Transcript Soft Palate

ORAL HEALTH AND DENTISTRY
The anatomy of the oral cavity and salivary glands.
Borders:
roof = palate (hard, soft)
floor = tongue, mucosa, geniohyoid and mylohyoid m
Lat/ant
Outer fleshy wall = cheeks, gums
Inner bony wall = teeth and inner aspect of gums
communicates posteriorly with oropharynx
Divided into 2 areas: the oral vestibule, anterior to
the teeth and buccal side of gingiva (gums) & oral
cavity proper, which is the space behind the teeth
and gums
Oral Vestibule = Cheeks, Lips, Gingivae
Lips
Lips contain the orbicularis oris m, and
sup/inf labial m, a/v/n.
Covered externally by skin externally, and
mucosa internally.
Epithelium of skin transitions from normal
skin –> red vermillion portion –> to inner
mucosal layer. The border line b/w skin and
red portion = transition zone.
Structures to identify in relation to the lips:
upper lip = b/w nose & opening of oral cavity
nasolabial grooves = seperate lips from cheeks, 1 cm
lat to angle of mouth
philtrum = a shallow depression below the nose,
bordered by 2 lateral crests – not everyone has one
lower lip = b/w opening of oral cavity and labiomental
groove, separating lower lip from chin.
labial frenula = a mucosal membrane fold that
attaches the lips to the ant surface of the vestibular
gingiva (gums facing the oral vestibule) — NOTE diff
from lingual frenula, that attaches the tongue to the
floor of the mouth
Blood supply = sup/inf labial a (facial a)
upper lip = br of facial/ infraorbital = sup
labial br
lower lip = br of facial/mental a = inf labial
br
Innervation
upper lip = sup labial br of V2
lower lip = inf labial br of mental n from V3
(mental n comes from inf alveloar n)
Lymph Drainage =
submandibular/submental lymph nodes
Cheeks
over lie the zygomatic process
contain the buccinator m - that holds
cheeks taught when exhaling forcefully
contains the buccal fat pad (of Bichat)
Blood Supply = buccal br of maxillary a
(terminal br of ext carotid), n = buccal
br of mandibular n (V3)
Gums
are fibrous tissue covered with mucosa
hold teeth in place
supplied by many a/v/n
Blood Supply
upper (maxillary) lingual gingiva of incisors, canines =
nasopalatine n,a/v – most ant, this makes sense because
nasopalatine structures go through incisive foramen at most
ant part of hard palate
upper (maxillary) lingual gingiva of premolars, molars = gr.
palatine n, a/v – post, makes sense b/c gr. palatine structures
go through gr palatine foramen at post/lat part of hard palate
lower(mandibular) labial buccal gingiva of incisors, canines,
premolars = inf alveolar n/a/v
lower(mandibular) labial buccal gingiva of molars = buccal n
lower(mandibular) lingual gingiva = lingual n/a/v
Palate
Made up of hard and soft palate
Hard palate
is bony and makes up the ant 4/5 of the palate = palatine process of the
maxilla, and horizontal plate of palatine bone
border b/w nasal and oral cavity
@ midline of hard palate, running back from incisive foramen = palatine
raphe – where the 2 palatine shelves fused in embryonic life
3 foramina:
Incisive foramen (ant/med) = nasopalatine n/a/v
In the netter, it looks like sphenopalatine a goes through there, but do not
say this in a test, it will be considered incorrect.
NOTE – makes the location of the fusion b/w primary/secondary palate in
embryonic life
Greater and Lesser Palatine foramen (post/lat) – right next to 3rd molar
(wisdom tooth) = the gr/lsr palatine n/a/v go through them.
Gr palatine structures run ant and supply hard palate
Lsr palatine stuctures run post and supply soft palate
Soft Palate
is fibromuscular fold that makes up post 1/5 of palate
moves agains the pharyngeal wall to close oropharynx while swallowing or speaking
as mentioned earlier, supplied a/v/n by lesser palatine structures.
Laterally, is continuous with palatoglossal and palato pharyngeal folds
These folds are form the lateral border to the exit of oral cavity = Isthmus of
Fauces, that leads to Oropharynx (More on that in pharynx)
b/w them is the tonsillar bed = palatine tonsils
CLINCAL NOTE – are frequently inflamed and removed, along with pharyngeal
tonsils (see pharyn) aka adenoids
CLINCAL NOTE = Since lingual gingiva is connected to mucosa of soft palate, can inject
anasthetic there to numb soft palate
Has numerous palatine glands, that secrete mucus
Blood Supply: Gr and Lsr palatine a (more the 2nd one), Asc palatine a (Facial a),
Palantine br of Asc Pharyngeal a
Innervation : SS = lsr palatine n, SM = CN X
Venous Drainage: hard and soft palate v drain in pterygoid venous plexus
NOTE that Hard palate has no SM innervation – no musc there.
Muscles of Palate: all innervated by CN X via
pharyngeal plexus – except Tensor Veli Palatini (V3)
Tensor Veli Palatini - tenses soft palate, has a large
tendon that strengthens the soft palate = palatine
aponeurosis
Levator Veli Palatini – elevate soft palate
Palatoglossus - elevates tongus (Just uses palate as an
origin site, doesn’t do anything to palate itself)
Palatopharyngeus – elevates pharynx, to help close
off nasopharynx from oropharynx in swallowing
Uvulus – @ termination of soft palate, no real
function, but helps to identify issues with CN X, b/c if
this doesn’t move when saying, “Ahhh”, then poss
malfunction w. CN X
Tongue
•is almost purely made of muscle
•the ant 2/3 is called the oral part = originates from 1st
pharyngeal arch
•post 1/3 = pharyngeal part, orginates from 3rd arch, behind
terminal sulcus of tongue
•@ midline of terminal sulcus is foramen cecum, the remnant
of thyroglossal duct
•root = from 4th arch
•Has midline sulcus on dosal surface = location of fusion of 1
lateral swellings of ant tongue over tuberculum impar.
Function: aid in speaking, allow for movement of food toward
oropharynx and within oral cavity
Parts:
Body – most of the tongue
Apex – pointed ant part
root – part fixed to hyoid bone and mandible, is located behind
palatoglossal fold, location of lingual tonsils.
Taste Buds: SEE HISTO
The inferior surface of tongue has a very thin mucus
membrane, so can see many veins, and is attached to floor of
mouth via another mucus membrane fold = lingual frenulum.
