CLEFT LIP AND PALATE- PART 2 – CLASSIFICATION, CLINIC FEATURES AND MANAGEMENT

Muhad Noorman P, Final year Team dentowesome.

CLASSIFICATIONS OF CLEFT LIP AND PALATE

Davis & Ritchie classification (1922)

Veau’s (1931)

Harkins and associates(1962)

Kernahan’s Classification (1971)

Spina (1974)

Tessiers’s Classification.

VEAU’S CLASSIFICATION

Group 1- Cleft of soft palate only
Group 2 – Cleft of hard and soft palate extending
no further extending than involving incisive foramen, (secondary palate only)
Group 3 – Complete unilateral cleft, extending from uvula
to incisive foramen in the midline, then deviating the one side and usually extending through the alevolus at the position of the future lateral incisor
Group 4- Complete bilateral cleft, extending forward through incisive foramen to alevolus. Premaxilla, suspended from the nasal septum .
Asian population have highest frequency often 

CLINICAL FEATURES:-

Incidence- 1in 500,With african population the lowest at 1in 250. Cleft lip alone more common in males. Isolated Cleft palate more common in female. 50% are syndromic, and are born with other congenital abnormalities.Cleft lip appear as unilateral / bi lateral. Line of cleft start on lateral part of upper lip and continues through philtrum of alveolus between lateral incisor and canine. When cleft lip continues from incisive foramen through palatal suture middle in palate,cleft lip with palate (unilateral/bilateral) present . . Cleft palate appears with involving soft palate only, involving uvula (bifid uvula),isolated cleft palate also.
.Patient have significant physical and physiological effects like, difficulty in eating and drinking with regurgitation of food to nose.
. Speech problem
. Ear infection: Malposition of Eustachian tubes result in middle ear infection
.Cosmetic deformities.

MANAGEMENT 

Management of Cleft lip and palate require, multidisciplinary coordinated approach by specialist including maxillofacial surgeon, pediatric surgeon, anesthetist, Prosthodontist, Orthodontist, Speech pathologist, otolaryngology ,audiologist  etc..

Management is aimed at closure and correction of lip and palate, secondary correction of palatal fistulae, orthodontic management of malocclusion, Orthognathic surgery, Rhinoplasty,and providing prosthesis for patients.

Pre operative criteria selected by physicians for surgery is Millards Rule of 10’s
1) 10lb weight
2) 10mg/l of haemoglobin
3) 10 weeks of age

  SURGICAL MANAGEMENT
1) Primary : Closure of lip & palate
2) Secondary : Closure of palatal fistula, Pharygoplasty  ,Bone grafting, orthodontic management Rhinoplasty and Scar revision.

Reference: Oral and Maxillofacial surgery, Balaaji. Textbook of general surgery for dental students, SRB

CLEFT LIP AND CLEFT PALATE- Part 1 ( Introduction, Etiology, Syndromes and embryogenesis)

Muhad Noorman P , team dentowesome, final year.

Cleft palate and Cleft lip comprises the complex of Orofacial clefts . Both comprises congenital malformations affecting oro-facial region.
Failure of fusion of nasal and maxillary process leads to cleft of primary palate which can lead to unilateral and bilateral. Cleft of secondary palate is medial, Varies from bifid uvula to complete cleft palate up to incisive foramen.

Etiology:-
Clinically, Isolated Cleft palate
and Cleft lip with or without Cleft palate has been established.

Factors playing  role in Development of Orofacial cleft comprises

1)Heredity (40%of cleft lip and 20% cleft lip appear genetically- single gene/polygenic mutation, Monozygotic twins far likely to get)
2)Nutritional disturbances (experimentally proved in rat fed on abnormal dietary regimen caused cleft palate) mostlty- Riboflavin,Folic Acid Deficiency.

