to the mixed stage Structureless V-pattern (amorphous) Common in man. cause root Don't cause resorption root resorption Patient will have pain No pain Periapical cemento-osseous dysplasia (early stage) vs periapical inflammation → rely on clinical information such as testing of the vitality of the involved tooth Periapical cemento-osseous dysplasia (mature stage) vs condensing osteitis (sclerosing osteitis) Periapical cemento-osseous dysplasia Condensing osteitis (sclerosing osteitis -Non-carious -caries -Dense radiopacity -PDL space widening -well-defined radiolucent ring -Diffuse scleritis -Not well defined  Radicular cyst A cysts that results when rest of epithelial cells (malassez) in the periodontal ligament are stimulated to proliferate and undergo cystic degeneration by inflammatory products from a non-vital tooth Lined by epithelial cells of malassez (present in perio Grow by osmotic pressure → pressure from fluid ligament) Radiographic features Location: epicenter at the apex of a nonvital tooth Periphery: well defined and corticated Shape: round and hydraulic Internal structure: Radiolucent Radicular cyst vs periapical radiolucency Note: a round shape, a well defined cortical border and a size GREATER than 2 cm in diameter are characteristic of a cyst Root resorption (2 types) → (external and internal) External Resorption of the surface of the tooth surface Etiology Localized Reimplanted tooth Tumors and cyst Excessive mechanical Impacted teeth inflammatory and occlusal forces Internal Resorption of the dentin surrounding the pulp chamber or canal → you would see that the pulp chamber is slightly widen bc its not communicating with the external root surface Etiology Acute trauma Direct and indirect pulp capping Pulpotomy Dense invagination SLOB TECHNIQUE: Internal vs External root resorption Internal Same position on 2nd radiograph External Moved to opposite Osteomyelitis: if infection stays for a long period of time Osteomyelitis Inflammation of bone involves bone marrow, cortex, cancellous portion and (background info) periosteum 3 ways to get osteomyelitis: ○ Abscessed teeth ○ postsurgical infection ○ hematogenous spread The hallmark of chronic osteomyelitis: formation of sequestrum (a pathognomonic feature) Can be either chronic or acute Sequestrum Necrotic bone (ischemic injury caused by inflammatory process) Scelrotic bone → blood supply is less (aka dead bone) With osteomyelitis there’s less blood supply ( hypovascularity) Chronic osteomyelitis → will be so sclerotic that it will be deprived of blood A) Visible bone is oral cavity B) Sclerotic bone C) Sclerotic bone Hypovascularity → can lead to death of bone (death of bone is called sequestrum formation) Image is showing how surrounding bone is separated from the actual bone Radiographic features Location: posterior body of mandible of osteomyelitis Periphery: ill-defined, better defined on chronic type Internal structure: both greater and lesser radiopacities Bone destruction (acute) → sclerotic bone (chronic) slightly Radiolucent Sequestrum Sequestrum: a pathognomic feature of osteomyelitis Effects surround structures Bone resorption: resorbed cortical bone Bone formation: ○ Periosteal new bone formation → proliferative periostitis (onion skin) more in the chronic type, enlargement of bone Loss of lamina dura and PDL space External root resorption Draining fistula (only chronic type) ○ Well-defined break in the outer cortex  Osteoradionecrosis Osteoradionecrosis Bone death resulting from exposure to therapeutic radiation doses greater than 50 Gy (general between 60-70 Gy) ← too much radiation ○ Lead to the 3 H’s Hypovascular Hypoxia Hypocellular Osteoradionecrosis Bone contains a number of other tissues that may be affected by radiation (one such tissue system is the vasculature) Many of the effects of radiation injury that are seen involving bone may arise as a consequence of damage to the vasculature Although vascular endothelial cells in large vessels are generally radioresistant- the thinner vessels walls of smaller vessels may have greater sensitivity The damage of this portion of cells lining the walls of small vessels may compromise their ability to proliferate, and the bone may become hypocellular and hypercellular as a result The lack of sufficient vascularity results in a hypoxic environment in which adequate healing of bone is