oral surgery 2

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oral surgery 2
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  1. TMJ Blood supply
    • • Masseteric arteryanterior
    • • Superficial temporal
    • artery-posterior
  2. TMJ Innervation
    • • Auriculotemporal nerve
    • • Masseteric nerve
    • • Posterior deep temporal
    • nerve
  3. TMJ function
    • Ginglyoarthrodial joint
    • • Hinge Movement allows rotation (lower, 15-25mm)
    • • Glide Movement allows translation (upper, 25-50mm)
    • • Articular Cartilage (fibrocartilage)
    • • Synovial Fluid- allows lubrication
    • • Meniscus- chondrocytes and matrix
  4. TMD Diagnosis
    • Intracapsular: Synovitis/ Capsulitis, Internal Derangement, Osteoarthritis, Dislocation (open lock)
    • Muscular: Myofascial Pain, Myalgia/Myositis
  5. Gold standard for TMJ disc imaging
    MRI
  6. TMJ Disorder tx
    • Understanding and empathy
    • • Patient education, stress management
    • • Thermal application (ice or heat)
    • • Soft, non-chew diet
    • • Behavioral changes (clenching/posture)
    • • Orthotic/ night guard
    • • Physical therapy
    • • Reassurance and follow-up
    • • Medication: Muscle relaxant (flexeril, soma), TCA
    • (amitryptiline) (Borg-Stein, 2006)
  7. TMJ arthrotomy/Open joint surgery indications:
    • • Disc degeneration with significant bony change/OA
    • • Severe trauma with extracapsular displacement
    • • Bony Ankylosis
  8. Diagnostic Arthroscopy indications:
    • • Best for closed lock > 6 months duration and osteoarthritis
    • • Same principle as arthrocentesis but can visualize the joint
    • • Can perform lysis of adhesions with direct and &/or indirect visualization
    • • Can perform operative arthroscopy
  9. TMJ Arthroscentesis:
    • • Minimally invasive, office-based
    • • Best for arthralgia and intermittent or acute closed lock (< 6 months)
    • • Lavage of the superior joint space
    • • Removal of inflammatory mediators
    • • Success rates similar to arthroscopy and disc “pinning” procedures
    • • Does not change shape of the disc
    • • Re-introduces lubrication into a collapsed joint
    • • Click that was gone usually returns
    • • Can also inject steroid or HA
  10. TMJ INTERNAL JOINT DERANGEMENT:
    • • Non-Surgical Management (3-6 months)
    • • “Conservative” Management:
    • • Joint injections (steroid, HA)
    • • Pumping Injection (single portal joint wash)
  11. DIFFERENTIATING MYOFASCIAL PAIN VS INTERNAL JOINT DERANGEMENT
    • Diagnostic Auriculotemporal Nerve Block
    • Trigger Point Injections
  12. DIFFERENTIATING INTERNAL JOINT DERANGEMENT VS MPD: DIRECT JOINT LOADING
    • Contralateral and specific (point with 1 finger): intracapsular
    • Ipsilateral and generalized: muscular
  13. 50 % of the population have joint sounds
    • • Pop/Click: Condyle slips under displaced disc producing noise
    • • Crepitus/grating: bone on bone contact
  14. MYOFASCIAL FACIAL PAIN THERAPY:
    • BOTOX
    • • Blocks Acetylcholine release at the neuromuscular
    • junction
    • • Reduces muscle hyperactivity to decrease local muscle ischemia
    • • Disrupts the normal neurophysiology of the trigger point
    • • Injected directly into the trigger point of the muscle
    • • Lower concentration at multiple sites is more efficacious
    • • Toxin will diffuse up to 1 cm
    • • Minor complications:
    • • Bruising, bleeding, tenderness at injection site
    • • Unfavorable cosmetic change due to muscle
    • weakness
    • • 70% success for TMD and 70% success for Migraines
    • (Song 2007, Karacalar, 2005)
    • • Full effect seen in 3-5 days and lasts 2-4 months
    • Injections may include:
    • • Corrugator, Procerus, Frontalis
    • (20-40 U)
    • • Masseter (25-50 U)
    • • Cervical and Occipital Muscles
    • (20-40 U)
    • • Temporalis (10-20 U)
    • • Lateral Pterygoid (7-10 U)
  15. TMD/MYOFASCIAL PAIN THERAPY: ACUPUNCTURE
    • • Acupuncture signals the brain to release seratonin and endorphins
    • • Goal is to remove Qi stagnations and return smooth flow of Qi through the meridians
    • • Acupuncturist’s “style” causes significant variation in studies
    • • Acupuncture “rule of thumb” is 1 month for every year of illness (6-10 sessions) (Noiman, 2010)
    • • Length of time, # of needles placed and # of sessions are not certain
    • • Overall, limited evidence that acupuncture is better than sham acupuncture (Jung, 2010)
  16. TMJ SYNOVITIS/CAPSULITIS
    • • intracapsular pain
    • • pinpoint preauricular pain
    • • intracapsular swelling
    • • little or no limitation in movement
    • • secondary to macro vs. microtrauma
  17. Superior compartment adhesions
    • cause the disk to become “fixed”
    • i. Surface adhesion, stickiness
    • ii. “filmy” adhesions (surface stickiness btwn surfaces)
    • 1. Temporal fossa / eminence
    • 2. Disk / posterior attachment
    • iii. “band-like” adhesions (fibrous band connecting)
    • 1. Soft tissues of fossa / eminence
    • 2. Synovial tissues of the recesses surrounding the disk
    • iv. “pseudo-wall” adhesions (massive layer of fibrous tissue usually seen in anterior superior joint space)
    • 1. Distinguishing actual capsule from pseudo-wall adhesion is difficult
    • 2. Often result of intracapsular bleeding secondary to trauma
  18. TMD Surgical care
    • Arthrocentesis: joint aspiration; clinical procedure of withdrawing synovial fluid from a joint space with a syringe
    • Arthroscopy: small incisions made for surgical instruments and small camera
    • Arthrotomy: incision of a joint
  19. Acute closed lock (painful) surgery
    • i. Arthrocentesis
    • 1. Single portal arthrocentesis = pumping procedure (older technique)
    • a. Fixed disk
    • b. Injection
    • c. Disk mobilization
    • d. Disk reduction
    • 2. Arthrocentesis double portal lavage
    • a. IV sedation
    • b. Double portal lavage
    • c. Mandibular manipulation and mobilization
    • d. Possible steroid injection
    • e. Jaw opening exercises / physical therapy
    • i. Post-op management physical therapy (before the pt leaves office)
    • ii. Physical therapy everyday that week
  20. Chronic closed lock
    • i. Characteristics
    • 1. Preauricular pain
    • 2. Hypomobile “stuck” TMJ
    • 3. NRAD (non-reducing anterior displacement) / “fixed” disk
    • 4. Adhesions / capsulitis
    • ii. What is the most common indication for TMJ arthroscopic surgery?