– Basically keeps tongue in mouth while allowing apex to
move about
Muscle of Tongue = all innervated by CN XII, except
palatoglossus, which we already said is innervated by
Pharyngeal plexus, via CN X
Intrinsic m - change the shape of tongue itself
Sup/Inf Longitudinal, Transverse, Vertical
Extrinsic m – change position of tongue
Genioglossus – protrudes and depresses tongue
Hyoglossus – depresses and retracts tongue
Styloglossus – retracts and elevate tongue
Palatoglossus – elevates tongue
How to remember them? Gay Hats STYLe Perfectly
Basic Taste sensations:
Sweetness = apex
Saltiness = lateral side
Sourness & bitterness = posterior part
Umami = used to taste the unusual tastes in cheese, meat, asparagus, & tomatoes
Blood Supply:
Lingual a from Ext carotid a, emerges @ lever of gr. horn of hyoid bone in carotid
triangle
Pathway: runs deep to hyoglossis (lateral lingual groove), and lies on middle
pharyngeal constrictorm
Br = dorsal lingual, suprahyoid,sublingual a, terminates as deep lingual a ( on top of
genioglossus m)
Lymph Drainage:
Post 1/3 = deep cervical lymph nodes
Medial ant 2/3 = inf deep cervical lymph nodes
lat ant 2/3 = submandibular l.n
apex = submental l.n
Innervation of Tongue:
Ant 2/3: SS = CN V3 via Lingual n, VS = CN VII via Chorda Tympani
Post 1/3: SS/VS = CN IX
Root: SS = CN X, no taste buds here, so no VS
Salivary Glands:
Parotid
Location: Retromandibular Space = Parotid Bed
Borders:
ant = Masseter m, Ramus of mandible
post = SCM, post digastric m
sup = zygomatic arch
inf = fascia b/w SCM and mandible
Lat = open
General Info:
covered by dense fibrous capsule from investing fascia of
neck
secretes serous saliva
largest of the glands
secretion of gland
Duct Pathway:
From widest part of gland –> across masseter and
deep to it –> lat/ant to Buccal fat pad –> peirces
Buccinator m, and opens @ 2nd maxillary (upper)
molar
Structures Passing through It:
Ext Carotid a - giving 2 terminal branches = Maxillary
a, Superficial temporal a
Superficial Temporal v & Maxillary v combine to give
Retromandibular v
Facial n peirces it and gives 5 terminal branches –
DOES NOT innervate the gland
Auriculo temporal n – carries PNS post synaptic fibers
with it to increase secretion of gland
Blood supply:
from branches of external carotid and superficial temporal a = Transverse facial a
Veins follow a and drain into Retromandibular v
Lymph Drainage:
superficial and deep cervical lymph nodes
Innervation:
Tympanic n arises from CN IX and emerges from jugular foramen
n enters the middle ear via the tympanic canaliculus in petrous part of temporal bone
tympanic n forms the tympanic plexus — and lesser petrosal n emerges from this
plexus
lesser petrosal leaves skull via foramen ovale
PNS fibers from it synapse in otic ganglion
post ggl fibers from ggl RUN W/ auriculotemporal n (from V3) to supply parotid gland
*Parotid and Submandibular gland separated by stylomandibular lig b/w styloid
process & angle of mandible
Submandibular Gland
Located: below mylohyoid & mandible
General Info:
Has Superficial and Deep part (deep part located b/w mylohyoid and
styloglossus)
secretes a mix of serous and mucus saliva
Duct Pathway:
ducts runs thru lat space of tongue w/ Hypoglossal n and lingual n =
lateral lingual groove —> then eventually goes to and open lat to
frenulum, b/w mylohyoid and styloglosses
lingual n loops under duct in the lateral lingual groove
Blood Supply: sunmental a (Facial a), V run with a.
Lymph Drainage: deep cervical l.n. –> jugulo-omohyoid nodes
Innervation:
Pre ggl PNS fibers from CN VII by chordatympani –> submandibular ggl –
> post ggl fibers run w/ lingual n
SNS post ggl fibers come from sup cervical ggl
Sublingual Glands
Location: b/w mandible and genioglossus m
General info:
smallest of the 3 glands
secretes both mucus and serous, but more mucus
Duct Pathway: duct opens @ floor of oral cavity w/
submandibular duct, just below mucus membrane of tongue,
lat to frenulum
Blood Supply : Submental and sublingual a (from facial and
lingual a)
Innervation:
Pre ggl PNS fibers from CN VII by chordatympani –>
submandibular ggl –> post ggl fibers run w/ lingual n
SNS post ggl fibers come from sup cervical ggl
Evaluation and examination of oral
cavity
Physical Examination of the Oral Cavity
Lips
Inspect landmarks – vermilion zone, commissures, nasolabial fold
Inspect color
Inspect surface for ulcerations, blisters, growths, thickness changes
Observe patient with mouth closed and patient smiling to look for
cranial nerve VII lesions
Palpate with gloved hands for surface irregularities not visible to the
eye, submucosal nodules, and areas of tenderness
Labial mucosa – reflect lips with gloved hands
Inspect color and surface for nodules, ulcerations, thickenings
Palpate upper and lower surfaces with two fingers from commissure
to commissure to detect submucosal changes
Buccal mucosa – have patient open mouth wide in
order to inspect and have good lighting.
Inspect color and surface for nodules, ulcerations,
thickenings
Identify normal landmarks: pterygomandibular
raphe and parotid papilla. Identify parotid papilla
on mucosal surface near upper molars. Palpate the
parotid gland and observe for expression of fluid
from Stensen’s duct
Palpate surface with two fingers to identify
submucosal lesions
Gingiva and alveolar mucosa
Gingiva and alveolar mucosa
inspect color of gingival and alveolar
mucosa.
Inspect texture of gingival and alveolar
mucosa – look for atrophy, recession,
hypertrophy or enlargement. Look for
ulcerations.
Palpate any areas of enlargement to
determine if enlargement is due to
edema, or an underlying bony or fibrous
process
Palate
identify hard and soft palate landmarks –
fovea palatinae, palatine raphe, alveolar
tuberosity, hamular notch, pillars of the
fauces, uvula. Inspect for any developmental
abnormalities of these landmarks
Inspect color of hard and soft palate and
inspect for ulcerations, thickenings, exudates.
petechiae
Palpate posterior hard palate and soft palate
for subcutaneous nodules
1.Tongue – inspect in normal resting position and
in a protruded position
1.Identify landmarks: terminal sulcus, median
sulcus, foramen cecum, lingual frenulum
2.Be familiar with normal appearance of
filiform, fungiform and circumvallate papillae
3.Inspect color and texture of dorsal, ventral
and lateral surfaces. Look for plaques,
ulcerations, thickenings, changes in papillae
4.Palpate dorsal and ventral aspects of the
tongue
5.Evaluate movement of tongue
1.Floor of the Mouth – have patient open mouth touch tip of
tongue to roof of mouth to inspect. Carefully retract tongue to
inspect distal aspects of floor.