3) Physiologic, Emotional stress, Traumatic also thought to cause
4) Circulating Alcohol ,Drugs ,toxins.
5)Environmental Factors– Teratogens (phenytoin, methotrexate, Corticosteroid, Sodium Valproate)
6)Syndromic Clefting
Treacher collins syndrome
Pierre Robin Syndrome
Stickler syndrome
Oro Facial Digital syndrome
Trisomy of 13,18
Van Der Voude syndrome ( lip pit syndrome, autosomal dominant , deletion of 1q32 , clinically presenting with cleft lip and palate and medial pits on lower lips on vermillion border.Also include ankyloglossia,high arch palate ,maxillary hypodontia and sygnathia)

EMBRYOGENESIS AND CLEFTING

During sixth and seventh weeks of development upper lips forms when median nasal process merges each each other and  fuses with maxillary process of 1st branchial arches. Mid portion of upper  lip is derived from median nasal process, lateral derived from maxillary process. Lateral nasal process involved in ala of nose. Primary palate is formed from merging of median nasal process to form intermaxillary segment, which give rises to premaxilla
(bone including 4 incisor teeth). Secondary palate make up 90% of palate formed from maxillary process of first branchial arches.Defective fusion of median nasal process with maxillary process forms cleft lip. Failure of palatal shelves to fuse result in cleft palate
45% are Cleft lip with palate
30% Cleft palate alone
25% with isolated cleft lip

 

Vander Woude syndrome with lower lip pits.
Van der Woude Syndome with lip pits , Cleft lip and palate.

Reference:- Textbook of maxillofacial surgery- Balaji. Textbook of embryology- Inderbir Singh. Neville Oral pathology. Images credits : Image 1 – Internet medscape (https://emedicine.medscape.com/article/950823-overview

Image 2 :- Internet, Children Hospital of Philadelphia , ( https://www.chop.edu/conditions-diseases/van-der-woude-syndrome)

WILSONS DISEASE

Muhad Noorman P, Team Dentowesome, Final year

Reference: Davidsons Internal medicine , Internet

Wilson’s disease, also known as hepatolenticular degeneration and progressive lenticular degeneration, is a rare genetic disorder that causes copper overload in the body.

Common cause of liver cirrohsis in children.

Etiology:- A mutation in the ATP7B gene, which codes for copper transportation, causes Wilson’s disease

Clinical Features:-

Liver related
Nausea, weakness, vomiting, jaundice, bloating, spider angiomas, muscle cramps etc..

Neurological
Memory, Speech impairments. Altered gait, personality changes, headache, insomnia etc…

Characteristic clinical signs:- SUNFLOWER CATARACT AND KAYSER-FLEISCHER RINGS. KF rings are golden brown ring like discoloration of eyes due to copper deposition.

Lab investigation:- Altered Liver enzymes
Elevated Serum copper level
Increased urinary copper excretion. Low Serum ceruloplasmin level. Liver biopsy will reveal copper deposition. Imaging like MRI/CT for lenticular imaging.

Treatment:-. Copper chelating agents like d-penicillamine, Trientine etc.. can be used. Oral Zinz tetrathiomolybdate can be given ti reduce dietary absorption of Copper.

HEAMOCHROMATOSIS

Muhad Noorman P, Final year, Team dentowesome

Abnormal accumulation of Iron in Liver , Pancreas and heart causing widespread damage of organs resulting in cirrohsis and diabetes mellitus.

Also known as Celtic Curse or Bronze diabetes

Autosomal recessive transmission due to HEF gene mutation.

Clinical features:-

Male : Female ratio = 10:1. Weaknesses, lethargy, diabetes mellitus, liver cirrohsis , arthralgia, skin hyperpigmentation, impotence, hepatomegaly, hypogonadism.

Lab investigation:- Serum Iron
Transferrin saturation > 45%. Plasma ferritin > 200 ng/ml. Liver biopsy (gold standard) > 1000 MCG/L. DNA Mapping study for gene mutation.

Treatment:- Venesection for all people with Iron biochemical overload. Chelating agents like Desferoxamine can be also taken.

References: DAVIDSONS INTERNAL MEDICINE, INTERNET

Characteristic Cells in Oral Pathology

Muhad Noorman P, Team dentowesome, Final year

Anitschkow cell: Modified macrophages with nuclei having caterpillar apperance ( linear bar of chromatin with peripheral radiating chromatins . Found in Recurrent Apthous stomatitis, Iron deficiency Anemia, megaloblastic Anemia, children receiving chemotherapy.