    • 1. Mandibular hypomobility secondary to:
    • a. Chronic closed lock
    • b. OA with adhesive capsulitis
    • iii. What is the most widely used operative procedure in TMJ arthroscopy?
    • 1. Arthroscopic lysis and lavage
    • a. Can be effective for OA even with disk perforation
  21. Arthrotomy (open joint surgery)
    • i. Indications
    • 1. Disk dislocation?
    • 2. Disk degeneration
    • 3. Severe osteoarthritis- condylar destruction w/ resultant malocclusion
    • 4. Ankylosis
    • ii. Preauricular approach to surgery
    • 1. Disk repair procedures- plication (folding)
    • 2. Diskectomy (menisectomy)
    • 3. Patient-fitted CAD/CAM total TMJ replacement system
  22. Soft tissue surgery
    • a. Frenectomy- cut the frenum and suture
    • b. Frenotomy- cut and remove a piece of frenum and then suture
    • c. Circumferential periodontal fiberotomy
  23. Impacted canines
    • i. 2% of all canines are impacted
    • ii. Maxillary canines
    • 1. Palatal impaction 3:1 (Bass)
    • 2. Palatal impaction 85% (Stellzig)
    • iii. Arch length deficiency
    • 1. Palatal 18%
    • 2. Buccal 46%
    • iv. Treatment options
    • 1. Leave them
    • 2. Remove them
    • 3. Retrieve them
    • a. Expose and bond
    • b. Transplant
    • c. Osteotomy
    • d. Distraction
  24. Orthodontic anchors
    • 1. Screws and plates
    • a. 1.5-2.0mm soft tissue collar
    • b. 1.5-2.0mm neck
    • c. 6.0-8.0mm thread length
    • d. 0.9mm (0.035”) diameter hole in head
    • 2. Easy to place
    • 3. Minimizes patient cooperation
    • 4. Minimizes headgear
    • 5. May eliminate orthognathic surgery
  25. Complications of surgery
    • a. Pain, bleeding, swelling, infection
    • b. Failure of procedure
    • c. Need for additional surgery
    • d. Damage to adjacent teeth
    • e. Damage to impacted tooth
    • f. Periodontal defects
    • g. Need for additional grafting
  26. Neoplastic neck masses
    • i. Matastatic epidermoid ca
    • ii. Primary head and neck
    • iii. adenoca
  27. Congenital/developmental neck masses
    • i. Sebaceous cysts
    • ii. Branchial cleft cysts
    • iii. Thyroglossal duct cysts
  28. Inflammatory neck masses
    • i. Lymphadenopathy
    • ii. Tuberculosis
    • iii. Sialdenitis
    • iv. Congenital cysts
  29. B. Three zones of the neck
    • a. Used mainly for decision making with penetrating neck trauma
    • b. Zone I: Extends from the cricoids cartilage to the clavicles and sternum
    • c. Zone II: Extends from the angle of mandible to the cricoids cartilage
    • d. Zone III: Area above the angle of mandible
  30. Anatomic borders of the anterior cervical triangle
    • i. Medial portion of the SCM
    • ii. Lower border of the md
    • iii. Midline of neck
    • Anterior triangle contains
    • i. Carotid art
    • ii. Jugular veins
    • iii. Thyroid gland
    • iv. Esophagus
    • v. Trachea
    • vi. Larynx
    • vii. Vagus nerve
  31. Anterior triangle contains
    • i. Carotid art
    • ii. Jugular veins
    • iii. Thyroid gland
    • iv. Esophagus
    • v. Trachea
    • vi. Larynx
    • vii. Vagus nerve
  32. Anatomic borders of the posterior cervical triangle
    • i. Lateral portion of the SCM
    • ii. Trapezius
    • iii. Middle third of clavicle
    • Post triangle
    • i. Subclavian art and vein
    • ii. Suprascapular artery
    • iii. Brachial plexus
  33. Post triangle contents
    • i. Subclavian art and vein
    • ii. Suprascapular artery
    • iii. Brachial plexus
  34. Facial planes of neck
    • a. Neck has several fascial planes
    • b. Superficial cervical fascia
    • i. Platysma muscle
    • ii. Superficial blood vessels
    • iii. Infection in this layer does not spread
    • c. Deep cervical fascia
    • i. Is contiguous with vital areas such as the mediastinum and thoracic cavity
    • ii. Need additional imaging
  35. Location of neck masses and common correlating dx
    • a. Ant triangle: infection, neoplasms, branchial cleft cyst
    • b. Post triangle: metatstatic cancer, lymphoma
    • c. Midline: thyroglossal duct cysts, thryroid masses
    • d. Lateral: multiple causes
    • e. Fascial layer: infection, neoplasm, adenopathy
  36. Overt stridor means:
    airway compromise and tracheal diameter of less than 10% of normal
  37. Fine needle aspiration biopsy
    i. Gold standard that separates inflammatory from neoplastic lesions
  38. Branchial cleft cyst
    • a. Develop from remnants of embryologic branchial clefts and are located ant to the SCM
    • b. Cyst present at any age and mostly in adults Most common congenital lesion in adults
    • c. They are slowly enlarging of neck, formed from buildup of cellular debris
    • d. Fistulas can form between skin and aerodigestive tract
    • e. Tx is complete excision
  39. Cysic hygroma
    • a. Develop from a malformation of lymphatic channels
    • b. Do occur elsewhere in body
    • c. Usually present in childhood, with 80-90% occurring prior to age two
    • d. Soft and painless
    • e. Because of their lymphatic origin, many are discovered after an URI.
    • f. Strong association between turner’s and down’s syndrome
    • g. Resection is usually curative, although recurrence is common.
  40. Teratoma
    • a. Can present as neck masses
    • b. Can occur at any age, commonly discovered in childhood
    • c. Derived from pluripotent embroyonic stem cells and contain all three germ latyers
    • d. Usually benign in infancy; however, after infancy, more than 50% of teratomas are malignant
    • e. Complete surgical resection is required for tx and workup for malignant spread is indicated.
  41. Thymic cyst
    • a. Remnants from the thymic tract and therefore are found lateral to the midline, either ant or deep to the SCM.
    • b. Very rare lesions and are usually asymptomatic
    • c. Surgical excision is curative
    • d. Thymic tissue can be seen histologically within the walls of the cyst
  42. Thyroglossal duct cyst
    • a. Midline mass arising from the descent of the thyroid gland from the base of the tongue to below the cricoid (pathognomonic for midline)
    • b. Cysts are mobile, esp with swallowing or protrusion of the tongue
    • c. Usu not tender, however, when infected can become very painful
    • d. If become infected, antibiotics are the initial therapy
    • e. Require complete surgical excision
    • f. If untreated, can result in increased risk of malignant transformation
  43. Neck masses caused by infection
    • a. Common cause of neck masses, esp in patients with poor dentition
    • b. Most common organism is group A beta hemolytic strep, strep pneumoniae and haemophilus influenza
    • c. Potentially fatal due to airway obstruction
    • d. Incision and drainage, abiotic coverage and removal of offending tooth/teeth is necessary (abiotics will not be effective unless there is I&D.
  44. Granulomatous infections (not very common)
    • a. Can present in neck from many dif causes, such as TB, syphilis, actinomycosis and tularemia
    • b. May need evaluation from possible surgical incision and drainage
    • c. Excisional bx and culture of infections will be necessary to make definitive dx
    • d. Result of these tests will guide tx with either antiTB or antifungal medication
  45. Infectious lymphadenopathy
    • a. Especially the result of the Epstein-barr virus (mononucleosis)
    • b. Can be quite painful on palpation
    • c. Multiple nodes may be involved
    • d. Other causes include AIDS-related lymphadenopathy, Kawasaki dz, tonsillitis, viral URI and dental abscesses
  46. Other causes of neck masses
    • a. Traumatic causes
    • b. Penetrating traumas should be evaluated systematically
    • c. Injury in Zone 2 lends itself to local exploration because of accessibility of its anatomical contents
    • d. Injuries in Zone 1 and 3 may need more invasive testing because their contents enter the thoracic cavity and the skull, respectively
  47. Neoplastic causes of neck masses
    • a. There masses tend to develop over months to years and are typically painless unless there has been significant invasion into surrounding tissue
    • b. Benign masses of the neck include lipomas, fibromas, hemangiomas
    • c. Malignant tumors of the neck include SCC of the pharynx, larynx or oral cavity, metastatic dz of the cervical nodes, thyroid cancers, melanoma, lymphoma, carotid body tumors, and salivary gland tumors
  48. Vascular causes for neck masses
    • a. Include vascular aneruysms, dissections or malformations
    • b. Carotid blowout can be caused by postoperative complications, aggressive infections, invasive tumors or radiation therapy
  49. Vascular masses tend to develop rapidly over minutes to hours and may be pulsatile.
  50. Idiopathic/ iatrogenic causes
    • a. Postoperative complications
    • b. Idiopathic etiologies would be a dx of exclusion
  51. Toxic and metabolic causes
    a. Several thyroid conditions such as hyperthyroidism and hypothyroidism can cause toxic or metabolic derangement that may present as neck masses, including hot and cold nodules, goiters and inflammatory thyroiditis
  52. Primary sites of growth in the face
    • 1. Free margins of the bony surfaces
    • a. Maxilla grows down and forward
    • b. Mandible grows out and back
    • 2. Sutures (maxilla)
    • 3. Synchondroses (spheno-occipital, spheno-ethmoid) of the cranial base (True growth centers)
    • 4. Nasal Septum
    • 5. Mandibular Condyle
  53. DFD Epidemilogy
    • a. Large percentage of US has significant malocclusion
    • i. 5% may be classified as handicapping
    • ii. 10% has Class II malocclusion
    • 1. 1% requires surgical advancement of the mandible to correct the skeletal deficiency
    • 2. A small percentage of the population requires sx to correct A-P maxillary excess to treat Class II malocclusion
    • iii. 2.5% of the population has Class III malocclusion
    • 1. ¼ as common as Class II
    • 2. 40% of these Class III cases are severe enough to require sx correction
    • 3. Many Class III malocclusions are attributed to mandibular excess
    • a. 50% may be at least partly caused by maxillary deficiency
  54. Functional matrix theory (Moss)
    1. The majority of growth in the bones of the face occurs in response to adjacent soft tissue and the functional demands placed on the underlying bone
  55. Area Relocation (Enlow)
    1. Growth of surrounding soft tissues translates the maxilla downward and forward, opening up space at its superior and posterior sutural attachments
  56. Acquired DFD
    • 1. Result from trauma or other external influences that alter facial morphology
    • 2. Examples: Malunion of facial fractures, Iatrogenic, Arthritis of the TMJ joints with resorption of the mandibular condyles
    • 3. Back braces with cervical support
    • 4. Rheumatoid Arthritis
  57. Developmental DFD
    • 1. Result from abnormal growth of facial structures
    • 2. More common than acquired DFD
    • 3. Subject to genetic, congenital, environmental, and functional influences
    • 4. The multifactorial nature of facial development precludes a prediction of an inherited pattern of a particular facial abnormality
    • 5. Environmental Influences:
    • a. AllergiesChronic nasal obstructionmouth breathingaltered tongue and mandible posturingExtended head postureexcess face height malocclusion
  58. Pre-Surgical Orthodonic Considerations
    • i. When to start Tx
    • 1. Excess Growth (CLASS III)
    • a. Child: consider growth modification
    • b. Adolescent: DELAY sx until growth is complete
    • c. Adult: START immediately
    • 2. Growth Deficiency (CLASS II)
    • a. Child: consider growth modification
    • b. Adolescent: CONSIDER Sx
    • c. Adult: START immediately
    • ii. Orthodontic preparations
    • 1. Align teeth within the dental arches
    • 2. Coordinate the dental arches
    • 3. Reverse dental compensations
  59. Dental Compensations for the skeletal deformity
    • i. Undesirable dental compensations occur as a response to DFD
    • ii. The pre-surgical goal is to reverse these compensations and reposition teeth over underlying skeletal component
    • iii. The malocclusion will necessarily be accentuated prior to sx
    • iv. Class II
    • 1. Deep bite
    • v. Class III
    • 1. Muscles of lips pull teeth back while keeping mouth closed
  60. Mandibular Deficiency (Class II malocclusion)
    • 1. Features:
    • a. Retruded chin (div I)
    • b. Weak jawline
    • c. Excess labiomental fold
    • d. Procumbent appearance of lower lip
    • e. Abnormal posture of upper lip
    • 2. Can be done for obstructive sleep apnea
  61. Distraction Osteogenesis (DO)
    • a. Currently used in the correction of large DFDs, concept of gradually lengthening the bone allowing soft tissues to adapt
    • i. Reduce the risk of sx relapse
    • ii. Avoid excessive loading of the TMJ
    • iii. Reduce the risk of sensory impairment
    • iv. Avoid the need for bone grafts
    • b. Stages:
    • i. Osteotomy
    • ii. Latency (7 days)
    • iii. Distraction (1mm/day)
    • 1. Rate: how much (0.5mm)
    • 2. Rhythm: How often (2x/day)
    • iv. Consolidation
    • 1. Regenerate/Remodeling period
    • c. Disadvantages
    • i. Technique sensitive
    • ii. Need for 2 procedures (have to remove the appliance)
    • iii. Increase cost
    • iv. Longer tx time
  62. Mandibular Excess (Class III)
    • 1. Features
    • a. Prominence of the lower 1/3 of the face
    • b. Straight or concave profile
    • c. Large reverse overjet precludes ability to obtain adequate lip closure without strain of orbicularis oris
  63. Maxillary Excess A-P (Class II)
    • 1. Features
    • a. Prominent upper lip
    • b. Acute nasolabial angle
    • c. Convex profile
    • d. Excessive gingival and incisal exposure
    • 2. Sx: Le Forte I Osteotomy and Set Back
  64. Maxillary Excess-Vertical
    • 1. Features
    • a. Long lower 1/3 of the face
    • b. Narrow nasal base
    • c. Lip incompetence with excessive incisal exposure or anterior open bite
    • d. Class I, II or III occlusion
    • 2. Sx: Advancing genioplasty, Le Forte I Posterior Impaction
  65. Maxillary Deficiency- A-P (Class III)
    • 1. Features
    • a. Retruded upper lip
    • b. Deficiency in paranasal and infraorbital areas
    • c. Inadequate tooth exposure during smile
    • d. Prominent chin relative to middle 1/3 of face
    • 2. Sx: LeForte I Advancement
  66. Maxillary Deficiency-Vertical (Class III)
    • 1. Features
    • a. Short compressed upper lip
    • b. Straight or concave profile
    • c. Pseudoprognathism
    • d. Insufficent upper tooth exposure during smile
    • 2. Sx: Lower maxilla to vertically lengthenrequires graft
    • a. Sources of bone graftmandbile, calvarium
  67. Cleft Lip Sx = takes ___ to heal
    10 weeks
  68. Cleft Palate Sx = takes ____ to heal
    9-10 months
  69. Usually the cleft is on the ___ side :
    • left
    • L: R = 2:1
  70. – Failure of fusion of the ________ unilaterally or bilaterally result in unilateral or bilateral cleft lip
    • with/without primary palate
    • maxillary and medial nasal prominences
  71. CLP epidemiolgy
    • asians>white>black
    • males>females
    • palate>lip
    • left>right>bilateal
  72. Associated syndromes
    • • Downs
    • • Pierre robin
    • • Apert’s syndrome
    • • Crouzon’s
    • • Treacher Collins
    • • Hemi-facial microsomia
    • • Goldenhars
    • • Skicklers
    • Associated Problems
    • • Heart, orbital ocular defects, seizures, neurologic impairment, vascular deformities, developmental delay, learning disabilities, psychological
  73. CLP Etiology
    • 1. genetic contribution to facial morphogenesis plays a role in syndromes asso with CLP-poorly understood. Transforming growth factor-alpha. Retinoic acid receptor – alpha
    • 2. envi modifying role may effect genetic activation/repression in non-syndromic CLP. Tobacco, anti-epileptic drugs, etc.
    • 3. Clefting of lip can interfere with palate closure. Isolated clefting of palate is etiologically independent entity from CLP
    • Genetic involvement
    • Two hypoth
    • 1. multi factorial threshold model: major genes, minor genes, environment, developmental
    • 2. single major gene with reduced penetrance (less than 40% CLP are directly genetic in origin
    • familial incidence
    • • both parents unaffected : 0.1% chance for first child
    • • first child affected: 4% chance for 2nd child
    • • two affected kids: 9% first child CLP
    • • one parent: 4% first child
    • • 1st child: 17% second child
    • • Both parents affected: 60% chance for all kids
  74. CLP failure of the facial primordial to fuse between the:
    • fifth and eighth week: FUSION (Meckel)
    • Stark pieces actually do come together, but not strong enough to stay together (FISSION)
  75. Mx growth
    • Four mx movements
    • 1. forward migration
    • 2. ant rotation
    • 3. verti elongation
    • 4. transverse expansion (for the tongue
  76. Facial growth
    • • the membranous sutures of the face must be responsive:
    • • the Vomerine-palatal suture is vital for adequate forces to be transmitted to the developing mx. Scarring of the suture will inhibit all aspects of growth.
    • • (if upset suture of vomer, mx won’t growth properly)
  77. Clft class
    • 1. normal bi-palate
    • 2. unilateral CL
    • 3. unilateral CLP-incomplete
    • 4. bilateral CLP-incomplete
    • 5. CP-incomplete
    • 6. Unilateral CLP-Complete
  78. Veau classification
    • Class I – incomplete cleft involving only the soft palate
    • – Class II – cleft involving the hard and soft palate
    • – Class III – complete unilateral cleft involving the lip and palate
    • – Class IV – complete bilateral cleft
  79. The “Y” (Kernahan)
    • 1. 1,4 lip
    • 2. 2,5: alveolus
    • 3. 3,6:
    • 4. 7 (incomplete palate)
  80. Microform – CL =
    obicularis Oris not connected
  81. Bilateral CL
    • • Microform: full thickness off mucosa, muscle never got across. Must open area up and close cleft lip together (Orbicularis oris not attached)
    • • Minimal: doesn’t go half way up lip (doesn’t pass the white roll)
    • • Incomplete: goes half way up or more (Passes through the white roll)
    • • Complete (All the way through)
  82. Lip musculature
    • 1. orbicularis oris: eighth muscle components, arising from modioli at either end of mouthStick your lip out
    • a. Blends fibers from: levator labii superioris Alaque Nasi, levator labii superioris, transverse muscles of the nares, zygomaticus minor, zygomaticus major, risorius
    • 2. superior and inferior horizontal band: act to shorten and bring lips together
    • 3. oblique bands (Nasolabialis): allow to take lips up and out. (cleft pts can’t bring out but can bring up.) horizontal fibers can bring lips together
    • 4. Superior Fibers
  83. Anatomy: Cleft
    • the muscles remain on the external sides; retracted and underdeveloped
    • the soft tissues and underlying skeleton is displaced
    • *need orbicularis oris to go horizontal rather than vertical, therefore you must reattach it during surgery
  84. Anatomy: Cleft Lip
    • normal anat is askew with deviation of philtrum, cupsids bow, tubercle
    • lateral lip element exhibits vertical discrepancy
    • mesodermal deficiency: muscle never grew across so can’t fn properly
  85. Surgical Correction of Cleft Lip
    • • DO NOT INTERFERE WITH MAXILLARY GROWTH!
    • • If left untreated:
    • o Facial growth is un-impaired
    • o Facial deformitiy remains the same as those present at birth
    • • If treated w/ sx
    • o Techniques must not interfere with growth factors
    • o In past, maxillary retardation in 3D resulted from sx intervention
    • • To allow the pre-maxillary-maxillary development, the surgeon must:
    • o Reconstitute the anatomy of the perioral and nasal musculature
    • o Unite the lateral segments of the clefted maxilla to the medial part to promote growth
    • o Respect the medial septum (frenum) to maintain its role as activator of sutural growth
    • o Normalize functions of breathing, mastication and swallowing
  86. Lip Adhesion
    • • Ideal Lip repair
    • o Independent correction of nasal and lip deficiencies
    • o No violation of relaxed skin tension lines (Langer’s)
    • o Minimal discarding of tissue)
    • o Proper muscle reorientation
    • o Symmetry of lip (vertical and horizontal)
    • o Ability to reoperate
    • • To be performed when child achieves RULE OF 10:
    • o 10wks old, 10lbs, 10g/dL Hemoglobin
    • • This procedure reduces a complete cleft lip to an incomplete cleft (early sx 2-3wks)
    • o Reduces tension deformities greater than 3mm
    • o Allows hard tissue deformity to be approximated during fxn
    • o No deleterious effect on growth and development, providing time for additional growth
    • o Decreases distoration of alar base
    • o DISADVANTAGE: requires additional sx in the future
  87. Definitive Lip Repair
    • • Commandments to Live By:
    • o Honor that which is normal. Return it to normal and retain it
    • o Thou shalt not throw away a living thing until it has been proven absolutely useless
    • o Thou shalt never steal from Peter to pay Paul unless Peter can afford it (Thou shall not commit tension)
    • o Thou shalt not have a routine or make any graven image or any likness of routine. Thou shall treat each case individually
  88. Cleft Palate Classification:
    • 1. submucous cleft: cleft of hard palate under mucosa.
    • 2. uvula
    • 3. soft palate
    • 4. soft and hard palate
    • NOTE: Primary palate in OS is the pre-maxilla, but primary palate to plastic surgeons is the soft palate! Watch out for a discrepancy in literature.
    • 5. They have class III because that’s what they have, not what the surgeons are doing. (Will always be Class III despite the sx)
  89. Cleft Palate Anatomy:
    • • Three types of mucoperiosteum that cover the palate
    • o Palatine: thin layer covering the middle and posterior vault
    • o Maxillary: thick layer overlying the mid-palate
    • o Gingival: Layer associated with the dento-alveolar region
    • • The thick mucoperiosteum is advanced medially to close the defect, and replaces the thin palatal mucosa usually seen in this area.
    • o Due to transposition of the tissue types, the normal widening of the maxilla during growth is INHIBITED
    • • Vomerine tissue advanced to close the nasal side of the defect prevents the vomerine-palatal suture’s normal growth potential from occurring
    • Palatal Anatomy (Musculature)
    • • Tensor veli palatine: transverse fibers control the opening and closing of the Eustachian tube (creates the sling when talking)Controlled by CNV
    • o If V isn’t working, can get middle ear pressure due to inability to equalize
    • o Cleft palate kids can’t open their Eustachian tube due to lack of function of this muscleneed to have PE tubes placed
    • • Palatal glossus, Levator veli palatine, palatopharyngeus, Uvular muscles: all four paired muscle groups function in phonation and swallowingControlled by CN IX/X
    • o Lavator muscle must be reoriented during sx
  90. Cleft palate
    • • Cleft soft palate demonstrates abnormal muscle insertion a the post edge of the hard palate, leading to dysfunction of muscles. CAN”T SPEAK.
    • • The valvular system is a continuum of movement that allows sound to be modified thru a change in pressure. Get Otitis media. Can’t equalize pressure. So lose hearing
    • • Vertical deficiency, retrodisplaced
    • • Transverse displacement
    • Goals of Palatal Surgery
    • • Release abnormal muscle insertion
    • • Establishment of muscle continuity
    • • Correct orientation of the velum to serve as a dynamic sling
    • • Establish functional velo-pharyngeal valve mechanism to allow closure between oral pharynx and nasal pharynx.
    • • Repair and reposition muscles of soft palate to restore function
    • • Close communication between nose and mouth
    • • Lengthen the palate to achieve velo-pharyngeal competency
    • • Restore function of Eustachian tube
    • • Allow normal growth to ensue
    • • Timing of Cleft Palate Repair:
    • o Early complete repair (5-9mos)
    • o Delayed complete repair (12-24mos)
    • o Late Complete repair (2-5yrs)
    • o Early soft palate repair with late hard palate repair (5-15yrs)
  91. Cleft Alveolus
    • • Mx alveolus is frequently involved in the cleft lip and palate deformity. It routinely presents as a subtle fistula in the labial vestibule following the repair of the lip.
    • • Repair of the Alveolar Cleft is required to:
    • o stabilitze mx arch-consolidat to one jaw
    • o establish functional nasal airway
    • o close oro-nsal fistula
    • o get osseous volume to support teeth
    • o eliminate depressed alar base
    • o allow for dental rehab
  92. Cleft Alveolous Repair techniques
    • • primary gingivoperiosteoplasty- should not be done
    • • primary alveolar bone grafting- do at time of lip repair.
    • • secondary gingivoperiosteoplaty-should not be done
    • • secondary alveolar bone grafting- done at a later time.
    • o Timing Of Alveolar Repair
    •  The alveolus is rarely primarily repaired due to the high incidence of transverse maxillary deficiency as well as impedance of anterior and inferior growth of the maxilla
    •  Additionally, primary repair does not eliminate the need for early secondary alveolar bone grafts
    •  Primary (Age 0-2.5)-High rate of failure and retardation of growth
    •  Early Secondary (2-5)-prior to eruption of central incisor and canine tooth-adequate bone to support these teeth (80% success)
    •  Secondary (6-9)-provides adequate bone for eruption of the canine, however ignores the central incisor
    •  Late (13+)-higher incidence of graft failure, does not satisfy most goals
    • o Classification of Repair
    •  Type I: complete ossification
    •  Type II: ¾ normal alveolar height
    •  Type III: Less than ½ normal alveolar height
    •  Type IV: no ossification, or only a bridge of bone across the defect
    • o Donor Site:
    •  Many sites have been utilized (cranium, mandible, iliac crest, alloplastic)
    •  Highest success rate with ILIAC CREST-sufficient volume of cancellous bone with high cellular contentration
    •  BMP-cytokine-osteoinduction (used in children)
    •  Graft success is completely dependent upon the ability of the surgeon to achieve water tight closure of the nasal floor
    • o Alveolar graft risk factors
    •  Infection from nasal cavity seepage if the oro-nasal fistula is not sealed
    •  Extraction of deciduous teeth at time of grafting
    •  Excessive sx and scarring in the area
    •  Large mucosal flaps employed to cover the graft
  93. CLP Patient Complaints
    • • Food and fluid come out of nose
    • • Inability to suck or blow
    • • Poor ability to keep teeth clean
    • • Decayed or deformed front teeth
    • • Missing or extra teeth in the cleft site
    • • Lack of boney support of adjacent teeth
    • • Mobility and deformity of primary palate
    • • Lack of support for nose and lip
  94. Primary Dysfunction
    • • Dysphagia
    • • Nourishment (sucking/eating)
    • • Esthetic
    • • Hearing
    • • Speech
    • o Isolated cleft lip rarely effects speech
    • o Unrepaired alveolar cleft produces minor speech impairment
    • o Cleft palate requires anatomic reconstruction to allow development of normal speech patterns
    • o Hard and soft palate repair is important in speech development
    • o Early repair is important to offset abnormalities in: articulation, resonance, nasal air emission, laryngeal voice quality, intelligibility, acceptability
    • • Infections
    • • Breathing
  95. CLP Management
    • • Immediately after birth
    • o Counsel parents: feeding (no sucking), determine if syndromic
    • • Week 1-4
    • o Team evaluation inc. hearing testing
    • • Week 10-12
    • o Repair lip, PE tube into ear if patient meets rule of 10s
    • • Month10-12
    • o Repair palate
    • • Month 15-18
    • o Team evaluation with emphasis on speech
    • • Years 2-5
    • o Speech therapy, fistula repair, eval veloparyngeal incompetency, consider alveolar repair
    • • Year 6-8
    • o Orthodontic orthopedics (maxillary expansion)
    • • GROWTH COMPLETION
    • o Evaluate for maxillary-mandbular correction (dental prosthetic) reconstruction
  96. Unrepaired clp
    • • Skeletal: mx protrusion. No md. Diff.
    • • Dental- cleft segment has tendency to rotate medially with cuspid crowss bite occurrence.
  97. Effect of lip repair
    • • skeL: ant mx is molded with reduction of protrusion. No md. Diff. overall appear is like non-cleft ind.
    • • Dental;mx and md incisors became more up right.. get post crossbite
  98. Unrepaired CPO
    • • Skel: mx and md retrusion. Md has steep plane angle
    • • Dent: no effect
    • • Palatal repair-CPO
    • • Skel: no effect on ant postion, however decreased vert ht
    • • Decrease md palne due to rotation. Get more of class III relationship
    • • Dental: see much greater post crossbite. (transverse growth of mx is restricted)
  99. Unrepaired UCLP
    • • Skel: mx is normal but md is rotated backwards
    • • Dental: collapse of segments, get post crossbite
  100. Repaired lip
    • • Mx retruded compared to unodperated cleft lips. Md unaffected. ANB is smaller than unoperated clefts but still pos
    • • Dental: no incr in ant crossbite. But yes post crossbite
  101. Lip and palate repair
    • • Skel: class III
    • • dentL ant crossbite and post cross bite
    • • findings:
  102. mx and md with repaired clefts are related to the presence of the cleft itself. Means: these pts with class III: thought it was result of surgical interference.
    Alv bone grafting repair: usually done at age 8 and 9 since canines haven’t erupted yet. so now, do cleft repair at 5-6
  103. Osteomyelitis
    • i) Bone infection limited to area of insult
    • ii) Etiology: Bacterial Infection
  104. Osteoradionecrosis
    • i) Bone death associated with limited area of radiation therapy
    • ii) Etiology: Radiation
  105. Osteonecrosis
    • i) Generalized changes in the bone metabolism secondary to drug reactions
    • ii) Etiology: Bisphosphonates
  106. Bisphosphonate Osteonecrosis
    • a) Bisphosphonate therapy leads to decreased bone metabolism
    • b) May not resorb dead bone and replace with new bone
    • c) At risk for spontaneous exposure of jaw bones following dentoalveolar surgery
  107. Bisphosphonate Indications
    • a) Primary Bone Cancers
    • i) Multiple Myeloma
    • b) Metastatic Cancers
    • i) Breast and prostate especially likely to metastasize in the jaw
    • c) Hypercalcemia of Malignancy
    • d) Osteoporosis
    • e) Paget’s Disease
  108. Bisphos Pharmacologic Action
    • i) Inhibition of bone resorption
    • ii) Works by inhibiting osteoclasts
    • (1) Prevents differentiation and recruitment
    • (2) Reduces osteoclast activity on bone surface
    • (3) Cytoskeletal disruption
    • (4) Increase apoptosis
    • (5) Anti-angiogenic properties
    • (6) Impair intracellular trafficking
    • iii) Effect on Osteoblasts
    • (1) May Decreased proliferation, increase differentiation
    • (2) May increase proliferation and differentiation
    • (3) Effects vary between different therapies
    • iv) Binds to exposed hydroxyapatite and is incorporated into bony matrix
  109. Bisphos Pharmacokinetics
    • i) Distribution:
    • (1) Rapid accumulation in sites of high bone turnover
    • (2) Low blood plasma levels
    • (3) Half life of years
    • ii) Not metabolized, but is excreted by the kidney
  110. Bisphosphonates and ONJ
    • a) Total People taking:
    • i) IV Bisphosphonates: 2-3 million
    • ii) Oral Bisphosphonates: Alendronate17 million, Risedronate6 million
    • b) Out of 100,000 people with each type of Bisphosphonate, the number affected
    • i) IV: 10,000
    • ii) Oral: 10
    • iii) 1,000 x more likely with IV Bisphosphonates
    • c) Initiating Factor
    • i) Up to 75% preventable
    • ii) More likely (7x) to occur after a dental procedure
  111. Why Necrosis occurs in the Jaws (as opposed to other bones)
    • a) Most unprotected bones in the body
    • b) Very thin overlying mucosa
    • c) Only bones with external projections (teeth)
    • d) Frequently exposed during surgery
    • i) Perio, extraction, apicoectomy, etc
    • e) Higher bone remodeling rate
    • f) Bone and mucosa in very close proximity
    • g) Toxicity to mucosal tissue
    • h) Existing Hypotheses
    • i) Osteopetrosis phenotype (???)