1.inspect normal landmarks – lingual frenulum, sublingual
folds, caruncles
2.inspect for color and texture changes
3.palpate entire sublingual and submandibular fossa areas by
bimanual palpation to detect nodules, differences in
consistency of sublingual glands and tissues
2.Teeth
1.Inspect for number and position of teeth – understand how
the number of teeth change from childhood to adulthood, look
for changes in teeth structure or number that indicate
congenital/genetic syndromes
2.Inspect color of teeth and look for surface changes indicative
of early dental decay
Orlal examination
Scope of responsibility
Diseases of the head & neck
Diseases of the supporting hard & soft
tissues
Diseases of the lips, tongue, salivary
glands, oral mucosa
Diseases of the oral tissues which are
a component of systemic disease
Many diseases (systemic or local)
have signs that appear on the face,
head & neck or intra-orally
Making a complete examination
can help you create a differential
diagnosis in cases of abnormalities
and make treatment
recommendations based on
accurate assessment of the signs &
symptoms of disease
Equipment
Assure that you have all the supplies
necessary to complete an oral
examination
Mirror
Tissue retractor (tongue blade)
Dry gauze
You must dry some of the tissues in order
to observe the nuances of any color
changes
Extra-oral examination
Observe: color of skin
Examination area of head & neck
Determine: gross functioning of cranial nerves
Normal vs. abnormal
Paralysis
Stroke, trauma, Bell’s Palsy
TMJ
Palpate upon opening
What is the maximum intermaxillary
space?
Is the opening symmetrical?
Is there popping, clicking, grinding?
What do these sounds tell you about
the anatomy of the joint?
When do sounds occur?
Use your stethoscope to listen to
sounds
Lymph node palpation
Refer to handout
Thyroid Gland Evaluation
Thyroid Gland
Palpation
Place hands
over the
trachea
Have the
patient
swallow
The thyroid
gland moves
upward
Exam: Lips
Observe the color & its
consistency-intra-orally and
externally
Is the vermillion border distinct?
Bi-digitally palpate the tissue
around the lips. Check for nodules,
bullae, abnormalities, mucocele,
fibroma
Exam: Lips
Evert the lip and examine the tissue
Observe frenum attachment/tissue
tension
Clear mucous filled pockets may be
seen on the inner side of the lip
(mucocele). This is a frequent, nonpathologic entity which represents a
blocked minor salivary gland
Exam: Lips-palpation
Color, consistency
Area for blocked
minor salivary glands
Lesions, ulcers
Frenum:
Attachment
Level of attached
gingiva
Exam: Lips-sun exposure
Palpate in the vestibule, observe color
Examination: Buccal Mucosa
 Observe
color, character of the mucosa
 Normal variations in color among
ethnic groups
 Amalgam tattoo
 Palpate tissue
 Observe Stenson’s duct opening for
inflammation or signs of blockage
 Visualize muscle attachments, hamular
notch, pterygomandibular folds
 Linea
alba
 Stenson’s
duct
Lesions – white, red
 Lichen Planus, Leukedema

Gingiva
Note color, tone, texture, architecture
& mucogingival relationships
How would you describe the gingiva?
Marginal vs. generalized?
Erythematous vs. fibrous
Drug reactions: Anti-epileptic, calcium channel
blockers, immunosuppressant
Exam: Hard palate
 Minor salivary glands, attached gingiva
 Note presence of tori: tx plan any preprosthetic surgery
Exam: Soft palate
 How does soft palate raise upon “aah”?
 Vibrating line, tonsilar pillars, tonsils,
oropharynx
Exam: Oropharanyx
 Color,
consistency of tissue
 Look to the back, beyond the soft
palate
 Note occasional small globlets of
transparent or pink opaque tissue
which are normal and may
include lymphoid tissue
Exam: Tonsils
 Tucked
in at base of anterior &
posterior tonsilar pillars
 Globular tissue that has “punched
out” appearing areas
 Regresses after adulthood
 May see white “orzo rice like” or
“torpedo” shaped white
concretions within the tissue
Exam: Tongue
The tongue and the floor of the
mouth are the most common
places for oral cancer to occur
It can occur other places; so
visualize all areas
You may observe:
Circumvalate papillae, epiglottis
You may observe lingual varicosities
You may observe geographic
tongue (erythema migrans)
You may observe drug reaction
Observe signs of nutritional deficiencies,
immune dysfunction
You may observe oral cancer
Palpation of the floor of the mouth
Exam: Floor of mouth
 Visualize,
palpate - bimanually
 Wharton’s duct
 Must dry to observe
 Does “lesion” wipe off?
 Where are the two most
likely areas for oral cancer?
 lateral border of the tongue
 Floor of mouth

Squamous Cell Carcinoma

Squamous Cell Carcinoma
Exam: Leukoplakic area
Edentulous Mandibular Ridge
 Oral
Cancer:
 Red
 White
 Red and White
 Does the patient have important risk
factors for oral cancer?
 Counseling for smoking and alcohol
Cessation
Squamous Cell Carcinoma
Triaging Lesions
*
Describe it’s characteristics
Size, shape, color, consistency, location
How long has it been present?
Is it related to a trauma?
Fractured cusp, occlusal trauma
Has it occurred before?
Can you wipe it off?
Does the patient have specific risk factors
for neoplastic lesions?
Any lesion that is suspicious
should be re-evaluated in 2
weeks
Lesions due to infectious
processes would have healed
in that time frame
If it remains, the lesions
should be biopsied
Exam: Maxilla & Mandible
• size, shape, contour
• pre-prosthetic treatment
•Tori removal
• tuberosity reduction
•Soft or hard tissue or both
Evaluate for Epulis fissuratum
If you make a new denture will the excess
tissue resolve?
Occlusion
Orthodontic
classification
Interferences
Breath
Oral odors can indicate:
Infection: caries, periodontal dx
URT infections
Chronic G.I. disturbances
Lung abscess
Diabetic acidosis
Uremia, kidney problem
Liver failure: mousy, musty odor
Self-medication with alcohol
Visualize all areas
Oral odors can indicate:
Infection: caries, periodontal dx
URT infections
Chronic G.I. disturbances
Lung abscess
Diabetic acidosis
Uremia, kidney problem
Liver failure: mousy, musty odor
Self-medication with alcohol
Disease of the hard tissue of teeth
Dental caries
Dental caries, also known as tooth decay
or a cavity, is an irreversible infection
usually bacterial in origin that causes
demineralization of the hard tissues
(enamel, dentin and cementum) and
destruction of the organic matter of the
tooth, usually by production of acid by
hydrolysis of the food debris accumulated
on the tooth surface .
If demineralization exceeds saliva and
other remineralization factors like from
calcium, fluoridated tooth pastes, these
tissues progressively break down,
producing dental caries (cavities, holes in
the teeth). Two groups of bacteria are
responsible for initiating caries:
Streptococcus mutans and Lactobacillus. If
left untreated, the disease can lead to pain,
tooth loss and infection.