compromised (should the dose, dose rate, or fractionation scheme of delivery exceed the tolerance of the bone to repair the bone may undergo cell death or necrosis → osteoradionecrosis Therapeutic radiation exposure can cause bone damage and changes without necrosis, although it is possible that such changes may make the bone more susceptible to necrosis, especially after surgical intervention What you see in osteoradionecrosis Bone formation and sclerotic bone formation (as you’ve seen in chronic osteomyelitis) Presence of sequestrum (as you seen in chronic osteomyelitis) ○ (a fragment of dead infected bone- which becomes separated from viable bone) OSTEORADIONECROSIS: Hypoxia Hypovascular Hypocellular How would you differentiate osteoradionecrosis from osteomyelitis? Medication related osteonecrosis of the jaw Medication Osteonecrosis associated with anti-resorptive medication especially bisphosphonate (reduce and necrosis function of osteoclasts, used for multiple myelo and osteoporosis to balance the osteoblast) of the jaw (metastatic tumors, metabolic bone disease and osteoporosis) Clinically ○ Exposed bone ○ Pain ○ Swelling at the site of extraction in the patient with history of antiresorptive medication use Radiographically ○ Same as osteoradionecrosis and chronic osteomyelitis ○ Thickening of lamina dura How would you differentiate between osteomyelitis/osteoradionecrosis or medication related osteonecrosis? Ask the patient their history Pericoronitis (crown, inflammation) Pericoronitis Inflammation of the tissues surrounding the crown of a partially erupted tooth Due to food and microbial debris trapped under the soft tissue More common in the mandibular 3rd molars Clinical presentation: pain and swelling, trismus Radiographic features Centered on the follicular space or the portion of the crown still embedded in bone or in close proximity to bone Ill-defined and scelrotic bone formation, enlargement of the follicular space  Lecture 10: Radiology caries Caries ○ Multifactorial: teeth, microflora, diet ○ Lactic acid produced by bacteria by fermentation on carbohydrates causes demineralization Radiographic: Caries Radiolucent (darker zone) → caries The demineralized area does not absorb as many x-ray photons as the unaffected portion Imaging gives assistance to detecting small caries that are difficult to detect clinically, especially in the INTERPROXIMAL REGION (hard to see in these region Cannot reveal if arrested or active (on x-ray) Type of radiographs to use for caries Bitewing radiographs ○ Bitewings with open contacts (no overlap) ○ Max and Man teeth and bone should be evenly distributed ○ Paralleling technique Reduces the number of overlapping contacts Improves image quality → minimizing interpretation errors ○ Goal: find interproximal caries Types of bitewings: horizontal vertical Periapical radiographs ○ Primarily for detecting changes in periapical bone (something at the end of the root) ○ Paralleling technique Reduces the number of overlapping contacts Improves image quality  Where can caries be found? → Always confirm radiographic dx with clinical exams Proximal caries ○ Early lesions Only In the enamel (demineralization) Caries begins as a triangle with its broad base at the tooth surface Chances are both sides are affected Once it’s extended into the DEJ it’s known as CARIES Second triangle with the apex directed to the pulp chamber Differential diagnosis for proximal caries Abrasion from a Cervical burnout Various morphological Dental anomalies Mach band effect clasps of a partial phenomena (pits and (hypoplastic pits and denture seen in the cervical region can fissures) concavities produced Optical illusion: exaggerates mimic a proximal caries (under by wear) the contrast in shades of gray Less dense area the contact) (radiolucent) Can be seen in proximal surface and occlusal surface Proximal caries begins below the contact point not below the free gingival margin Enamel (more radiopaque) Image above: Dentine (less radiopaque) Slight indentation Less enamel in that spot For cavity: you should be able to see or feel Common under restoration  Occlusal caries ○ Demineralization originates in enamel pits and fissures ○ Board based ○ Bowl shaped ○ Radiolucent zone often beneath a fissure ○ Little or no apparent changes in the enamel ○ May not be radiographically visible if it hasn't crossed