Palatal perforations/ dental implant courses

INDIAN DENTAL ACADEMY
Leader in continuing Dental
Education
www.indiandentalacademy.com

 The word “palate” comes from the latin word “palatine”
which essentially means the “the roof”.
 The Hard Palate is a partition between the nasal and
oral cavity.
 Its anterior 2/3rd are formed by the palatine processes
of the maxilla and its post 1/3rd by the horizontal plates
of the palatine bone.
 The interaction between the tongue and the hard palate
is essential in the formation of certain speech sounds.www.indiandentalacademy.com

 It separates the nasopharynx from the oropharynx and is
often looked upon as a traffic controller at the cross roads
between the food and air passages
 Palatal perforations creates a communication between the
oral cavity and nasal cavity or the maxillary sinus.
 A number of local and systemic factors could be attributed to
palatal perforation.
 Local signs and symptoms include nasal regurgitation,
swallow and phonation dysfunctions, hoarseness of voice etc.
 Management is two-fold as it requires treatment of thewww.indiandentalacademy.com

1. Developmental- Cleft Palate
2. Infectious
 Tertiary Syphilis
 Leprosy
 Tuberculosis
 Actinomycosis
 Diphtheria
 Rhinoscleroma,
 Zygomycosis, -fungal
 Leishmaniasis, -protozoal
3. Autoimmune
 Sarcoidosis,
 Wegener Granulomatosis.
 Crohn’s disease
Bacterial

4. Idiopathic – Midline lethal granuloma
5. Neoplastic
 Carcinomas
 Lymphomas
 melanomas
6. Drug related
7. Iatrogenic
 oro-antral fistula
 tumor surgery(maxillectomy)
 Intubation
8. Other causes
 Rhinolith
 osteoradionecrosis
 fictitious palatal perforatio

 The palate is formed by fusion of 3 components namely the right and
left palatal processes(arising from the maxillary process) ; and the
primitive palate (derived from the frontonasal process). Deficiency in
fusion leads to various forms of cleft palate.
 Approximately 1 in 700 children born have a cleft lip and/or a cleft
palate
 Palate cleft can occur as complete (soft and hard palate, possibly
including a gap in the jaw) or incomplete (a 'hole' in the roof of the
mouth, usually as a cleft soft palate).
 Cleft of the palate result in anomalous communication beetween the
mouth and the nose. These may be unilateral or bilateral.www.indiandentalacademy.com

1. Intrauterine moulding :
 Pressure against the developing face prenatally can lead to
distortion of rapidly growth areas. An arm is pressed across
the face in utero, resulting in severe maxillary deficiency at
birth. Featus head is flexed tightly against the chest in utero,
preventing the mandible from growth forward rapidly. This is
related to decreased in amniotic fluid.
 The result is an extremely small mandible at birth, usually
accompanied by a cleft palate because the restriction on

2. Teratogens :
 Teratogens are certain drugs or agents that cause disturbed growth
and development in the foetus. Drugs causing cleft lip and palate are
;
 Aspirin
 Dilantin
 6-metacaptopurine
 Valium
 Cortisone
 Methothrexate

3. Multivitamins :
 Play a role in etiology of clefting. Tolarova and Harris (1998) found that
greatest effectiveness of the multivitamin regimen in decreasing cleft.
Recurrence was in male, where 10 mg folic acid was given.
4. Heredity is considered to be important etiologic factor for cleft lip and
palate. Study by Drilien reported 1 in 3 children with cleft had some
relatives with similar congenital defects. Clefts of lip and palate can be
transmitted as a dominant or a recessive trait.
5. More than 200 syndromes include clefts
 Cleft Palate - Apert’s, Stickler’s, Treacher Collinswww.indiandentalacademy.com

Predisposing factors :
 Increased maternal age : Women who conceive late are
at an increased risk of having an offspring with some
form of clefting and cause unknown.
 Racial : Some races are susceptible to clefts than
others. Mongoloids show greatest percentage.
 Blood supply : Factors that reduces blood supply to
nasomaxillary area during embryological development
predisposes to cleft.www.indiandentalacademy.com

 Associated Dental Abnormalities
– Supernumery Teeth- 20%
– Missing Teeth- 50%
– Malocclusion- 100%
 Cleft Lip +Palate- 2 Male: 1 Female
 Cleft Palate - 2 Female: 1 Male
 Cleft Lip +Palate- Native Americans > Oriental and Caucasians > Blacks
 Airway obstruction may present in children with a cleft palate, especially
those with mandibular hypoplasia (ie, a Pierre Robin sequence). Upper
airway obstruction results from posterior positioning of the tongue, which is
prone to prolapse into the pharynx with inspiration.