Tooth decay is caused by specific types of acidproducing bacteria that cause damage in the
presence of fermentable carbohydrates such as
sucrose, fructose, and glucoseThe mineral content of
teeth is sensitive to increases in acidity from the
production of lactic acid. To be specific, a tooth
(which is primarily mineral in content) is in a
constant state of back-and-forth demineralization
and remineralization between the tooth and
surrounding saliva. For people with little saliva,
especially due to radiation therapies that may
destroy the salivary glands, there also exists
remineralization gel
These patients are particularly susceptible to
dental caries. When the pH at the surface of the
tooth drops below 5.5, demineralization
proceeds faster than remineralization (meaning
that there is a net loss of mineral structure on
the tooth's surface). Most foods are in this
acidic range and without remineralization, this
results in the ensuing decay. Depending on the
extent of tooth destruction, various treatments
can be used to restore teeth to proper form,
function, and aesthetics, but there is no known
method to regenerate large amounts of tooth
Classification
Caries can be classified by location,
etiology, rate of progression, and
affected hard tissues. These forms
of classification can be used to
characterize a particular case of
tooth decay in order to more
accurately represent the condition
to others and also indicate the
severity of tooth destruction.
Etiology
Rampant caries.
In some instances, caries are described in other ways
that might indicate the cause. "Baby bottle caries," "early
childhood caries," "baby bottle tooth decay," or "Bottle
Rot" is a pattern of decay found in young children with
their deciduous (baby) teeth. The teeth most likely
affected are the maxillary anterior teeth, but all teeth can
be affectedThe name for this type of caries comes from
the fact that the decay usually is a result of allowing
children to fall asleep with sweetened liquids in their
bottles or feeding children sweetened liquids multiple
times during the day. Another pattern of decay is
"rampant caries", which signifies advanced or severe
decay on multiple surfaces of many teeth
Rampant caries may be seen in
individuals with xerostomia, poor oral
hygiene, stimulant use (due to druginduced dry mouth and/or large sugar
intake. If rampant caries is a result of
previous radiation to the head and
neck, it may be described as radiationinduced caries. Problems can also be
caused by the self destruction of roots
and whole tooth resorption when new
teeth erupt or later from unknown
.
Three factors for dental caries
1 Carbohydrate substrate
2 Acid that caused dissolution of
tooth minerals
3 Oral micro-organisms that
produce acid and also cause
proteolysis.
Rate of progression
These descriptions can be applied to caries to
indicate the progression rate and previous
history. "Acute" signifies a quickly developing
condition, whereas "chronic" describes a
condition that has taken an extended time to
develop, in which thousands of meals and
snacks, many causing some acid
demineralization that is not remineralized,
eventually results in cavities. Fluoride treatment
can help recalcification of tooth enamel.
Recurrent caries, also described as secondary,
are caries that appears at a location with a
previous history of caries. This is frequently
found on the margins of fillings and other dental
restorations. On the other hand, incipient caries
describes decay at a location that has not
experienced previous decay. Arrested caries
describes a lesion on a tooth that was
previously demineralized but was remineralized
before causing a cavitation. Using fluoride
treatments can help with recalcification.
Affected hard tissue
Depending on which hard tissues are affected, it is
possible to describe caries as involving enamel,
dentin, or cementum. Early in its development, caries
may affect only enamel. Once the extent of decay
reaches the deeper layer of dentin, "dentinal caries" is
used. Since cementum is the hard tissue that covers
the roots of teeth, it is not often affected by decay
unless the roots of teeth are exposed to the mouth.
Although the term "cementum caries" may be used to
describe the decay on roots of teeth, very rarely does
caries affect the cementum alone. Roots have a very
thin layer of cementum over a large layer of dentin,
and thus most caries affecting cementum also affects
Signs and symptoms
A person experiencing caries may not be aware of the
diseaseThe earliest sign of a new carious lesion is the
appearance of a chalky white spot on the surface of the
tooth, indicating an area of demineralization of enamel. This
is referred to as an incipient carious lesion or "microcavity".
As the lesion continues to demineralize, it can turn brown but
will eventually turn into a cavitation ("cavity"). Before the
cavity forms, the process is reversible, but once a cavity
forms, the lost tooth structure cannot be regenerated A lesion
that appears brown and shiny suggests dental caries were
once present but the demineralization process has stopped,
leaving a stain. A brown spot that is dull in appearance is
probably a sign of active caries.
As the enamel and dentin are destroyed, the cavity
becomes more noticeable. The affected areas of the
tooth change color and become soft to the touch.
Once the decay passes through enamel, the dentinal
tubules, which have passages to the nerve of the
tooth, become exposed and causes a toothache. The
pain may worsen with exposure to heat, cold, or
sweet foods and drinks Dental caries can also cause
bad breath and foul tastes In highly progressed cases,
infection can spread from the tooth to the
surrounding soft tissues. Complications such as
cavernous sinus thrombosis and Ludwig's angina can
be life-threatening.
Causes
There are four main criteria required for caries formation: a tooth
surface (enamel or dentin); caries-causing bacteria; fermentable
carbohydrates (such as sucrose); and time The caries process does not
have an inevitable outcome, and different individuals will be susceptible
to different degrees depending on the shape of their teeth, oral hygiene
habits, and the buffering capacity of their saliva. Dental caries can occur
on any surface of a tooth that is exposed to the oral cavity, but not the
structures that are retained within the bone All caries occurs from acid
demineralization that exceeds saliva and fluoride remineralization, and
almost all acid demineralization occurs where food (containing
carbohydrate like sugar) is left on teeth. Though most trapped food is
left between teeth, over 80% of cavities occur inside pits and fissures on
chewing surfaces where brushing, fluoride, and saliva cannot reach to
remineralize the tooth as they do on easy-to-reach surfaces that
develop few cavities.
Dental Plaque and Gum Disease
A build-up of plaque and calculus can lead to
inflamed and infected gums. Mild gum disease
is called gingivitis and is not usually serious.
More severe gum disease, called periodontitis,
can lead to teeth falling out. Good oral hygiene
which includes regular tooth brushing and
cleaning between teeth (eg by flossing) can
usually prevent gum disease, and treat mild-tomoderate gum disease. Specialist dental
treatments may be needed for severe gum
disease.
Dental plaque is a soft deposit that forms
on the surface of teeth. It contains many
types of bacteria (germs). You can usually
remove plaque quite easily by tooth
brushing and cleaning between teeth.
Calculus is hardened calcified plaque. It is
sometimes called tartar. It sticks firmly to
teeth. Generally, it can only be removed by
a dentist or dental hygienist, with special
instruments.
Gum disease (periodontal
disease) means infection or
inflammation of the tissues that
surround the teeth. Depending
on the severity, gum disease is
generally divided into two types
- gingivitis and periodontitis.
Gingivitis
Gingivitis means inflammation of the gums.
Most cases of gingivitis are caused by plaque.
This is then called plaque-associated gingivitis.
Periodontitis
Periodontitis literally means 'inflammation
around the tooth'. It occurs if gingivitis becomes
worse and progresses to involve the tissue that
joins the teeth to the gums (the periodontium),
and/or the supporting bone.
As a consequence of periodontitis, a gap (pocket) develops
between the tooth and gum. If left untreated, the tooth may
slowly loosen and eventually fall out.
Dentists assess the severity of periodontitis by measuring the
depth of the pockets that form between the gum and tooth.
Plaque can be removed from shallow pockets (up to about 3
mm deep) by brushing and cleaning teeth in a normal way.
However, deeper pockets need to be treated by a dentist, as
normal brushing and cleaning will not reach the bottom of
the pocket.
Dental Pulp Diseases
Poor dental hygiene is the main reason for tooth
decay, tooth pain, and other oral health
conditions. If you don't maintain good oral
health habits, including brushing and flossing
regularly, plaque can develop and lead to
cavities. Left untreated, a cavity can eventually
affect the soft center (or pulp) of your tooth,
which contains sensitive nerves and delicate
blood vessels. And if pulp diseases aren't
properly managed, you can lose your teeth.
Symptoms of Pulp Diseases
Depending on the type of pulp
disease, symptoms may vary in
intensity and can include:
Pain in a tooth or teeth when you
eat something very sweet, hot, or
cold
Sudden, intense pain in the mouth
Infection in the mouth
Types of Pulp Diseases
There are several different pulp diseases, including:
Reversible pulpitis, or mild inflammation of the pulp.
Symptoms typically include pain upon eating or drinking
something very sweet, hot, or cold. Without treatment, the
inflammation can progress to a dental abscess, a collection of
bacteria and pus. Good oral health habits can help offset
reversible pulpitis, but in many cases, a filling is eventually
needed. Pulpitis can also occur if you crack or break a tooth.
Irreversible pulpitis, or severe inflammation of the pulp that
can't be cured. Symptoms include sudden intense pain. Left
untreated, it can result in a widespread gum and connective
tissue infection. Irreversible pulpitis is generally treated with a
root canal procedure. If that doesn't work, your dentist may
have to remove the tooth.
Dental pulp calcification (also
known as dental pulp stones). This
is a condition in which hardening,
or calcification, of pulp tissue
results in hypersensitivity and
extreme pain because the dental
nerves become compressed. A root
canal is usually necessary to clear
away hardened tissue.
Dental pulp exposure. This condition
comes on when damage to the external
covering of a tooth, such as a cavity or
crack in the tooth, exposes the normally
protected pulp to bacteria and irritating
food particles. Pain is the most frequent
symptom and without proper dental care,
a mild infection can progress into a serious
abscess. Depending on the degree of pulp
exposure, a filling, root-canal procedure, or
even tooth extraction may be required.
Pulp Diseases Treatment: Root Canal
Therapy
If damaged pulp in your tooth isn't taken
out, a severe infection can spread to
surrounding tissue, including your jaw
bone. A root canal procedure to remove
the pulp tissue is usually performed over
several visits by a regular dentist or a pulp
specialist, called an endodontist. The root
canal therapy may spare you from having
to get the infected tooth removed.
Here's what you can expect from root canal therapy:
First visit. The diseased pulp is removed and the empty space,
the root canal, is cleaned out and enlarged. Special
medications may be placed in the canal to disinfect the area.
A temporary filling may be placed as well, or your dentist may
choose to leave the canal open and let the tooth drain for a
few days. An oral antibiotic may also be recommended to
treat infection in the tissues surrounding your tooth.
Second visit. The temporary filling is removed and a
permanent filling is placed.
Final visit. A crown is placed over the tooth to reinforce the
tooth and make it stronger.
Some pulp diseases may be caused by an injury that broke a
tooth. But many other pulp diseases are simply caused by
poor oral health habits. If you brush and floss regularly and
seek out regular dental care, you are less likely to develop
Tooth extraction
Definition
Tooth extraction is the
removal of a tooth from
its socket in the bone.
Indcations And ContraIndications Of Extractions
Dental Extraction:
Dental Extraction is defined as :
“The removal of a tooth from oral
cavity by means of elevators and
forceps”.
Also referred as “Exodontia”.
Indications Of Extraction:
Indications advocated for dental
extraction:
-Unrestorable carious tooth.
-Pulp necrosis and irreversible
pulpitis;untreatable by
endodontic therapy,calcified root
canal,patient refusal.
Severe periodontal
disease; Bone loss,grade 3
mobility,furaction
involvement.
-
-Impacted teeth ;Malalligned,resorption of
roots of adjacent teeth.
Orthodontic treatment ;
Crowding,Space
creation.Maxillary and
st
Mandibular 1 Pre-molar.
-Mal-alligned teeth ;
Tissue trauma,malpositioning,esthetics.
Esthetics ; Stained teeth,
excessively protruded
teeth,mal-alligned.
-Cracked and fractured
tooth ;Tooth in fracture
line,pain,Dialceration,heal
ing, infection.
Pre-prosthetic extraction ;
Unsuitable
abutments,interference with
appliance
-Supre-numerary teeth ;
Impacted,resorption,
displacement,failure for
erruption.
-Pre-radiation therapy ;
Osteoradionecrosis.
-Economical reason ;
Unaffording patient.
-Lack of time ; Unavailability
of time for other options.
Contraindications for Dental
Extraction
Systemic
Local
Systemic Contraindications:
-Uncontrollable metabolic disease e.g
Diabetes, End stage renal disease,
Uremia.
-Uncontrollable leukemia and
lymphomas.
-Uncontrollable cardiac diseases ;
Severe M.I.,Angina Pectoris, Recent
M.I., Dysarrythmias.
Uncontrolled hypertension ;
Risk of myocardial insufficiency,
C.V.A.
-Bleeding diathesis ;
Hemophilia, Thrombocytopenia.
-Pregnancy ; 1st and 3rd
Trimester ; Relative contraindication.
Local Contraindications:
-Therapeutic irradation ;
osteoradionecrosis.
-Teeth in area of malignant tumor.
-Severe pericoronitis.
-Acute dento-alveolar abscess.
Types
Extractions are often
categorized as "simple"
or "surgical".
Simple extractions are performed on teeth that
are visible in the mouth, usually under local
anaesthetic, and require only the use of
instruments to elevate and/or grasp the visible
portion of the tooth. Typically the tooth is lifted
using an elevator, and using dental forceps,
rocked back and forth until the Periodontal
ligament has been sufficiently broken and the
supporting alveolar bone has been adequately
widened to make the tooth loose enough to
remove. Typically, when teeth are removed with
forceps, slow, steady pressure is applied with
Surgical extractions involve the removal of teeth
that cannot be easily accessed, either because
they have broken under the gum line or because
they have not erupted fully. Surgical extractions
almost always require an incision. In a surgical
extraction the doctor may elevate the soft tissues
covering the tooth and bone and may also
remove some of the overlying and/or surrounding
jawbone tissue with a drill or osteotome.
Frequently, the tooth may be split into multiple
pieces to facilitate its removal. Surgical
extractions are usually performed under a general
anaesthetic.
Post-extraction healing
Following extraction of a tooth, a blood clot
forms in the socket, usually within an hour.
Bleeding is common in this first hour, but its
likelihood decreases quickly as time passes, and
is unusual after 24 hours. The raw open wound
overlying the dental socket takes about 1 week
to heal. Thereafter, the socket will gradually fill
in with soft gum tissue over a period of about
one to two months. Final closure of the socket
with bony remodeling can take six months or
more.
TootExtraction Complications
A tooth extraction is a routine dental
procedure. In the majority of the procedures
no complications are expected during or after
the tooth extraction. But difficulties with
extractions are unpredictable and sometimes
complications
do
occur.
Tooth extraction difficulty increases when
the following conditions exist: strong
supporting tissues, difficult root morphology,
teeth with weakened crown surfaces due to
large restorations, teeth with deep caries,
Tooth extraction complications
during the procedure
Potential tooth extraction complications during
the procedure include :
Damage to nearby teeth. The adjacent
teeth or dental restorations (e.g., crowns,
bridges, implants) next to the extracted tooth
may occasionally be damaged during the
procedure. Nearby teeth may become
fractured, chipped or loosened during the
extraction of a tooth or teeth, sometimes
requiring more dental work.
Fracture of the tooth. The tooth may
fracture during the extraction process,
complicating the procedure and requiring more
time and effort to complete the extraction.
Tooth sectioning may be needed.
Incomplete extraction. A small part of the
tooth root may be left in the jawbone.
Although it may increase the risk of infection,
sometimes the dentist will prefer to not try to
extract it because its removal may be too
risky e.g. if it is very close to a nerve.
Damage to the sinus. The extraction of a molar from
the upper jaw may damage the sinus cavities above it,
by creating a hole that might become a source of
sinus infections. Normally the hole will heal and close
by itself, but if not it may require corrective surgery.
Nerve damage. A mistake during an extraction of
a tooth from the lower jaw may damage the inferior
alveolar nerve. Numbness in the lower lip and chin are
common symptoms of a damaged nerve. The nerve will
heal in a few weeks up to some months depending on
the extend of the damage. In rare cases, the nerve is
unable to heal completely, leaving the patient with a
permanent numbness.
Jaw fracture. Patients with a weak
jawbone structure (e.g. older
women with osteoporosis) may
have a risk of jaw fracture. Even if
the actual tooth extraction
procedure is performed smoothly
without any problems, there are
cases of complications during the
healing process.
Tooth extraction complications after the operation
Possible tooth extraction complications after
the operation include :
Dry socket. A dry socket following a tooth
extraction is a common complication in about
5% of people who have a tooth extracted. The
condition occurs when a blood clot does not
form normally in the tooth socket or the blood
clot is washed out or dissolved prematurely. In
a dry socket situation, the underlying bone and
nerves are exposed to air and food, causing
intense pain and sometimes bad odor or taste.
A dry socket needs to be treated with a
Infection. The wound of the
tooth extraction can be a
doorway for bacteria causing
an infection, particularly in
patients with a weakened
immune system. If a patient
has a high risk of infection the
dentist will generally prescribe
antibiotics before and
after the extraction.
Excessive bleeding and/or
swelling, redness or fever.
If you have any of these
symptoms, especially if they
continue after the first 24
hours, contact your dentist or
oral surgeon for advice.
Why you must replace an extracted
tooth
After a tooth extraction, dentists
will always recommend that the
extracted tooth has to be replaced
by a bridge or an implant (unless the
extraction was made as part of
preparation for full dentures). If the
tooth is not replaced, its absence
may cause a series of problems in the
long term.
These complications because of tooth
extractions include :
Teeth misalignment. The teeth next
to an extracted tooth tend to shift in the
empty space left by the extracted tooth
causing problems with the alignment of
teeth. Potential long term risks of teeth
misalignment include tooth wearing, teeth
grinding (bruxism) and
temporomandibular joint disorders.
Chewing problems. The loss of a tooth, especially if it
was a molar, may affect the chewing ability. Besides
that, the opposing tooth will press hard foods against
the soft tooth socket of the extracted tooth,
causing irritation and pain.
Loose teeth. The neighboring teeth on the sides
of a tooth extraction site loose their lateral support
and have increased risk of becoming loose over time.
Cosmetic problems. The patient’s appearance is
severely affected by the loss of one or more front
teeth.
The best treatment after tooth extractions is
to replace missing teeth with dental
implants.
T
he cost involved with dental
treatments needed to replace an extracted
tooth is significant and many patients can
not afford it if they are not covered by
their dental insurance. Learn how to choose
a dental insurance that will help you provide
the best dental treatment to yourself and
your family.
Anesthesia and Pain Control in Dentistry
Introduction
The practice of various psychological,
physical, and chemical approaches to
the prevention and treatment of
preoperative, operative, and
postoperative anxiety and pain.
Methods of pain control
Anesthetic agents
Inhalation sedation
Antianxiety agents
Intravenous sedation
General anesthesia
Anesthetic Agents
The numbing of a specific site or area.
Topical Anesthesia provides a temporary
numbing effect on nerve endings that are
located on the surface of the oral mucosa.
Supplied as:
Ointments
Liquids
Sprays
Local Anesthesia What are local anesthetics?
Local anesthetic: produce loss of sensation to pain in a
specific area of the body without the loss of consciousness
Agents most frequently used for pain control in
dentistry.
Criteria for use:
Be nonirritating to the tissues in the area of the
injection.
Produce minimal toxicity.
Be of rapid onset.
Provide profound anesthesia.
Be of sufficient duration.
Be completely reversible.
Be sterile.
Method of Action
Local anesthesia temporarily blocks the normal
generation and conduction action of the nerve
impulses.
Local anesthesia is obtained by injecting the
anesthetic agent near the nerve in the area
intended for dental treatment.
Induction time is the length of time from the
injection of the anesthetic solution to complete
and effective conduction blockage.
Duration
Length of time from induction until the reversal
process is complete.
Short-acting:
Local anesthetic agent lasts less than 30
minutes.
Intermediate-acting:
Local anesthetic agent lasts about 60 minutes.
Long-acting:
Local anesthetic agent lasts longer than 90
minutes.
Vasoconstrictor
Criteria for use:
Prolongs the duration of an anesthetic
agent by decreasing the blood flow in the
immediate area of the injection.
Decreases bleeding in the area during
surgical procedures.
Types:
Epinephrine
Levonordefrin
Norepinephrine
Ratio of vasoconstrictor
to anesthetic solution:
1:20,000
1:50,000
1:100,000
1:200,000
Contraindications for the use of
vasoconstrictors
Unstable angina.
RecentContraindications for the use of
vasoconstrictors
Unstable angina.
Recent myocardial infarction.
Recent coronary artery bypass surgery.
Untreated or uncontrolled severe
hypertension.
Untreated or uncontrolled congestive
heart failure.
myocardial infarction.
Recent coronary artery bypass surgery.
Untreated or uncontrolled severe
Contraindications for the use of
vasoconstrictors
Unstable angina.
Recent myocardial infarction.
Recent coronary artery bypass surgery.
Untreated or uncontrolled severe
hypertension.
Untreated or uncontrolled congestive
heart failure.
Types of Local Anesthesia Injections
Infiltration is achieved by injecting
the solution directly into the tissue
at the site of the dental procedure.
Most frequently used to anesthetize
the maxillary teeth.
Used as a secondary injection to
block gingival tissues surrounding
the mandibular teeth.
Block anesthesia
The solution is injected near
a major nerve, and the
entire area served by that
nerve is numbed.
Type of injection required
for most mandibular teeth.
Inferior alveolar nerve block
Obtained by injecting the
anesthetic solution near the branch
of the inferior alveolar nerve close
to the mandibular foramen.
Type of injection for half of the
lower jaw, including the teeth,
tongue, and lip.
Incisive nerve block
Injection given at the site of the mental
foramen.
Used when the mandibular anterior teeth
or premolars require anesthesia.
Periodontal ligament
Alternative infiltration anesthesia method
by which the anesthetic solution is injected
directly into the periodontal ligament and
surrounding tissues.
Local Anesthesia Setup
Anesthetic carpule: Care and caution
of use
Cartridges should be stored at room
temperature and protected from
direct sunlight.
Never use a cartridge that has been
frozen.
Do not use a cartridge if it is cracked,
chipped, or damaged in any way
Never use a solution that is
discolored or cloudy or has passed
the expiration date.
Do not leave the syringe preloaded
with the needle attached for an
extended period of time.
Never save a cartridge for reuse.
Local Anesthetic Cautions
Injection into a blood vessel
Infected area
Localized toxic reaction
Systemic toxic reaction
Temporary numbness
Paresthesia
Electronic Anesthesia
A noninvasive method to block
pain electronically by using a
low current of electricity
through contact pads that
target a specific electronic
waveform directly to the nerve
bundle at the root of the tooth.
Benefits to the patient:
No needles.
No post-operative numbness or
swelling.
Chemical-free method of anesthesia.
No risk of cross-contamination.
Reduces fear and anxiety.
Patients have control over their own
comfort level.
Dental Injuries
An average of 22,000 occur annually among children less than
18 years of age.
Over 80% of all dental injuries involve the upper teeth.
30% of preschoolers have had a dental injury of some kind.
Of all sports, baseball and basketball were associated with the
largest number of dental injuries.
Children with primary teeth, less than 7 years old, sustained
over half of the dental injuries in activities associated with
home furniture.
Outdoor recreational products and activities were associated
with the largest number of dental injuries among children
ages 7-12 years of age.
Management and dental trauma evaluation
Check airway, breathing, and, circulation
Determine if there are any other lifethreatening injuries present.
Perform a neurological exam.
Assess the cervical spine.
Evaluate extra oral soft tissue injuries.
Conduct intraoral examination
Determine if the injury is to primary or
permanent teeth
Assess availability of dental care
Three broad categories of injuries result
from impacts during play to the soft
tissues, the jaws and teeth:
Soft Tissues – bruises, lacerations and cuts to
the lips, cheeks and tongue.
Jaws – Dislocations of the lower jaw (mandible)
or fractures of the upper arch (maxillary).
Dental – Tooth related; this can be as simple as
a chipped tooth or as serious as an avulsion
(tooth removed from the socket)
The goal is to try to save the teeth
that have been affected.
Avoid tooth loss
Assessment, diagnosis and
treatment will differ in damaged
baby teeth compared to adult
teeth.
Keep the child comfortable.
Immediate treatment – within 5 minutes
For a tooth that has been completely knocked out
(avulsed tooth)
Physically try to place the tooth back into the socket
Rinse the tooth with clean water: do not scrub or
scrape the root surfaces.
Hold the tooth’s crown and push it back into the
socket. You will need to hold the tooth in the socket
for several minutes to keep it from extruding back
out of the socket.
It is okay if the tooth is not completely aligned. The
dentist can adjust it later.
What if no one can replant the
tooth?
Control the bleeding with pressure.
Place the tooth in either cold milk
or the patient’s saliva to keep it
from drying out.
The person needs to transported to
their dental provider/ emergency
room immediately.
Why replant the tooth within 5
minutes?
Evidence suggests that placing the
tooth back into the socket is an
important factor for long term
survival of knocked out teeth.
More than 5 minutes
Transporting the tooth in milk
or the person’s own saliva will
keep the tooth from drying out.
If the tooth dries out, it will be
unable to regenerate the
periodontal ligament cells.
What if a baby tooth is completely
knocked out?
Primary teeth (baby) are different than
adult teeth and the treatment is different.
Primary teeth are generally not replanted
into the socket.
The reason is for not replanting is that the
primary tooth may cause an infection to
spread to the permanent tooth. It may
also affect the eruption pattern of the
permanent tooth.
Urgent Treatment – Within 6 hours
A painful injury from a permanent tooth moved from
its original position
This will cause the tooth/teeth to be driven in or out
of the jaw.
This may cause a fracture to the roots of the teeth.
The person should seek treatment as soon as
possible.
If the person has a dental provider it’s best to contact
them immediately.
The dentist may be able to splint the teeth back
together.
Primary (baby) Tooth Injuries
If the child is unable to bite and close his teeth
together normally, you should contact the child’s
dental provider as soon as possible, or go to the
emergency department of the nearest hospital.
Primary teeth can be treated in up to 6 hours. This
will usually not have an impact on long-term
outcomes.
Contact the child’s medical and or dental provider.
Following treatment with pain control and some rest
may result in the child being more comfortable with
treatment.
Less Urgent Treatment – Within 12
Hours
Fractured or Chipped Permanent Tooth
Crown fractures are the most common
traumatic injury.
These teeth will be sensitive to
temperature. These will need
medical/dental follow up, but treatment of
the pulp nerve exposure will not affect long
term outcomes.
Contact the child’s dental/medical provider.
Mouthguards
Mouthguards are designed to absorb and
distribute the forces of impact received while
participating in athletic activities.
Properly fitted mouthguards help protect the
soft tissues of the lip, cheeks, gums, and tongue
by covering the sharp surfaces of the teeth.
They can also reduce the potential for jaw joint
fractures and displacement by cushioning
against the impact.
They can reduce the force upon impact helping
to protect the jaws from fracture.
Your Role in Injury Prevention
It is far better to prevent injuries than to have to
deal with them after they occur. Anterior
trauma can have life-long consequences
affecting aesthetics, self-image, and
pocketbook. Raising awareness and stressing
prevention to parents of young children are
important public health messages. A trusted
clinician is in a powerful position to provide
preventive recommendations to parents.
Cleft Lip & Palate
Birth defects
Malformations
alterations in normal development
Deformations
abnormal mechanical force on an
otherwise normal fetus
Disruptions
disruption of an otherwise normal
developmental process
Introduction
Most common craniofacial
malformation
Cleft lip with or without cleft palate
(CL/P) or isolated cleft palate (CP).
CL/P and CP differ with respect to
Embryology, etiology, candidate
genes, associated abnormalities,
and recurrence risk.
Prevalence
CL/P is more common than CP and varies by
ethnicity.
CL/P
High in American Indians and Asians (1/500
newborns)
Low in American blacks (1/2000 newborns)
Intermediate level in Caucasians (1/1000
newborns)
Isolated CP occurs in only 1/2500 newborns and
does not display variation by ethnicity
Cleft Lip
Complete closure at 35 days
postconception:
7 weeks from the LMP.
Lateral nasal, median nasal, and
maxillary mesodermal processes merge.
Failure of closure can produce unilateral,
bilateral, or median lip clefting.
Left side unilateral cleft is the most
common
Cleft lip Severity
Mild, involving only the lip
Extend into the palate and
midface thereby affecting the
nose, forehead, eyes, and brain.
Cleft Palate
Lack of fusion of the palatal shelves.
Abnormalities in programmed cell
death may contribute to lack of
palatal fusion(?).
Isolated disruption of palate shelves
can occur after closure of the lip
Palatal closure is not completed
until 9 weeks post-conception.
Etiology
Genes
Control cell patterning, cell
proliferation, extracellular
communication, and differentiation
Clefting usually represents a genetically
complex event
Single Mendelian disorders associated
with clefting are rare
2 to 20 genes are thought to interact to
Dlx gene
Direct the destination of the distal skeletogenic
mesenchyme elements to the palate.
Mutations of these genes result in isolated palatal
defects.
Sonic hedgehog gene
Protein that mediates ectodermal functions, might
regulate the outgrowth and fusion of the facial
domains.
TGF-alpha variant
Receptor ligand, usually a rare variant of TGF-alpha
Family histories of cleft defects
Additive teratogenic effect with agents such as
cigarette smoking and alcohol
TGF-beta-3 gene
Expressed just prior to palatal
fusion.
Results in isolated cleft palate.
IRF 6
Identified in autosomal dominant
van der Woude syndrome.
Environmental agents
Several agents that are associated with an
increased frequency of midfacial
malformation.
Medications —phenytoin, sodium
valproate, methotrexate.
With corticosteroids there is no evidence
of an increase in malformations.
Possible association could not be
excluded
Etiology
Cigarette smoking
Noted with mothers of children with facial clefting,
both CL/P and CP.
Teratogenesis has been attributed to hypoxia as
well as a component of tobacco (cadmium).
Alcohol
Associated with an increased risk of fetal facial
clefting.
Alterations in cell membrane fluidity or reduced
activity of specific enzymes such as superoxide
dismutase.
Folate deficiency
Contributes to a range of birth defects.
Evidence is emerging for a similar association with
the development of CL/P.
Prenatal Diagnosis
Diagnosed until the soft tissues of the
fetal face can be clearly visualized
sonographically (13 to 14 weeks).
The majority of infants with cleft lip
also have palatal involvement:
85% of bilateral cleft lips
70% associated with cleft palate.
Cleft palate with an intact lip
comprises 27% of isolated CL/P
The sensitivity is highest when is associated
with other structural anomalies.
Isolated CL/P in a low risk population, the
sensitivity may only reach 50 percent.
Cleft palate with an intact lip is the most
difficult orofacial malformation to diagnose
prenatally.
Detected in only 13 of 198 cases in one
large series.
Three-dimensional ultrasound, can provide
a clear image of the malformation
Syndrome ?
A thorough examination of the
newborn or stillbirth is always
warranted.
Orofacial clefting is noted in over
300 syndromes.
3 deserve additional comment.
frequency, variable presentations,
and modes of inheritance
Deletion of chromosome 22q11
DeGeorge syndrome.
Spectrum in addition to cleft palate:
Conotruncal cardiac defects, thymic
hypoplasia, and velopharyngeal webs.
Majority of cases represent a new
microdeletion
In families with conotruncal
malformations and/or CP, further
evaluation is appropriate.
Oral-facial-digital syndrome, type I
X-linked dominant syndromes.
Manifestations in affected
females are variable and subtle:
hyperplastic frenula
cleft tongue
cleft lip/palate
digital anomalies
Treacher-Collins syndrome
Autosomal dominant disorder
Downward slanting palpebral fissures,
micrognathia, dysplastic ears, and
deafness.
Mental development is normal.
The mutations appear to increase cell
death in the prefusion neural folds.
A family history with deafness, ear
abnormalities, or CP.
Obstetrical
Amniocentesis for karyotype should be
Management
offered.
high rate of chromosomal defects
Difficulty in prenatal sonographic diagnosis
supports chromosomal evaluation
As of January 2002, "in utero" correction
had been attempted only once in Mexico
The child delivered prematurely and died
at two months of life
Recurrent Risk
Affected relative
Risk in child, percent
Cleft lip with or without cleft palate
Parent
Sibling
2%
Recurrent
RecurrentRisk
Risk
4 – 7%
11 – 14%
Parent and Sibling
Two Siblings
10%
Cleft palate only
Parent
7%
Sibling
2 – 5%
Parent and sibling
14 – 17%
Postnatal Management
repair, but also more immediate needs
such as feeding.
Primary lip repairs can often be undertaken
at three months of age with palatal repairs
around six months.
Additional surgeries as well as speech and
orthodontic therapies are often needed.
Cleft lip repair. The edges of
the cleft between the lip and
nose are cut (A and B). The
bottom of the nostril is formed
with suture (C). The upper part
of the lip tissue is closed (D),
and the stitches are extended
down to close the opening
entirely (E).
Feedings
Infants with CL/P have few feeding problems.
If the cleft involves the hard palate, the infant is
usually not able to suck efficiently.
Experiment (special nipples or alternate
feeding positions)
The infant should be held in a nearly sitting
position during feeding
Prevents flowing to the back into the nose.
Should be burped frequently, (q 3-4min).
It is important to keep the cleft clean
Breastfeeding is extremely challenging
.
Haberman Feeder
Activated by tongue and gum pressure.
Milk cannot flow back.
Replenished continuously as the baby
feeds.
Prevents the baby from being
overwhelmed with milk.
A gentle pumping action to the body of
the nipple will increase flow.
Family Care
Have a family meeting with both parents
present.
Infant should be brought to the parents as
soon the mother and the infant are in
satisfactory condition.
Allow the parents to observe, react and
ask questions about the infant.
Explained the defect and the how the
surgeon will most likely correct the clefts.
Before and after pictures are helpful.
Emphasize as possible to the
parents the normal healthy features
of the baby.
The baby should be present when
the defect is explained, as ugly as
the cleft might be.
Training the mother about feeding
techniques and avoiding
complications
.