This document provides information on cleft lip and cleft palate, including epidemiology, etiology, embryology, classifications, symptoms, problems, and treatment. It discusses that cleft lip and palate is a common birth defect affecting the lip, alveolus, and palate. Prenatal diagnosis and counseling is important. Treatment involves a multidisciplinary team and stages of presurgical nasoalveolar molding, lip and palate repair surgery, followed by postoperative care and long-term orthodontics and speech therapy. Surgical techniques aim to reconstruct the lip and palate while minimizing complications and achieving optimal function and appearance.
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Dr. Ahmed M. Adawy
Professor Emeritus, Dep. Oral & Maxillofacial Surg.
Former Dean, Faculty of Dental Medicine
Al-Azhar University
The condition of being prognathic indicates abnormal forward projection of one or of both jaws beyond the established normal relationship with the cranial base. The skeletal manifestation can be due to mandibular anterior positioning (prognathism) or growth excess (macrognathia), maxillary posterior positioning (retrognathism) or growth deficiency (micrognathia), or a combination of both. The prevalence of mandibular prognathism, the etiologic factors, evaluation of patients, and treatment modalities are presented.
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
offering a wide range of dental certified courses in different formats.for more details please visit
www.indiandentalacademy.com
Dr. Ahmed M. Adawy
Professor Emeritus, Dep. Oral & Maxillofacial Surg.
Former Dean, Faculty of Dental Medicine
Al-Azhar University
The condition of being prognathic indicates abnormal forward projection of one or of both jaws beyond the established normal relationship with the cranial base. The skeletal manifestation can be due to mandibular anterior positioning (prognathism) or growth excess (macrognathia), maxillary posterior positioning (retrognathism) or growth deficiency (micrognathia), or a combination of both. The prevalence of mandibular prognathism, the etiologic factors, evaluation of patients, and treatment modalities are presented.
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Cleft lip and palate is the most common developmental anomaly of the craniofacial region, and they have been depicted throughout in the past civilizations.
presentation about impacted canine incidence, prevalence,classification,diagnosis, localization and treatment options including surgical and non surgical modalities
Cleft Lip and Palate - Presentation.
Cleft Lip and Palate is the 2nd most common Congenital Anomaly after Clubfoot. This presentation goes in depth about the Presentation, eitiology, Genetics, Medical management, Nasoalveolar Moulding, Surgical management of Cleft Lip & Palate
The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and
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The Indian Dental Academy is the Leader in continuing dental education , training dentists in all aspects of dentistry and offering a wide range of dental certified courses in different formats.
Cleft lip and palate is the most common developmental anomaly of the craniofacial region, and they have been depicted throughout in the past civilizations.
presentation about impacted canine incidence, prevalence,classification,diagnosis, localization and treatment options including surgical and non surgical modalities
Cleft Lip and Palate - Presentation.
Cleft Lip and Palate is the 2nd most common Congenital Anomaly after Clubfoot. This presentation goes in depth about the Presentation, eitiology, Genetics, Medical management, Nasoalveolar Moulding, Surgical management of Cleft Lip & Palate
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offering a wide range of dental certified courses in different formats.for more details please visit
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Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
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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.
Acute scrotum is a general term referring to an emergency condition affecting the contents or the wall of the scrotum.
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Testicular torsion refers to twisting of the spermatic cord, causing ischaemia of the testicle.
Testicular torsion results from inadequate fixation of the testis to the tunica vaginalis producing ischemia from reduced arterial inflow and venous outflow obstruction.
The prevalence of testicular torsion in adult patients hospitalized with acute scrotal pain is approximately 25 to 50 percent
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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.
NVBDCP.pptx Nation vector borne disease control programSapna Thakur
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Title: Sense of Smell
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 primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
3. Introduction
Facial clefting is the second most common
congenital deformity (after clubfoot).
Most common congenital malformation of the
head & neck
Problems are cosmetic, dental, speech,
swallowing, hearing, facial growth, emotional
4. EPIDEMIOLOGY:
Cleft lip and palate is a global problem.(0.28-3.74/1000 live
births globally)
Least incidence in negro (0.4%) and maximum in
afghans(4.9%)
The incidence of oral clefts is seen more in males than in
females.
Cleft lip alone- more in males than female
Cleft palate- more in females than males
5. ETIOLOGY:
1.) Heredity:
Transmitted through a male as sex linked recessive gene.
Predisposition for cleft lip is 40% while only 18-20% for cleft palate.