 Nasal obstruction can also result from the tongue protruding
into the nasal cavity
 Otitis media in 50% children with associated conductive
hearing loss. Although this problem tends to improve with age,
hearing loss in young children during the critical language
developmental can be as high as 60%

 Team Approach : management of defect, speech disorders, ear diseases,
airway problems
Surgical Repair
 Several Techniques- Trend is towards less scarring and less tension on
palate; Scarring of palate may cause impaired mid-facial growth(alveolar
arch collapse, midface retrusion, malocclusion)
 Generally, 1-stage closure of the soft palate and/or the hard palate can be
accomplished when the patient is aged 11-12 months. However, some
advocate a 2-stage closure, with repair of the velum (soft palate) when the
patient is aged 3-4 months.
 This procedure results in narrowing of the hard palate cleft, facilitating
closure at a later date, usually when the patient is aged 18 months. Similar

 When cleft palate repair is deferred to later childhood or
adulthood, repair often involves a pharyngeal flap. Incorporating a
pharyngeal flap into the repair can help close a large defect and
compensate for velopharyngeal dysfunction and speech problems.
Non-Surgical Treatment
Dental Obturator
– For high-risk patients or those that refuse surgery.
– Advantage- High rate of closure
– Disadvantage- Need to wear a prosthesis, and need to modify
prosthesis as child grows.

 Chronic infectious granulomatous disease caused by mycobacterium tuberculosis.
 Poor nutrition, general debilitating diseases, overcrowded living conditions and certain respiratory
diseases such as silicosis are predisposing factors.
 Trasmitted exclusively by air droplets less than 8 µm in size although bovine TB can be
transmitted by milk.
Clinical features-
 Episodic fever, chills, weight loss, persistent cough, easy fatigability, (classic symptoms- aftrenoon
rise in temp of 0.5 to 2 degree F, nightsweats and cavitary pneumonia.)
 Scrofula- TB of the cervical lymph nodes from consumption of raw bovine milk.
 Pott’s disease
 Lupus vulgaris- involvement of skin
 Miliary TB –most common to kidneys

Oral manifestations-
 Lesions are secondary to pulmonary disease, mostly in advanced disease
resulting from contact from infected sputum.
 Tongue most commonly affected followed by cheeks,palate and lips
 The usual presentation is an irregular, superficial or deep, painful ulcer
which tends to increase slowly in size. Long standing ulcers on palate can
lead to palatal perforation.
 Frequently found in areas of trauma.
 Tuberculous gingivitis-diffuse, hyperemic,nodular or papillary proliferation
of gingival tissue.
 Diffuse involvement of maxilla or mandible –tuberculous periostitis may

A 48-year-old lady from lower
socioeconomic group with palatal
perforation
Biopsy from the edge of the perforation
showed caseating epithelioid cell
granulomas with Langhans’type giant cells
J. Maxillofac. Oral Surg, 2009www.indiandentalacademy.com

 tubeculin test : 5 tuberculin units of PPD subcut
 Chest X ray
 Presence of acid fast bacilli and growth of these bacilli on sputum culture
 Histologic features: Foci of caseous necrosis surrounded by epitheloid
cells, lymphocytes, occasional multinucleated giant cells
 PCR
 Multiagent therapy : 8-16 week course ; combination of or more drugs-
INZ, rifampacin , pyrimidazole, streptomycin and ethambutol.

 It is a chronic infectious systemic disease caused by the spirochaete
Treponema pallidum
 It may be congenital or acquired; although in primitive overcrowded
conditions non venereal forms such as endemic syphilis, yaws and pinta
may be seen.
 Transmission can occur via direct contact with syphilitic lesions or infected
blood. Entry is gained through epithelial breaks and spread occurs via the
lymphatic and circulatory systems.
 Incubation period lasts from 10 to 90 days after which the first two stages
are highly contagious.