Langerhans cells : Bone marrow derived antigen presenting cells found in epidermis positive for CD1a and Bierbeck Granules. Increased in Langerhans cell histocytosis and decreased in Psoriasis etc.. Named after Paul Langerhans

Tzank Cells: Enlarged , Balooned up degenerating keratinocytes with enlarged vesicular hyperchromatic nucleus, basophilic cytoplasm and diminished nucleoli and perinuclear halo appearance. Named after Arnault Tzank. Found in Herpes Simplex infection, Herpes Zoster, Pemphigus vulgaris, Varicella.

Langhans Giant cells: They are formed by the fusion of epithelioid cells and contain multiple nuclei arranged in a horseshoe-shaped pattern in the cell periphery or are arranged circumferentially. Named after Theodor Langhans. Found in granulomatous lesions like Tuberculosis, tuberculous Leprosy.

Downey cells : Atypical lymphocytes, abundant pale blue cytoplasm and irregular chromatin . Found in infectious mononucleosis. Named after Hal Downey.

Warthin Finkeldy Giant cells : Giant cells with upto 100 nuclei, cytoplasmic and nuclear inclusions. Pathognomic of measels infection. Named after Warthin and Finkeldy.

Reed–Sternberg cells: They are named after Dorothy Reed Mendenhall and Carl Sternberg. They are large cells that either are multinucleated or have a bilobed nucleus (having an “owl’s eye” appearance) with prominent eosinophilic nucleoli.Reed–Sternberg cells are giant cells found in Hodgkin’s lymphoma (HL).

Gaucher Cells : Glucocerebroside laden macrophages containing tubular cytoplasmic inclusions. (Crumbled tissue paper apperance) Hallmark of gaucher disease. Staining positive for Wright and PAS stain.

Rushton bodies : Peculiar linear , curved- hyaline homogeneous structure found in wall of ODONTOGENIC cysts like periapical cyst, dentigerous cyst etc..

Ghost cells: Well defined, eosinophilc, elliptoid fused epithelial cells with blurred apperance. Found in Ghost cell odontogenic tumor, Calcifying epithelial odontogenic cyst, odontoma, craniopharyngioma etc..

Rusells bodies : Large eosinophilc immunoglobulin containing inclusion bodies found in plasma cells. Distented endoplasmic reticulum staining positive for PAS, CD38 etc. Found in chronic inflammations. Aggregate Is called Mott bodies.

Reference : Internet, Shafers oral pathology, Neville Oral pathology

Unique Clinical appearance in Oral pathology and Medicine

Muhad Noorman, Team dentowesome , Final year

Apple jelly nodules in nasal septum: It is the nodular form of the tuberculosis in nasal mucosa. It begins in the vestibule and extends to adjoining skin and mucosa.

Arnold head: In Cleidocranial dysplasia, the fontanelles may remain open until adulthood, but the sutures often close with interposition of wormian bones

Blue Sclera: Osteogenesis imperfecta , EHLER danlos syndrome, Fetal Rickets, MARFANS Syndome etc.. Asymptomatic bluish discoloration of sclera due to thinning of sclera and exposing underlying vascular choroid.

Ash-leaf spots: Hypomelanic macules in Tuberous sclerosis.

Buffalo hump: Cushing’s syndrome, the fat relocalization in nape of the neck resembling the buffalo’s hump

Bull neck: Diptheria, Cherubism

Cerebriform tongue: Pemphigus vegetans. Also known as Furrowed tongue with numerous sulci and gyri

Chipmunk facies: Thalassemia and Sickle cell anemia. The bones of the head and face become enlarged and deformed causing an abnormal appearance resulting in a typical “chipmunk/ rodent facies” appearance. This occurs because the bone marrow, the site of red blood cell production, becomes hyperactive in an attempt to produce sufficient red cells to over profound anemia.

Cobble stone appearance: Lymphangioma, Inflammatory papillary hyperplasia, Heck’s disease

Forschemmier spots : Forscheimer spots are enanthem seen as small, red spots (petechiae) on the soft palate in patients with rubella. Also found in palatal mucosa of Scarlet fever.