It is transferred as:
a) Monogenic/ single gene disorder-conform to mendelian inheritance
b) Polygenic/ multifactorial inheritance- show familial tendency but not
mendelian inheritance
c) Chromosomal abnormalities:
- Down’s Syndrome
- Edwards Syndrome (trisomy 18)
-
6. 2.) Environmental Factors:
Usually occurs due to various influences during Ist trimester.
• Environmental terratogens:
-Cigarette smoking- 30% increase in cleft lip and palate and 20%
increase in cleft palate in smoking during pregnancy.
-Anti seizure drugs.eg: di-phenyl hydantoin and trimethadione.also
causes growth retardation, craniofacial dysmorphism, mental deficiency
7. MALNUTRITION:
Hypervitaminosis A: acute maternal exposure to 13-cis retinoic
acid during first trimester causes cell death in the pharygeal
arch leading to facial clefting. Vit A analogue used as an anti-
acne drug. Also proved by animal experiments.
Folic Acid: Deficiency of folic acid affects virtually every organ
system. It affect the neural tube- neural crest cell migration and
differentiation.
Anaemia
INFECTION DURING PREGNANCY:
Rubella infection during the first 3 months associated with
clefting.
PARENTAL AGE:
Shaw et al presented evidence that women above the age of 35
had a doubled risk of having a child with CLCP.
above 39- tripled risk.
Consanguineous marriages- increased risk of CLCP in child.
8. SYNDROMES WITH CLEFT LIP AND PALATE
Van der woude Syndrome
Treacher Collins Syndrome Autosomal Dominant
Stickler’s Syndrome
Roberts Syndrome
Appert Syndrome
Christian Syndrome Autosomal Recessive
Meckel Syndrome
9. EMBRYOLOGY
The first pharyngeal arch (mandibular arch),
develops two prominences at the end of 4th
week
The maxillary prominence
The mandibular prominence
14. As the medial nasal prominences merge with the
maxillary prominence, they form an intermaxillary
segment.
(Intermaxilla
ry segment)
15. The intermaxillary segment gives rise to :-
1. philtrum of the upper lip.
2. The median part of the maxillary bone with its four
incisor teeth
3. The primary palate.
21. Cleft Anatomy
Unilateral Cleft Lip
and alveolus
lack of mesodermal
proliferation
cleft of orbicularis
o medial portion to
columella
o lateral portion to
nasal ala
cleft of alveolus
27. Airway Problems
Cleft Palate patients
e.g. Pierre-Robin Sequence
Micrognathia
, Cleft Palate,
Glossoptosis
CYANOSIS
develop airway distress from tongue
fall and touch pharanyx
lodged in palatal defect
28. FEEDING PROBLEM
FEEDING IN HEAD ELEVATED POSITION
FEEDING WITH SPCIAL CP BOTTLES OR
D/SYRINGE OR DROPPER
AFTER FEED LAY BABY ON SHOULDER AND
SLAB ON BACK TILL RETCHING
29.
30. Hearing problem
ETD- Due to abnormal insertion of levator veli
palatini and salpingo pharyngeus muscle into
hard palate
milk enter into eustachian tube and lead to serous
otitis media and infective otitis media and finally
ankylosis of oscicles
30% develop permanent deafness
31. Speech Disorders
Errors in Articulation: Fricatives, Affricates
Velopharyngeal Competence- competence after
initial palate surgery
Incompetence- nasal emission or snort
Evaluation- Direct exam , Fiberoptic Exam
32. When to Operate
Generally (Rules of 10’s)
Weight > 10 pound (4500 gm)
Hb > 10 gm
Age > 10 weeks
Cleft lips between 3-6 months
Cleft palate between 12-18 months (preferred before
speech devolops)
35. Nagpur classification
Group I - Cleft of lip
Group I(A) - Cleft of lip & alveolus
Group II - Cleft of palate
Group II(S) - Submucous cleft of palate
Group III - Cleft of lip & palate
36. DAVIS AND RITCHIE CLASSIFICATION (1922):
They classified congenital clefts based on the position of the cleft
in relation to the alveolar process.
Group I-Pre alveolar clefts Lip
clefts only with subdivisions for
unilateral, median, bilateral.
Group II-Post alveolar clefts
degrees of involvement of soft and
hard palate to be specified till the
alveolar ridge, submucous clefts
included.
Group III-Alveolar clefts is
complete clefts of palate, alveolus
ridge and lip with subdivisions for
unilateral, median, bilateral.
37. Classification
Veau Classification - 1931
Veau Class I: isolated soft palate cleft
Veau Class II: isolated hard and soft palate
Veau Class III: unilateral CLAP
Veau Class IV: bilateral CLAP
38. II VEAU’S CLASSIFICATION
(1931):
Group I - Cleft of
soft palate only
Group II - Cleft of hard and
soft palate, extending no
further than the incisive
foramen thus involving the
secondary palate alone.
39. Group III - Complete
unilateral cleft of soft and
hard palate, lip and
alveolar ridge
Group IV - Complete
bilateral cleft of soft and
hard palate, lip and
alveolar ridge on both
sides.
40. III KERNAHAN’S STRIPED “Y”
CLASSIFICATION (1971):
In this classification the
incisive foramen is taken as the
reference point
“Y” logo are each divided into
three sections, representing the
lip, the alveolus and the hard
palate as far back as the incisive
foramen. The stem of the “Y” is
also divided into three parts,
representing varying degrees of
clefting of the hard and soft
palates.
41. V MILLARD’S CLASSIFICATION
(1977):
A modification of Kernahan’s
striped “Y” classification.
. The inverted triangles represent the
nasal arch the upright triangles
represent the nasal floor.
42. Striped Y
1 & 5 - Floor of nose on right & left
sides
2 & 6 - Lip
3 & 7 - Alveolar ridges
4 & 8 - Premaxilla to incisive foramen
9 & 10 - Each half of the hard palate
11 - Soft palate
12 - Congenital velopharyngeal
incompetence without obvious clefts
13 - Protrusion of premaxilla
43. Iowa Classification
Group I
Clefts of lip only
Group II
Clefts of palate only (2o)
Group III
Clefts of lip,
alveolus, palate
Group IV
Clefts of lip and
alveolus (primary
cleft palate and
lip)
Group V
Miscellaneous
44.
45. LAHSHAL Classification
Kriens (1989)
Rt. Side of pt. is on lt. side of formula
L - cleft lip of Rt. Side
-L cleft lip of Lt.side
Complete cleft-Capital letters
Partial cleft – lower letters
Microform - Asterisks
46. Cleft Variants
1) Isolated Incomplete
Intact skin/muscle between the lip and nose
Less distortion brought on by abnormal muscle
pull
Bilateral/Unilateral
Cleft Lip
Expressed in structures anterior to incisive foramen
- prepalatal alveolus, maxilla, lip, nasal
structures
Gaping cleft of alveolus/lip structures to
mere ‘scar’ (forme fruste)
Deficiency in skin, muscles, mucous membranes,
maxillary/nasal bones, nasal cartilages
47. Unilateral Cleft Lip
Nasal floor communicates with oral cavity
Maxilla on cleft side is hypoplastic
Columella is displaced to normal side
Nasal ala on cleft side is laterally, posteriorly, and
inferiorly displaced
Lower lat on cleft side -lower, more obtuse
Lip muscles insert into ala and columella
48. Cleft Variants
Isolated Cleft Palate
Complete/Incomplete
Soft Palate
-cleft can extend into the hard
palate to any extent
Hard
Palate
Primary Palate (CL)
Secondary Palate
50. PRIMARY MANAGEMENT Antenatal Diagnosis
Diagnosed By US 3D After 18
Weeks’ Gestation
Parents Need Counseling
Reassure The Parents
Explain Functional Problems
Advise On
Feeding
Timing Of Surgery
Ideally, The Newborn Infant With
A Cleft Is Evaluated By Cleft
Team In 1st Weeks Of Life
51. PRESURGICAL MANAGEMENT1:Presurgical infant orthopedics:
Appliances
latham appliance for collapsed alveolar
arch
2:Presurgical nasoalveolar molding :
objective of NAM :
To align & approximate the alveolar
segment
To correct the malposition of the nasal
cartilage & alar base on affected side
To idealize the position of philtrum &
columella
52. When a cleft lip is present, it may be difficult for the baby
to make a good seal around the nipple.
Babies with cleft palate usually need special bottles and
techniques to feed properly.
There are three types of bottles for feeding babies with
clefts –
the Mead-Johnson Cleft Palate Nurser,
the Haberman Feeder and
the Pigeon Nipple:
FEEDING TECHNIQUES
53. Feeding obturator
The feeding obturator is a prosthetic aid that is designed to
obturate the cleft and restore the separation between the
oral and nasal cavities.
It creates a rigid platform
The obturator also prevents the tongue from entering the
defect and interfering with spontaneous growth of the
palatal shelves.
reduces nasal regurgitation,
reduces the incidence of choking,
also helps in the development of the
jaws and contributes to speech
54. Naso Alveolar Moulding-(PRESURGICAL NASO
ALVEOLAR MOULDING )
(Grayson etal, 1999)
Nasoalveolar moulding is a nonsurgical method of
reshaping the gums, lip and nostrils before cleft lip and
palate surgery, reducing the severity of the cleft. Surgery is
performed after the molding is complete, approximately
three to six months after birth.
Actively mould and reposition the deformed nasal cartilages
and alveolar processes and lengthen the deficient
collumella.
65. POSTOPERATIVE CARE
Soft arm restrain for 2 weeks
Analgesics
Feeding
Suture line care
Stitch removal
Avoid oral suction
66. POSTOPERATIVE CARE
Fluids for one week
Water after every feed
Semi solids for next two weeks and water after
every diet
Solids are allowed after three weeks
No need to remove stiches (vicryl)
67. Cleft Palate
Affects 1/2500 living births
More often in girls
Heredity is less affects
69. Goal of Palatal Repair
Separation of oral and nasal
cavities
Understanble speech
Avoiding maxillary retrusion
Preservation of hearing
Good occlusion
70. Submucous Cleft Palate
Anatomic problem
Muscles are not fused middle of palate (muscular diastasis)
notch at the back of the hard palate
Bifid uvula
persistentear disease
swallowing difficulties
Mostly asymptomatic
% 15 velopharengeal insufficiency
Short soft palate
Limited motion
Easy to get tired while speaking
When light goes through nose, light can be seen from oral
side
It is not necessary surgical treatment until child growth
enough to cooperate
71. •Treatment of Submucous Cleft
Palate
Submucous cleft palate only requires surgery
if it is causing problems for the individual
The most common reason for treating a
person with a submucous cleft palate is
because of abnormal, nasal-sounding speech
72. Surgical Repair- Cleft Palate
Several Techniques-
less scarring and less tension on palate
Scarring of palate may cause impaired mid-facial
growth(alveolar arch collapse, midface retrusion,
malocclusion)
Facial growth may be less affected if surgery is
delayed until 18 months, but feeding, speech,
socialization may suffer.
73. Surgical techniques
Von langenback operation
Veau, Wardill, Kilner push back palatoplasty
Intravelar veloplasty
Furlow z – plasty
Bordeck palatoplasty
75. “Double opposing Z Plasty”
Von Langenback
Method
Surgical treatment of isolated cleft palate
76. Secondary surgery for cleft lip and
palate
Cleft lip revision
malaligned vermilion
Asymmetrical cupid’s bow
Poor nasal tip projection
Deviation of cartilaginous nasal septum
Alveolar bone grafting
Closure of palatal fistula, veloplasty,
pharyngoplasty
Rhinoplasty
77. Take home message
Common orofacial defect
Counselling of parents
Feeding techniques
Look for other genetic syndrome like down’s
78. References
1. Cleft lip and palate, Bailey & Love, a short practice of surgery.
2. Advanced Trauma Life Support Manual. Chicago: American College of Surgeons; 1997. pp. 103–112.
3. Haemostasis and Blood Coagulation, textbook of medical physiology, Guyton and hall.
4. Management of bleeding following major trauma:Rolf Rossaint1, Bertil Bouillon2,Critical Care 2010,
14:R52
5. Initial assessment and treatment with the Airway, Breathing, Circulation, Disability, Exposure
(ABCDE) approach, Troels Thim, International Journal of General Medicine 2012:5 117–121.
6. Nanavati RS, Kumar M, Modi TG, Kale H. Anaphylactic shock management in dental clinics: An
overview. J Int Clin Dent Res Organ 2013;5:36-9
7. Surgical Complications After Implant Placement, Dental Clinics of North America, Volume 59, Issue 1,
Pages 57-72.
8. Use of a Collagen Matrix as a Substitute for Free Mucosal Grafts in Pre-Prosthetic Surgery: 1 Year
Results From a Clinical ,The Open Dentistry Journal, 2016, 10, 395-410 Prospective.
9. Shastry SP,Kaul R, Baroudi K, Umar D. Hemophilia A: Dental considerations and management. Journal of
International
10. Society of Preventive & Community Dentistry. 2014;4(Suppl 3):S147-S152. doi:10.4103/2231-
0762.149022.
11. Cleft lip and palate, Rajiv Borle, Textbook Of oral and Maxillofacial Surgery
12. Anaphylaxis: an update for dental practitioners NG Maher,* J de Looze,* GR Hoffman*†
13. Medical Emergencies in Dental Office Stanley F Malamed.
14. Management of Syncope in Dental Camps, Gururaju CR, Journal of Oral Health.