 All features arise from endarteritis obliterans.
 Primary syphilis uncommonly manifests as an oral chancre.
 Secondary syphilis can cause greyish ulceration in ‘snail track’ or ‘mucous
patch’ formations.
 Tertiary syphilis is a non-infective multi-organ stage characterised by a
painless localised granuloma (gumma) which classically presents on the
midline of the palate.
 Degradation of the mass leaves a deep pale ulcer with necrotic rolled
margins.
 Chronic necrosis destroys the palatal bone to leave a clean perforation.
 Healing occurs with severe scarring which causes distortion or destruction

 Histological changes can be non-specific and do
not therefore form the basis of diagnosis.
 Non-specific serological testing (eg VDRL)
indicates active disease and is positive in
untreated tertiary syphilis.
 Dark field microscopy- not useful in oral lesions
 Specific tests (eg FTA) remain positive even in
treated cases.www.indiandentalacademy.com

 Penicillin forms the mainstay of treatment and is supported with preventive
advice and regular sexual health check-ups.
 Pn –G -2.4 million units i.m /week for 3 weeks
 Or Tetracyclin or Eythromycin 500 mg 4 times a day for 30 days.
 Treatment of late syphilis will not reverse the tissue damage but it may
result in some improvement.
 Dental management can resume once the VDRL is negative
 Obturators are a successful method of managing the speech and
masticatory problems.
 Surgery is another option but extensive scarring in syphilitic lesions makes
any attempt at palatal repair hazardous

 Chronic granulomatous infection caused by mycobacterium leprae
Classification –
 Tuberculoid leprosy, Borderline tuberculoid, Borderline leprosy,
Borderline lepromatous, Lepromatous leprosy
Clinical features
 Tuberculoid lesions- single or multiple macular, erythematous
eruptions, with dermal and peripheral nerve involvement with loss of
sensations.
 Lepromatous lesions lead to progressive thickening of skin and
nodule formation, producing disfigurement

 The oral lesions in leprosy develop insidiously, are generally asymptomatic
and are secondary to nasal changes; most frequently affected site is the
hard palate
 M. leprae favors temperatures a little below the body temperature for its
multiplication, Based on this fact, a pathophysiologic mechanism is
postulated for oral involvement: a nasal lesion with obstruction of the air
flow leads to oral breathing (mouth breathing), which is very common in
lepromatous leprosy. This causes a decrease in the intra-oral temperature,
mainly in sites near the air intake, the anterior areas, facilitating the
harboring of the bacillus
 Sequence of pathological alterations: congestion, infiltration,and formation

A patient with a history of leprosy.
 There may be macrocheilia(caused by infiltration) or
microstomia (caused by ulceration and subsequent
repair with fibrosis of perioral or lip lepromas).
 Gums are usually affected in the area behind the
upper central incisors, often by contiguity, of lesions
of the hard palate. Chronic gingivitis, periodontitis
and periodontoclasia may occur
 In the advanced stages, there may be deformities
and functional alterations, such as fibrosis and
retraction of the soft palate or perforation of the hard
palate, with serious disturbances in phonation, andwww.indiandentalacademy.com

 Definitive diagnosis is based on clinical presentation and
demonstration of acid fast organisms on a smear or on a tissue.
 Histologic features:
 Granulomatous nodule shows collection of epitheloid cells and
lymphocytes in fibrous stroma
 Vacuolated macrophages called leprae cells are scattered throught
the lesion and contain bacilli.
Treatment :
 Paucibacillary : 6 month regimen of rifampacin and dapsone
 Multibacillary : 24 months of rifampacin,dapsone and clofazimine
 After resolution of infection, therapy should be directed towards
reconstruction and physiotherapy

 Caused by non acid fast, gram positive filamentous bacteria
called Actinomycosis, (A.israelli, Aviscosis)
 May be either a cute rapidly progressing lesion or a chronic
slowly spreading lesion ass with fibrosis.
 Formation of abscess with tendency to drain by sinus
formation.
 Pus shows presence of sulfur granules or colonies of
organisms which appear in suppurative material as tiny
yellow grains.