DEJ Differential diagnosis for occlusal caries Superimposition of the image of the buccal pit Non-metal restoration Mach band effect Rampant caries ○ Serve,rapidly progressing carious destruction of teeth ○ Population pediatric - poor oral hygiene, baby bottle caries Adults with xerostomia due to Systemic disease Poly pharmacy Salivary gland dysfunction Adults abusing drugs (met mouth) Radiographically- tooth destruction  Caries of buccal and lingual surfaces ○ Enamel pits and fissures of teeth ○ Lesions may be round early on ○ Evolve to elliptical or semilunar as it grows ○ Difficult to differentiate on radiographs ○ Clinical evaluation necessary Caries associated with restorations ○ Differentiate from Residual caries which are left due to proximity of the pulp Radiolucent restoration Cervical burnout restoration still in place but caries at the margin Radiolucent restoration: well defined margins Root caries ○ Involve both cementum and dentin associated with gingival recession (seen clinically) ○ Usually detected clinically ○ Difficult to differentiate from cervical burnout Radiation induced caries Radiation to the head and neck Loss of salivary gland function Xerostomia Change in the bacterial flora Rampant caries looks pretty aggressive Lecture 10, part 2: Periodontal disease What is periodontal disease? Dental plaque forms → gums inflamed (gingivitis) → periodontitis Gingivitis Gingival inflammation without detectable destruction of the host tissues Gingival swelling, edema, erythema (not seen on a radiograph) May or may not progress to periodontitis NOT A RADIOGRAPHIC FINDING (CLINICAL DIAGNOSIS) Periodontitis Bone loss ○ Localized vs generalized ○ Horizontal and/or vertical ○ Mild/moderate or severe Clinically: ○ Pocket formation ○ Gingival swelling, edema, erythema ○ Chronic Aggressive Manifestations of systemic disease Diagnostic images Complimentary to the clinical examination Part of the assessment ○ Extent of destruction ○ Local contributing factors ○ Periodontal features that affect prognosis ○ Crown to root ratio ○ Periodontal therapy Checklist for radiographic Limitation of intraoral images 2D view of 3D structure Difficult to evaluate the bucco-lingual aspect (CBCT: you can see buccal-lingual) Reflect less bone loss than what is actually present No soft tissue to hard tissue relationship (pocket depths) → can’t see pocket on bitewing Lack of proper reference point of measurement Diagnostic imaging Invaluable role in diagnosis and tx planning Supplements a thorough clinical exam Radiographic modalities: Bitewings Prescribed depending on: ○ Degree of bone loss ○ Clinical gingival recession (loss of attachment) Note: for bitewing that is horizontal you want to see an equal portion of mandibular and maxillary teeth ○ Vertical bitewing: better assessment of bone level Radiographic modalities: Periapical imaging Periapical for anterior teeth Sometimes bone level isn't accurate May present a distorted view of the relationship of teeth to alveolar bone Normal bone appearance Cortical bone covering the alveolar crest 0.5 to 2 mm below CEJ → (greater than 2mm can be bone loss) Parallel to a line connecting adjacent CEJs Periodontal ligament space slightly widened around the cervical portion Major imaging features of periodontal disease Changes in the morphology of bone ○ Loss of the interproximal crestal bone ○ Loss of the bone overlapping the buccal or lingual aspects of the tooth root Changes in the dentistry of bone ○ Reduction reflects as increased radiolucency ○ Increase in the thickness and number of trabeculae reflects as sclerosis (whiter/more dense) Shades of gray Buccal/lingual cortical plate loss If one plate starts to lose bone- you’ll find trabeculae Lingual/buccal plate of bone See trabeculation because either the lingual/buccal side has bone loss Changes in morphology of bone Early bone changes ○ Localized erosion of the interproximal alveolar bone crest What do you see in this image? Looking at the molar ○ Decayed, endo treatment, bone loss in furca (on either the buccal or lingual, but not both plates) White arrow: Alveolar crest (bone at the crest) Horizontal bone loss ○ Loss in the height in the horizontal pattern ○ Parallel to an imaginary line connecting the CEJs of adjacent teeth ○ Crest of buccal and lingual cortical plates resorbs ○ Interdental bone resorbs ○ Bone loss MILD: