Ankylosis of the temporomandibular joint (TMJ) is a fusion of the condyle to the glenoid fossa that results in limited or no mobility of the jaw. Surgical treatment involves aggressive excision of the bony mass and reconstruction of the joint space using interpositional materials or costochondral grafts to prevent reankylosis. Post-operative physiotherapy and early mobilization are important to restore function and prevent recurrence, while additional procedures may be needed to correct facial asymmetries. Complications can include open bite, deviation on opening, infection, and reankylosis if not properly managed.
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
The presentation deals with the basics required for studying TMJ ankylosis. The text has been simplified and presented. It is well supported with illustrations.
Suggestions and feedback will be well appreciated. :)
Phase I periodontal therapy is the first in the chronologic sequence of procedures that constitute periodontal treatment. It is also referred to as cause related therapy or non-surgical periodontal therapy.
REFERENCES TAKEN FROM CARRANZA'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND LINDHE'S TEXTBOOK OF CLINICAL PERIODONTOLOGY AND IMPLANT DENTISTRY. CONTAINS ENOUGH AND MORE DETAILS OF THIS TOPIC FOR BDS STUDENTS.HOPE THIS PRESENTATION WILL HELP U GAIN SOME KNOWLEDGE ABOUT PERIODONTAL PLASTIC AND ESTHETIC DENTISTRY.
The presentation deals with the basics required for studying TMJ ankylosis. The text has been simplified and presented. It is well supported with illustrations.
Suggestions and feedback will be well appreciated. :)
Dear Readers,
this is my ppt was made from a book of BAGHERI ( Current therapy in oral and maxillofacial surgery)- 2012 PLUS other sources.. hope you find it beneficial.
have a nice day,
hanan
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Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
NVBDCP was launched in 2003-2004 . Vector-Borne Disease: Disease that results from an infection transmitted to humans and other animals by blood-feeding arthropods, such as mosquitoes, ticks, and fleas. Examples of vector-borne diseases include Dengue fever, West Nile Virus, Lyme disease, and malaria.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
These lecture slides, by Dr Sidra Arshad, offer a quick overview of physiological basis of a normal electrocardiogram.
Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
5. Enlist some common indications for obtaining an ECG
Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
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Ethanol (CH3CH2OH), or beverage alcohol, is a two-carbon alcohol
that is rapidly distributed in the body and brain. Ethanol alters many
neurochemical systems and has rewarding and addictive properties. It
is the oldest recreational drug and likely contributes to more morbidity,
mortality, and public health costs than all illicit drugs combined. The
5th edition of the Diagnostic and Statistical Manual of Mental Disorders
(DSM-5) integrates alcohol abuse and alcohol dependence into a single
disorder called alcohol use disorder (AUD), with mild, moderate,
and severe subclassifications (American Psychiatric Association, 2013).
In the DSM-5, all types of substance abuse and dependence have been
combined into a single substance use disorder (SUD) on a continuum
from mild to severe. A diagnosis of AUD requires that at least two of
the 11 DSM-5 behaviors be present within a 12-month period (mild
AUD: 2–3 criteria; moderate AUD: 4–5 criteria; severe AUD: 6–11 criteria).
The four main behavioral effects of AUD are impaired control over
drinking, negative social consequences, risky use, and altered physiological
effects (tolerance, withdrawal). This chapter presents an overview
of the prevalence and harmful consequences of AUD in the U.S.,
the systemic nature of the disease, neurocircuitry and stages of AUD,
comorbidities, fetal alcohol spectrum disorders, genetic risk factors, and
pharmacotherapies for AUD.
Knee anatomy and clinical tests 2024.pdfvimalpl1234
This includes all relevant anatomy and clinical tests compiled from standard textbooks, Campbell,netter etc..It is comprehensive and best suited for orthopaedicians and orthopaedic residents.
Prix Galien International 2024 Forum ProgramLevi Shapiro
June 20, 2024, Prix Galien International and Jerusalem Ethics Forum in ROME. Detailed agenda including panels:
- ADVANCES IN CARDIOLOGY: A NEW PARADIGM IS COMING
- WOMEN’S HEALTH: FERTILITY PRESERVATION
- WHAT’S NEW IN THE TREATMENT OF INFECTIOUS,
ONCOLOGICAL AND INFLAMMATORY SKIN DISEASES?
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- GENE THERAPY
- BEYOND BORDERS: GLOBAL INITIATIVES FOR DEMOCRATIZING LIFE SCIENCE TECHNOLOGIES AND PROMOTING ACCESS TO HEALTHCARE
- ETHICAL CHALLENGES IN LIFE SCIENCES
- Prix Galien International Awards Ceremony
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
2. • Ankylosis is a greek word meaning “Stiff
joint” and denotes hypomobility or no
mobility. Inability to open the mouth
beyond 5 mm of interincisal opening due
to fusion of head of the condyle with the
articulating surface of the glenoid fossa is
termed as ankylosis of TMJ.
3. • Definition:- Ankylosis refers to the
partial or complete inability to open
the mouth which results in functional
and growth deformation of the
mandible.
4. ANATOMY OF TMJANATOMY OF TMJ
TMJ is highly specialised ,diarthroidal
non weight bearing synovial joint of
condylar variety
ARTICULAR SURFACES:-
upper surface :-
a) articular eminence
b) anterior part of the mandibular fossa
lower surface:- Head of the mandible
5. BONY COMPONENT:-
º consist of glenoid fossa of the temporal
bone & mandibular condyle.
º condyle is roughly elliptical in cross
section with mediolateral width being
two times the anteroposterior width.
6. º the glenoid fossa is a smooth depression in
the temporal bone which is thinnest in its
deepest part which separates the joint
from the middle cranial fossa.
º articular surface is covered by
fibrocartilage.
7.
8. SOFT TISSUE COMPONENT:-
1) Intraarticular disc or meniscus
2)Synovial membrane
3) Lateral pterygoid muscle
4)Capsule of joint
5) Ligaments-
a) temporomandibular (lateral) ligament
b) sphenomandibular ligament
c) stylomandibular ligament
d) anterior malleolar ligament
11. APPLIED PHYSIOLOGYAPPLIED PHYSIOLOGY
Movement produced by muscle of
mastication in the upper joint cavity gliding
movements and in the lower joint cavity
hinge movements take place.
movements are:-
- Protrusive -Retraction
-Depression -Elevation
-Lateral or side to side movements
14. ETIOLOGYETIOLOGY
1. TRAUMA- Most common cause of
ankylosis. Trauma to the chin forcing
the condyle against the glenoid fossa,
particularly with bleeding into the
joint.
2. INFECTION- From middle ear &
mastoid (otitis media,mastoiditis).
15. 3. INFLAMMATORY-
. primary inflammation of the joint
. secondary to local inflammatory
process. (osteomyelitis)
.Secondary to blood streaminfections
- septicemia
- scarlet fever
- gonorrhea
. Rheumatiod arthritis
18. GENERAL FEATURESGENERAL FEATURES
• AGE- Seen in young age (1 to 10 years)
• Symptoms – Trismus (inability to open
mouth)
. Oral problems – poor oral hygiene
carious teeth
periodontal problems
malocclusion
19. UNILATERAL FEATURESUNILATERAL FEATURES
1. Mouth opening is very limited
2. Asymmetry of face with fullness of
the affected side & relative
flattening of the unaffected side.
3. Face is deviated towards the
affected side.
20. 4. Chin is retracted on the affected side
& slightly bypass the midline.
5. Slight gliding movement towards the
affected side.
6. Cross bite is present.
7. Well defined antegonial notch on
affected side.
21.
22. BILATERAL FEATURESBILATERAL FEATURES
• Bird face appearance/ micrognathia.
• No gliding movement neither
protrusive nor lateral movement.
• Presence of scar on the chin (possibly
due to trauma)
23. • Class II malocclusion, protrusive
incisors & anterior open bite.
• In a long standing case there is
atrophy or fibrosis of muscle.
• In congenital case-difficulty of
introducing the nipple into the mouth
of newborn infants.
26. HISTOPATHOLOGYHISTOPATHOLOGY
1. Atrophy or destructive changes in the
cartilagenous component of the joint with loss
of meniscus.
2. Normal soft tissue is replaced by thick
fibrous bands.
3. An overall flattening of articulation.
4. Glenoid fossa & articular eminence become
less pronounced.
5. The condyle become enlarged, composed of
dense sclerotic bone.
27. INVESTIGATIONSINVESTIGATIONS
• For definitive diagnosis & to confirm the
extent of bony growth imaging may be
required.
1. Lateral oblique view
2. O. P. G. view
3. Cephalometric radiograph
4. Submentovertex view
5. PA view
6. C T Scan
28. • FINDINGS –
1. Decreased ramus height on
the affected side.
2. The joint space is completely
or partially obliterated with
dense sclerotic bone.
3. The condyle can be replaced by
shapeless mass of bone.
29. 4. Prominent antegonial notch on the
affected side of mandible.
5. Elongation of coronoid process.
6. Sometimes A transverse or oblique dark
line crossing the mass of dense bone
showing fibrous ankylosis.
30. MANAGEMENTMANAGEMENT
• Ankylosis can only be treated surgically
there is no form of pharmacological
management.
• The type of surgery depends on the
patient & extent of deformity.
• Treatment also varies if ankylosis is
unilateral or bilateral.
31. Surgery for ankylosis is done in two
stages
1. in first operation only a release of
ankylosis is done, Jaw mobility is
brought about.
it is belived that growth takes
place after ankylosis release.
2. Second procedure, an orthognathic
surgery can then be planned to restore
facial esthetics. (especially in children)
32. GOALS OF TREATMENTGOALS OF TREATMENT
1. To create mobility in the joint to a
satisfactory limit.
2. To restore vertical height of the ramus.
3. To restore the mandible & TMJ to normal
anatomic & functional state.
4. To create a new joint space.
5. To allow the jaw to grow normally in child
treated for ankylosis.
6. To restore the facial esthetics.
7. To prevent recurrence of ankylosis.
34. CONDYLECTOMYCONDYLECTOMY
• This is a procedure done in ankylosis where the
anatomic feature of the joint are not
completely changed as in areas of fibrous.
• COMPLICATIONS-
1.Loss of vertical height of ramus
2. in bilateral condylectomy it create an
anterior open bite.
3. In unilateral condylectomy there is
deviation of the jaw on opening.
35. GAP ARTHRPLASTYGAP ARTHRPLASTY
• Gap arthroplasty involves creation of an
anatomical gap in the ankylosed segment to
form an artificial joint space.
• The gap is created at a level lower than the
original joint space.
• Two horizontal bony cuts are made in the
most superior aspect of the ramus and the
wedge of bone.
• A gap of 1-1.5 cm. is created & first
interposed with any material.
36. • COMPLICATIONS-
1. Chances of creating excessive gap
& reducing vertical height of ramus.
2. Anterior open bite due to excessive
bone removal.
3. Reankylosis due to bony contact b/w
the cut ends.
37. INTERPOSITIONALINTERPOSITIONAL
ARTHROPLASTYARTHROPLASTY
• Placing the interpositional material
material b/w the two cut ends avoids
contact b/w the bony ends.
• It minimises the chance of reankylosis.
• I.P. material may be-
biological- dermis, facia lata, bone &
cartilage.
Alloplastic- Vitallium, Tantalum,Silastic
& Acrylic.
38. COMPLICATIONS-
1. Second surgical site is necessary.
2. Foreign body reaction to alloplastic
material.
3. Difficulty in suturing or stablizing
the interpositional material on
the medial aspect of joint.
4. Doner site complication such as
pleuritic pain, pneumothorax.
40. OPERATION BY TEMPORALOPERATION BY TEMPORAL
APPROACHAPPROACH
1.It is the approach through a curvilinear
preauricular incision, extending 3 cm. long
into the temporal region for the exposure
of temporal facia.
2.The dissection of soft tissue is proceeded
up to zygomatic arch.
3.The capsule of the joint is opened with a T
shaped incision of the facia.
41. 4.Once the joint region is exposed and
ankylosed site is identified, aggressive
excision of the fibrous & bony mass
carried out.
5. Special attention is directed to the
medial extension of the callus to ensure
adequate excision.
6. Glenoid fossa is recontoured as needed.
7. Coronoidectomy & stripping of muscles
are done.
42. 8.It is observed that nearly 1/3 of the
height of the ramus is lost following
condylectomy & coronoidectomy.
9.Costochondral graft is removed
through inframammary incision.
10.Through submandibular approach
ramus is exposed.
11.Masseter & temporalis are stripped
from the ramus.
43. 12.Then the surface of the graft and
ramus are freshened to produce good
bony interface.
13.The graft is placed in position & fixed
with stable internal fixation so that
2mm. of posterior open bite is created
to compensate for remodelling of the
costochondral graft.
44. 14.The length of the graft is determined
by the ramus height discrepancy & the
facial asymmetry to be corrected.
15. A drain is placed & the wounds are
closed in layers.
16. After inter maxillary fixation for a
few days, jaw is mobilized vigorously &
physiotherapy is continued.
46. 3. Inter incisial opening should be
critically evaluated to ensure that it
should be more than 35 mm.
4. If step 1,2,3 do not create enough
opening opposite side coronoidectomy
is done.
5. A suitable interpositional material must
be placed to avoid the risk of
reankylosis.
6. Reconstruction of ramus with
costochondral graft helps to maintain
the ramus height.
47. 7. Rigid fixation of the graft with ramus is
necessary for early mobilization of the joint.
8. Creation of open bite on affected side to
permit setting of graft for 3-6 months.
9. Early mobilization with minimum IMF less
than 3 weeks.
10. Post operative physiotherapy 6-8 weeks.
48. 11.If no further improvement is noticed
postoperatively, joint is stretched
under GA.(Brisement Force given.)
12.Later on, if needed, excessive growth
of the costochondral graft may have to
be recontoured so that no disturbance
in occlusion & jaw relationship develop.
49. REASONS OF RECURRENCEREASONS OF RECURRENCE
1.Incomplete excision of callus at the
ankylosed site.
2.If the mouth opening during surgery is
less than 35 mm & if coronoid process is
not excised, recurrence develops.
3.Insufficient & unsatisfactory
physiotherapy.
50. 4.Failure to maintain the ramus height
leads to narrowing of the inter-
fragmentory gap.
5.Failure to provide a satisfactory
interpositional material.
6.Heigher osteogenic & periosteal
reaction may be responsible for high
rate of recurrence in children.
51. COMPLICATION OFCOMPLICATION OF
ANKYLOSIS RELEASEANKYLOSIS RELEASE
SURGERYSURGERY
A. Preoperative consideration
B. Intra operative consideration
a. complication due to incision
b. complication during
osteotomy procedure.
c. Postoperative complications.
52. COMPLICATIONS DUE TOCOMPLICATIONS DUE TO
INCISIONINCISION
1. Damage to facial nerve.
2. Bleeding from superficial temporal
artery or facial vessels.
3. Damage to parotid gland.
55. MANAGEMENT SUMMARYMANAGEMENT SUMMARY
1.Prior to 1951, it was considered to be
incurable.
2.Brisment force (forceful opening under
GA) was tried without success.
3.Esmarch suggested- wedge resection of
the body of the mandible.
4.Condylectomy in early cases.
56. 5. gap-arthroplasty led to recurrance.
6. osteoarthrotomy(gap & interpositional
arthroplasty) improved the prognosis.
7. Excision of callus & joint
reconstruction become the treatment
of choice.
57. R E F E R E N C E SR E F E R E N C E S
• B. SHRINIVASAN – Text book of oral
& maxillofacial surgery. (second edition)
• CHITRA CHAKARWARTI - Text book
of oral & maxillofacial surgery. (first
edition)
• ANIL GOVINDRAO GHOM- Text book
of oral medicine. (first edition)