    • ii) Inhibition of angiogenesis
    • iii) Constant microtrauma from function
    • iv) Bacterial Infections
    • v) Mucosal toxicity
  112. Staging of ONJ
    • a) Stage 1
    • i) Exposed bone that is asymptomatic with no sign of soft tissue infection
    • b) Stage 2
    • i) Exposed bone with pain, soft tissue and/or bone infection
    • c) Stage 3
    • i) Exposed bone associated with soft tissue infection or pain that is not manageable with antibiotics
    • ii) Pathologic fracture
  113. ONJ Treatment
    • a) Minimal surgical intervention
    • b) Biopsy if metastasis suspected
    • c) CHx rinse
    • d) Oral antibiotics prn
    • e) Surgical removal-only extreme cases
    • f) RCT for suspicious teeth
    • g) Dentures over areas of necrosis may aggravate/inflict pain
  114. Bisphosphonate Treatment Protocols
    • a) Prior to IV Bisphosphonate
    • i) Full dental examination
    • ii) Remove abcessed, non-restorable and perio compromised teeth. Also remove teeth with poor prognosis
    • iii) Rehab remaining dentition
    • iv) Education and OHI
    • b) During IV Bisphosphonate
    • i) Avoid dental procedures that may expose bone
    • ii) Routine dental cleanings
    • iii) Ensure good fit of prostheses
    • iv) Manage infections non-surgically (RCT)
    • v) Reassess regularly
    • c) Oral Bisphosphonates
    • i) Lower risk, but non-zero
    • ii) Dentoalveolar surgery NOT CONTAINDICATED
    • iii) No change in normal treatment protocol
    • d) Already Established ONJ
    • i) Consultations: General dentist, oral surgeon, oncologist
    • ii) Bony debridement to reduce sharp surfaces
    • iii) Protective stent may be used to protect adjacent tissues
    • iv) Avoid invasive dental procedures
    • v) Biopsy only if strongly suspect metastases
    • e) Prevention
    • i) Pre-treatment dental visit
    • (1) Do surgeries, extractions, etc FIRST
    • (2) Very thorough cleaning
    • (3) Adjust prostheses
    • ii) Traumatic procedures and Dental implants controversial for Oral BP but not contraindicated
  115. Long-term complications of ONJ
    • a) Secondary infection
    • b) Loss of adjacent teeth
    • c) Fracture
    • d) Fistula
  116. Neuropraxia
    • i. Bruised nerve, injured the nerve to the point where it stops functioning temporarily
    • ii. Continuous axonal connection to the pain
    • iii. Most common with removal of impacted third molars
    • iv. Recover spontaneously , start recovering within a few weeks
  117. Axonotmesis
    • i. Crushed the epineurium, broken axons inside but the epineurium is still intact
    • ii. Regeneration can occur as long as the nerve body is still alive
    • iii. All of the axons distal are cut off from the energy of the nerve body and therefore die off
    • iv. At the edge where the axons are disrupted, continue to grow and follow the epineurium
    • v. Axons can grow about 1mm per day
    • vi. Could take a long time to start seeing some recovery
    • vii. Less chance of recovery than neuropraxia
  118. Neurotmesis
    • i. The entire nerve is cut
    • ii. Possibility that the two ends of the nerve are not close to one another
    • iii. The proximal ends that can regeneration do not have an epineurium to follow for regeneration
    • iv. Example: IAN regeneration is more likely o spontaneously recover than the lingual nerve due to the presence of the IAN canal
  119. Wallerian degeneration
    i. Process that results when a nerve fiber is cut or crushed, in which the part of the axon separated from the neuron's cell body degenerates distal to the injury
  120. Neuroma
    i. Attempt of the body to repair a nerve injury but results in a clump of axons and a sensitive spot
  121. Paresthesia-
    abnormal sensation, spontaneous or evoked
  122. Dysesthesia-
    paresthesia that is unpleasant
  123. Hyperesthesia-
    increases sensitivity to all stimuli
  124. Hyperalgesia
    ncreased sensitivity to noxious stimuli
  125. Hypoesthesia-
    decreased sensitivity to all stimuli
  126. Hypoalgesia
    decreased sensitivity to noxious stimuli
  127. Anesthesia-
    absence of sensitivity to all stimuli
  128. Analgesia-
    absence of sensitivity to noxious stimuli
  129. Allodynia-
    pain from a normal non-painful stimulus
  130. Types of nerve surgery
    • a. Decompression- removal of source of pressure
    • b. Partial excision- removal of a small portion of an injured nerve
    • c. Resection- through-and-through nerve injury, remove the bad part and then try to reapproximate them and place very small sutures through the epineurium to put the nerve back together
    • d. Primary anastomosis
    • e. Nerve grafting

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