Fournier’s molars: congenital syphilis, Mulberry molars

Hamman’s crunch: Cervicofacial emphysema. It’s a crunching, rasping sound, synchronous with the heartbeat, heard over the precordium .

Hebra nose: Rhinoscleroma. Epistaxis, nasal deformity, and destruction of the nasal cartilage are also noted.

Iris pearl’s: Leprosy. Miliary lepromas or iris pearls near the pupillary margins, which are spherical yellowish opaque micronodules

Koplik’s spots: Measles. Koplik spots are a prodromic viral enanthem of measles manifesting two days before the measles erythmatous cutaneous rash itself. They are characterized as clustered, white lesions on the buccal mucosa ( table salt appearance) near each Stensen’s duct (on the buccal mucosa opposite the maxillary 2nd molars) and are pathognomonic for measles.

Lisch nodules: Neurofibromatosis. A Lisch nodule is a pigmented hamartomatous nodule found in iris which is an aggregate of melanocytes.

Pastia’s lines: Scarlet fever. Pastia’s sign, Pastia lines or Thompson’s sign is a clinical sign in which pink or red lines formed of confluent petechiae are found in skin creases, particularly the crease in the antecubital fossa. Caused by erythrogenic toxins staphylococcus.

References : Shafers Oral pathology. Burkets Oral Medicine

Clinical Signs In Oral Pathology/ Medicine

Dentowesome- Muhad Noorman P
Final year

Asboe-Hansen sign (also known as indirect Nikolsky sign) refers to the extension of a blister to adjacent unblistered skin when pressure is put on the top of the intact bulla.

Auspitz’s sign is the appearance of punctate bleeding spots when psoriasis scales are scraped off, named after Heinrich Auspitz.This happens because there is thinning of the epidermal layer overlying the tips of the dermal papillae and blood vessels within the papillae are dilated and tortuous, which bleed readily when the scale is removed.

Button-hole sign: Neurofibromatosis. invagination of a nodule when pressed with a finger, a characteristic of neurofibromatosis

Carpet tack lesions: Discoid lupus erythematosus. There are follicular hyperkeratotic plugs causing a carpet tack appearance as they project from the undersurface of the scale when it is removed from advanced lesions.

Charcot’s triad: Seen in multiple sclerosis, characterized by intention tremor, nystagmus, dysarthria

Crowe’s sign: Found in Neurofibromatosis. Presence of axillary freckling in people with neurofibromatosis type I.

Gorlin sign: Ehler -Danlos Syndrome. Ability to touch the tip of the nose with tongue and touch the elbow with the tongue

Higomenakis’s sign: Congenital syphilis. A unilateral enlargement of the sternoclavicular portion of the clavicle, seen in congenital syphilis

Millian sign: Erysipelas. Involvement of the ear (Milian’s ear sign) is a distinguishing feature for erysipelas since this region does not contain deeper dermis tissue.

Nikolsky’s sign: Epidermolysis bullosa, pemphigus, Severe Steven –Johnson syndrome etc. Application of lateral oblique pressure to skin yeild formation of new blisters.

Oil drop sign: Psoriasis. A translucent discolouration in the nail bed that resembles a drop of oil beneath the nail plate.

Reference: Neville Textbook of oral Pathology. Cawsons essential oral pathology
Regezi and Batsakis Oral pathology

Powerful ways to remember what you study.

Muhad Noorman P – Final year -Team Dentowesome

Most often we get frustrated by studying for days before exams, often we fail to recollect or forget while writing exams. It’s a quite natural process for a human body to forget.
However there are tricks to master our hippocampus and remember for long. Excelling in exams are only possible based on how much you remember topics.

According to Ebbinghaus curve of forgetting information is lost from brain and we’re inable to recollect it.A typical graph of the forgetting curve purports to show that humans tend to halve their memory of newly learned knowledge in a matter of days or weeks unless they consciously review the learned material.

In oder to master long term memorization, we need to practice following methods

Revision : You still remember, A for apple and mitochondria is power house of cell. Constant and frequent revison makes your hippocampus to convert short term memory to long term memory.

Spaced repetition learning technique
Review Your Notes. Within 20-24 hours   of the initial intake of information, make sure the information is written down in notes and that you have reviewed them.
Recall the Information for the First Time. Recall the Materials Again.
Study It All Over Again
Difficult topics are checked regularly while easy topics could be reviewed occasionally

Take a break method
  Study for 20 minutes take a 5 minute break repeat pattern for 3 to 4 hours. It helps to gain more focus, At the end you’ll be happy for the productive hours. Without break in intervals your brains rejects input eventually your output becomes non productive. Mastering this techinque daily, your graph of productivity hits up.

Use body movements while learning,helps to Tigger muscle memory.


Make a story to memorize long topics. Pieces of information are always connected each other when a story link is given.

Organise your study table. Neat study table and fresh environment boost your intake . Bright light, fresh air, erect spine enhance brain functioning. Feel comfortable stay away from cluttered environment

Try to understand what you learn,  things you understand and studied are memorised 9 times.


Learn opposite things .

Switch your topics frequently. Similiar memory get’s intermixed (interference theory).

Things learned at the beginning and end are most memorized. Plan your topics accordingly.


Dicatate your topics and record in dictaphone you can download in your phone. Hear audios before you sleep, going to a beach or restaurant… Brain makes short term memory to long term memory while relaxed.

Visualise your topics. You still remembers the colour of precipitate and titration from your 12th chemistry lab practicals. Visualized memory is far beyond your imaginations.

Read first from books, 2 or 3 days later watch related topics videos from Youtube or any informative apps. Audio+ video learning brushes your previous stored information

Always make use of Sticky notes of alternating colours (prefer light colours- eye rejects dark colour for long time. Use sticky notes apps In your phone screen ( numericals, years etc.could be written in it).

  Last days before your exams should be used for rough reading or revison not for studying. Brain rejects things learned in stressed or a state of anxiety .( Your neurotransmitters makes it mess. Respect them 🤣)

Credits : 1) Forgetting curve definition:Wikipedia. Image : Internet. 2) Spaced repetition technique images from Internet and Osmosis.org website . Spaced repetition method content from Google.

How to study efficiently and score more marks in exams.

Muhad Noorman P, Final year Student – Team Dentowesome

Scoring good and better marks are always priority of any student irrespective of their level and class .  Hard work and smart work helps to score good marks.

Some tips to study smart and score more marks

1) Always organise yourself, Never procrastinate. Don’t think about wasted days ,look forward days ahead and make efficient planning.

2) Give importance to every subject equally, start with easy and end in hard nuts.


3) Identify your best time, and place to study. Ignore and never seek how you’re peer group works. Always your peer lies about studies, focus on yourself 🙂

4) Cut your social distraction, even though it sounds like a rocket science, regular practice helps to cut your Distraction. Utilise focus mode in android phones, Install Forest app. It Helps to prioritise your study hours.


5) Teach yourself as if you’re a teacher, trust me you’ll crack a million topics.


6) Teach you’re peer group , it’ll help to recollect and brush up your brain.


7) Regularly shift your studyplace , between a period of 1 hour or 2 hour later,  brain and mind always rejects learning from a same environment.


8) Get familiarise with the exam layout, use previous year question, understand nature of questions , prepare accordingly.


9) Always finish with previous questions first and if time allows study other topic left, mentioned in  University syllabus.


10) Reading a book not studying :  Revise topic after 1 or 2 hour, Prepare notes, put away books . Attempt topic as an exam question. Self realization is best methodology to improve yourself.


11) Never cut too many corners: Often we get devastated listening rumors , predictable questions . And the  truth is anything can come.


12) Practice mock exams during free times. Practice always make a man perfect.


13) Organize your answer while writing in exam papers. Never forget, Presentation matters. Include as much as figures, flowcharts, pie diagrams..etc.. Proove examiner you have an edge over topics. Underline important points with seperate ink.


14) Last but not least get an adequate sleep.(Ideally 6 to 7 hours)  Give some time for your brain and hippocampus to process your memory.

References: Image : Google

Seqeulae of wearing denture

Muhad Noorman P- Dentowesome 2020

1.DENTURE STOMATITIS

Denture-induced stomatitis is a common inflammatory reaction related to the wearing of dentures usually involving Candida (yeast) species. Less common forms of denture stomatitis may be due to mechanical trauma or a contact reaction.

Predisposing factors

Denture-related stomatitis is very common, with over 50% of denture wearers affected in some populations. It is the most common clinically important condition developing in the mouth

  • Complete upper (maxillary) denture – probably due to the large contact area between denture and oral mucosa
  • Acrylic dentures – Candida species seem to have a particular binding affinity for acrylic resin
  • Poor dental hygiene – Candida species and Lactobacillus bacteria stick to denture surfaces and should be removed chemically and/or mechanically at least daily
  • Poorly fitting dentures – mechanical trauma damages the mucosa, making it more prone to infection
  • Denture age – old dentures are commonly associated with denture stomatitis probably due to poor fitting and rough surface in which Candida can hide
  • Continuous wearing of denture – failure to remove at night increases the risk
  • Men – are twice as likely to develop denture stomatitis than women
  • Diabetes mellitus – diabetics are more prone to developing yeast infections
  • Dry mouth (xerostomia) – saliva normally helps flush the mouth and clean the denture surface

CLINICAL FEATURE , Denture stomatitis usually does not cause any symptoms ,Some complain of burning sensations in mouth . But on examination the mouth lining in contact with the denture will be red and swollen sometimes with small red dots (petechial haemorrhages).

Treatment: regular oral hygiene, oral nystatin gargle, cleansing denture in nystatin solution, Not wearing denture at night.

2.DENTURE INDUCED FIBROUS HYPERPLASIA aka EPULIS FISSURATUM

Denture-induced fibrous hyperplasia (DIFH) is a persistent lesion caused mostly by the prolonged wear of an ill-fitting, over-extended denture. Although the condition frequently coexists with denture stomatitis, it is a distinct entity .Develops as a reactive lesion to chronic mechanical irritation produced by the flange of a poorly fitting denture.More simply, epulis fissuratum is where excess folds of firm tissue form inside the mouth, as a result of rubbing on the edge of dentures that do not fit well. It is a benign entity.

CLINICAL FEATURE: The lesion is usually painless.The usual appearance is of two excess tissue folds in alveolar vestibule/buccal sulcus, with the flange of the denture fitting in between the two folds. It may occur in either the maxillary or mandibular sulci,although the latter is more usual.Anterior locations are more common than posterior. Less commonly there may be a single fold, and the lesion may appear on the lingual surface of the mandibular alveolar ridge.

Surgically excised, reconstruction of denture, denture rebasing can be done

3. DENTURE INDUCED ULCER

Traumatic ulcers caused by dentures with overextended or unbalanced occlusion are seen in about 5% of denture wearers.Overextention of flanges,sequestration of bony spicules, illfitting, sharp boders are cause of Traumatic ulcer.

CLINICAL FEATURE: Superficial, Painful, shallow ulceration often with erythematous halo and greyish membrane covering the ulcer.

Symptomatic relief by topical analgesic,steroid oinments and repair of denture.

4. INFLAMMATORY PAPILLARY HYPERPLASIA OF PALATE

Inflammatory papillary hyperplasia (IPH) is a benign lesion of the palatal mucosa. It is usually found in denture-wearers but also has been reported in patients without a history of use of a maxillary prosthesis use.The lesion almost exclusively involves the hard palate

CLINICAL FEATURES:

Inflammatory papillary hyperplasia is usually asymptomatic. It presents as a cluster of individual papules or nodules that may be erythematous, somewhat translucent, or normal in surface coloration. Mucosa is erythematous and has a pebbly or papillary surface. Many cases are associated with denture stomatitis.

Often the entire vault of the hard palate is involved .Has a female prediliction.

This may be aided by use of topical antibiotic or antifungal therapies. Small lesions are also typically treated with mouthrinses such as chlorhexidine mouthrinse at 0.12% or antifungal mouthrinse/ gels. Larger lesions recquired surgical excision.

References: Neville Textbook of Oral pathology.

Shafers textbook of pathology. Cover photo image: Internet