2ND EXAM ORTHO 2.pdf

LECTURE 3: ETIOLOGY OF MALOCCLUSION: LOCAL & GENERAL FACTORS DR. ROCACURVA MALOCCLUSION...

LECTURE 3: ETIOLOGY OF MALOCCLUSION: LOCAL & GENERAL FACTORS DR. ROCACURVA MALOCCLUSION CLASS II MALOCCLUSION “An occlusion in which there is a mal-relationship between the arches → maxillary prognathism or mandibular retrognathism in any one of the planes of space or in which there are anomalies in → positive overjet tooth position beyond the limits of normal” → usually associated with short faces (brachycephalic) -Samuel S. Flitch CLASS III MALOCCLUSION ETIOLOGY → maxillary retrognathism or mandibular prognathism → pre- and post natal etiologic factors include: → negative overjet o genetic → usually associated with long facial types (dolichocephalic) o environmental o developmental OPEN BITE o congenital → hereditary o functional → sucking habit → various ways to classify the etiologies: → tongue posture → excessive eruption of posterior teeth Graber general and local factors CONGENITAL DEFECTS Moyer heredity, trauma, habits, physical agents, → most common: diseases, malnutrition o cleft lip and palate Proffit specific, genetic, environmental o cerebral palsy White and dental base, pre- & post-natal abnormalities o Crouzon’s syndrome Gardiner o cleidocranial dysostosis/cleidocranial dysplasia CLEFT LIP AND CLEFT PALATE General Factors Local Factors → can be: → heredity → anomalies in number o unilateral cleft lip and palate incomplete → congenital defects → anomalies in size o bilateral cleft lip and palate incomplete → environmental → abnormal tooth shape o unilateral incomplete → predisposing diseases → abnormal labial frenum o normal palate → soft tissue factors → premature loss of teeth o cleft lip → habits → prolonged retention o bilateral cleft lip → tonsils & adenoids → delayed eruption o cleft palate → posture → abnormal eruptive path o unilateral cleft lip and palate → trauma & accidents → ankylosis o bilateral cleft lip with full palate → caries → treated with appliances called obturators which are made from → improper dental restoration self-cure acrylic that covers the discrepancies o obturators prevent asphyxiation for babies when feeding GENERAL FACTORS as they create a vacuum movement HEREDITY o used until baby can undergo surgery → plays a role in: o constantly adjusted as the baby grows o tooth size and shape → can cause: o oligodontia/anodontia (caused by the genes–MSX 1 & o crossbite Pax9) o malposition and rotated maxillary incisors o supernumerary teeth o defect in eruption pattern o crowding/spacing o arch length and width CROUZON SYNDROME o height of palatal vault → genetic disorder that presents premature fusion of skull bones o overbite/overjet → affects head, neck & face (patient presents with small head) o tongue size and shape → branchial arch syndrome: o position and configuration of muscles o affects branchial arch 1 which forms the maxilla and o size and position of jaws mandible o congenital deformities → intra- and extraoral findings: o facial symmetry o brachycephalic o exophthalmos Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 3: ETIOLOGY OF MALOCCLUSION: LOCAL & GENERAL FACTORS DR. ROCACURVA o absent zygomatic prominence HYPOPITUITARISM o class III malocclusion → decreased cranial base measurements o high palatal vault → open bite o crowding → delayed tooth eruption o anterior & posterior crossbite INFECTIOUS DISEASE CLEIDOCRANIAL DYSOSTOSIS/DYSPLASIA → viral such as: → birth defect affecting the bones & teeth → prominent brow area and lower jaw Mumps dental hypoplasia → wide nasal bridge Rubella delayed tooth eruption → shoulder & collarbones are missing or have abnormal development which allows the shoulders to be hyperflexed (most common) NUTRITIONAL DEFICIENCY → deciduous teeth do not exfoliate at the right time → also have an effect on the growing dentition: ENVIRONMENTAL Cleft Lip and Palate → hypervitaminosis A PRENATAL TRAUMA → vit. B12 deficiency → common causes: → folic acid deficiency o intrauterine molding Retarded Eruption → vit. A and D deficiency o trauma to the mandible during birth process → protein deficiency POSTNATAL TRAUMA Early Loss of Deciduous Teeth → vit. D deficiency → common causes: and Open Bite o after an injury with tremendous scarring = restricted normal growth movements SOFT TISSUE FACTORS o with more scarring & restriction on one side = asymmetric → muscles affect dentition and pattern of growth growth → major factor in determining tooth position MUSCLE DYSTROPHY Incompetent Lips → short upper lip → a missing muscle, such as the masseter muscle, will cause facial → mandibular retrognathia asymmetry → incisor protrusion Short Upper Lip → proclination of anteriors PREDISPOSING DISEASES → increased overjet ENDOCRINE DISTURBANCES → open bite HYPERPARATHYROIDISM → early eruption of deciduous and permanent teeth → loss of lamina dura and cortical bones → early tooth loss due to CLASS II DIVISION 1 not enough anchorage → failure of lower lip to control the position of upper incisors HYPERTHYROIDISM CLASS III → early loss and eruption of permanent teeth → deep mentolabial sulcus → low tongue position HYPOTHYROIDISM → lingually inclined mandibular incisors → reduced jaw growth → mandibular prognathism ORAL HABITS → delayed eruption → can be induced by anxiety or stress; important in determining → retained deciduous teeth cause → abnormal resorption pattern → factors: o frequency HYPERPITUITARISM o duration → class III accelerated mandibular development o intensity → early dental development and eruption o position Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 3: ETIOLOGY OF MALOCCLUSION: LOCAL & GENERAL FACTORS DR. ROCACURVA THUMB/FINGER SUCKING → abnormal swallowing pattern → abnormal location of teeth Normal Subclinical birth to 3 years old ABNORMALITY IN TOOTH SIZE Clinically Significant 3 to 7 years old → macrodontia cause crowding Intractable Habit beyond 7 years → microdontia cause diastema or spacing → causes: ANOMALIES IN TOOTH SHAPE o improper/inadequate nursing → peg-laterals o insecurity/attention → taurodontism o feeling of hunger → Hutchinson’s teeth o simple learned habit with no underlying neurosis → talon’s cusp → effects of prolonged thumb sucking: o result of evagination o increased overjet o pulp can be exposed if this is removed o anterior open bite o most common in maxillary incisors o flaring or labial inclination of maxillary incisors o can be unilateral or bilateral o lingual inclination of mandibular incisors → fusion and gemination o narrow arch and high palatal vault → dens en dente o incompetent lips o invagination of enamel and dentin before calcification o posterior crossbite o prone to caries and infection o mandibular retrognathism and maxillary prognathism o dens invaginatus o maxillary arch constriction o abnormal lip and tongue activity ABNORMAL LABIAL FRENUM o speech defects → may be too low and cause diastema → treated with frenectomy LIP BITING AND SUCKING → effects: PREMATURE LOSS OF DECIDUOUS TEETH o lower lip lingually inclined → developing permanent teeth have no space and may be o maxillary proclination of incisors impacted o open bite → permanent teeth are given a wrong path of eruption → midline shift NAIL BITING → labial proclination of incisors → same concept with thumb sucking → spacing → narrow maxillary arches → speech defects → crowding of teeth → common causes: → brittle or attrition of the incisal edges o trauma o caries MOUTH BREATHING → could be treated with appliances or lip taping PROLONGED RETENTION OF DECIDUOUS TEETH → permanent teeth erupt in wrong location LOCAL FACTORS → results in: ABNORMALITY IN TOOTH NUMBER o labial/buccal or palatal/lingual eruption of succedaneous SUPERNUMERARY TEETH teeth → extra teeth cause crowding o impaction of permanent teeth → rotation → delayed eruption or deflection of erupting teeth to an abnormal DELAYED ERUPTION OF PERMANENT TEETH pattern → may be caused by: → diastema o early loss of adjacent primary teeth with flaring or spacing → torsiversion between erupting permanent tooth → root resorption of adjacent teeth o mucosal thickening over succedaneous tooth or bone → prevention of tooth movement deposition over succedaneous tooth o hereditary CONGENITALLY MISSING TEETH o presence of supernumerary teeth, cysts, root fragments of → diastema deciduous teeth, or ankylosed deciduous teeth Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 3: ETIOLOGY OF MALOCCLUSION: LOCAL & GENERAL FACTORS DR. ROCACURVA o congenitally lost permanent tooth o endocrine conditions (hypothyroidism) ABNORMAL ERUPTIVE PATH → a secondary manifestation of a primary disturbance caused by: o arch length deficiency o supernumerary teeth, retained deciduous teeth or root fragments o traumatic displacement of tooth buds o impacted molars o coronary cyst IMPROPER DENTAL RESTORATION → teeth drift occlusally/proximally → functional shift of jaw → collapse of occlusion → results in: o decrease in arch length o overcontoured restoration → decreased space for erupting tooth o premature contact → functional shift of mandible during jaw closure o undercontoured restoration → supraeruption of opposing dentition Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 4: BIOLOGIC & MECHANICAL BASIS OF ORTHODONTIC TOOTH MOVEMENT DR. TAN TOOTH MOVEMENT PHYSIOLOGIC → naturally occurring or expected such as tooth eruption or movement of the tooth into the oral cavity at the level of the occlusal plane, tooth migration, supraeruption, or mesial drifting → mastication → internal/biological force ORTHODONTIC (OTM) → movement of tooth from one area to the next due to an external force → “the result of biologic response to interference in the physiologic equilibrium of the dentofacial complex to an externally applied force” → a PDL phenomenon; there is no change in the tooth only the position ORTHODONTIC FORCE The positive charge or convex area is where bone resorption occurs → “force applied to the teeth for the purpose of effecting tooth while the negative charge or concave area is where bone deposition movement having a magnitude generally lower than orthopedic happens. force” SUMMARY THEORIES OF TOOTH MOVEMENT external force prolonged force (even of low magnitude) ↓ ↓ alveolar bone bends physiologic response: ↓ remodeling of the adjacent bone deformation of crystalline structure ↓ ↓ orthodontic tooth movement piezoelectric signals ↓ BONE REMODELING cellular differentiation Bone Resorption → bone under pressure ↓ → compression of PDL tooth movement Bone Formation → bone under tensile force → stretching of PDL BIOELECTRIC THEORY → Bassett & Barber, 1962 → connected to previous theory called “Bone Bending Theory” → changes in bone metabolism controlled by electric signals produced when alveolar bone flexes and bends to light pressure → electric signals (piezoelectric) alter metabolism of bone that might initiate tooth movement → endpoint is bone remodeling → force is only in seconds but good enough to initiate remodeling The concave side (-) of the periosteum is where osteoblastic activity PIEZOELECTRICITY occurs while the convex side (+) is where osteoclastic activity → phenomenon observed in crystalline materials happens. → cause: o deformation of a crystal structure produces a flow of electricity current as electrons are moved from one part of PRESSURE-TENSION THEORY the crystal lattice and displaced to another → Schwarz, 1932 Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 4: BIOLOGIC & MECHANICAL BASIS OF ORTHODONTIC TOOTH MOVEMENT DR. TAN → classic theory of OTM → if force is applied, there is stretching or tension where force is CHANGES IN OXYGEN TENSION AND and pressure on the opposite side RELEASE OF CHEMICAL MEDIATORS → osteoblasts on tension side and osteoclasts on pressure side → importance of oxygen reduction after orthodontic force application: Pressure Tension o stabilizes RANKL expression in the PDL Blood Flow ↓ ↑ - increased osteoclast differentiation - resorption on pressure side Cell Replication ↓ ↑ o stimulates cell proliferation & angiogenesis due to product of HIF-1 (hypoxia inducible factor-1) which activates VEGF Fiber Production ↓ ↑ (vascular endothelial growth factor) Oxygen Level ↓ ↑ - regeneration of the PDL and its blood supply → hypoxia is a critical factor for orthodontic tooth remodeling Carbon Dioxide Level ↑ ↓ CELL MEDIATORS → depending on the force applied, there is tension and → experiments have shown that prostaglandin & interleukin-1 beta compression in different areas of the tooth, creating now the levels increase within the PDL within a short time after the different types of orthodontic tooth movement (rotation, application of pressure, and it is clear now that both are extrusion, intrusion, etc.) important mediators of the cellular response SUMMARY Compression Tension external force ↓ Increase PGE2 IL-10 tooth shifts its position within PDL space RANKL ↓ Decrease OPG RANKL pressure and tension in some areas ↓ Outcome ↑ osteoclasts ↓ osteoclasts ↑ resorption ↓ resorption if force is maintained: changes in blood flow, oxygen tension, and ↓ apposition ↑ apposition release of chemical mediators ↓ bone resorption & bone formation RANK/RANKL/OPG SIGNALING PATHWAY ↓ orthodontic tooth movement RANKL RANK OPG receptor activator of CHANGES IN BLOOD FLOW nuclear factor kappa beta ligand expressed by expressed by expressed by osteoblasts osteoclasts osteoblasts role in osteoclast located in osteoclast decoy receptor for formation precursors RANKL; binds to RANKL receptor for RANKL if present, RANKL will be inhibited and osteoclasts will not be activated → a force that will close the blood supply is not ideal → change in blood flow is related to the amount of force applied Kirsten M. Abarquez | Cebu Doctors’ University | DMD-3B  LECTURE 4: BIOLOGIC & MECHANICAL BASIS OF ORTHODONTIC TOOTH MOVEMENT DR. TAN FRONTAL AND UNDERMINING RESORPTION AND HYALINIZATION Frontal Resorption Undermining Resorption on frontal edge of the bone on the underside or within bone direct resorption backward resorption → when blood flow is totally cut off: o differentiation of osteoclasts within PDL space is not possible o cells are recruited from undermining side of lamina dura o undermining resorption occurs HYALINIZED ZONE IN PDL (HYALINIZATION) → cellular component of PDL disappears → ground glass appearance → sterile necrosis (no microorganisms but due to force) More Hyalinization slow OTM more cells lost Less Hyalinization fast OTM less cells lost Cells lost must be repaired first before orthodontic tooth movement happens. PHYSIOLOGIC RESPONSE TO SUSTAINED PRESSURE AGAINST A TOOTH Time Light Pressure Heavy Pressure