Clinical features-
 Cervicofacial-typically enters through an area of prior trauma
produce swelling and induration of tissues which develop into
abscess and tend to drain on the skin liberating pus containing sulfur
granules.
 Skin overlying abscess is purplish red, indurated and fluctuant.
 Sinuses heal and form in other areas producing scarring.
 May cause necrosis of the underlying bone leading to formation of
fistulas
 Most common site to be involved is the tongue followed by the

A rare case of co-infection with
pulmonary tuberculosis and oronasal
actinomycosis causing perforation of
the hard palate
J. bras. pneumol. vol.35 no.11 São
Paulo Nov. 2009 www.indiandentalacademy.com

Histologic features-
 Central abscess in which microorganisms are seen.
 Colonies appear to float in a sea of PMN associated with
multinucleated giant cells and macrophages around periphery of
lesion.
 The colonies appear round or lobulated and made up of meshwork
of filaments
Treatment :
 Abscess drainage and excision of sinus/fistula tracts, adequate
debridement

 Rapidly spreading gangrene of oral and facial tissues that
usually occurs in debilitated or nutritionally deficient patients.
 mortality rate as high as 70–90% if not promptly treated
 Fusobacterium necrophorum and Prevotella intermedia –
main org
 Predisposing factors : poverty,malnutrition,dehydration, poor
oral hygiene, poor sanitation,proximity to unkempt livestock,
malignancy, immunodeficiency disoders
 Begins as small ulcer of gingival mucosa which rapidly
spreads to involve the surrounding tissues of jaws,lips andwww.indiandentalacademy.com

 Overlying skin becomes inflamed, edematous and necrotic
 A line of demarcation develops between healthy and dead tissue and
large masses of tissue slough out leaving jaw exposed.
 Necrosis can extend to the deeper tissues extending to involve large
areas of bone resulting in osteomylitis
 Fetid odor, significant pain, fever,malaise, tachycardia, increased
respiratory rate, anemia,leukocytosis and regional lymphadenopathy
are additional features
Treatment :
 Antibiotics + local wound care+ adequate nutrition+ hydration +
maintain electrolyte balancewww.indiandentalacademy.com

 is one of the most rapidly progressing and lethal form of fungal infection in
humans which usually begins in the nose and paranasal sinuses
 This fungus invades the arteries, forms thrombi within the blood vessels that
reduce blood supply and cause necrosis of hard and soft tissues
 The predisposing factors : uncontrolled diabetes (particularly in patients
having ketoacidosis), malignancies such as lymphomas and leukemia’s,
renal failure, organ transplant, long term corticosteroid and
immunosuppressive therapy, cirrhosis, burns, PEM and AIDS
 Nasal obstruction, bloody nasal discharge, facial pain or headache, facial
swelling or cellulitis
 If maxillary sinus involved – intraoral swelling of the maxillary alveolar

Radiographically cloudy opacification of
the sinuses in conjunctions with patchy
effacement of the bone walls of the
sinuses
Histological features
extensive necrosis with numerous large
branching nonseptate hyphae with
granulomatous inflammation
Treatment :
Surgical debridement of the area andwww.indiandentalacademy.com

 Rhinoscleroma is a chronic progressive inﬂammatory disease of the
upper respiratory tract affecting mainly the nasal passages caused
by a fram-negative coccobacillus, known as Klebsiella
rhinoscleromatis.
 usually starts in the nose, which is affected in most cases, and then
spreads to other parts such as the pharynx, which may be involved
in about 50% of cases.
 Other affected sites include the eustachian tube,maxillary antrum,
oral cavity, larynx, orbit,trachea and bronchi.

 condition characterized by a necrotizing granulomatous condition of
respiratory tract, widespread vasculitis and necrotizing glomerulonephritis.
 Common presenting signs and symptoms include sinusitis, rhinorrhea,
nasal stuffiness and epistaxis with or without complain of fever, arthralgia
and weight loss.
Clinical features-
 Common in 4-5th decade
 Predilection for males
 Multisystem disease characterized by development of rhinitis, sinusitis and
otitis.
 Patient soon develops fever, cough, hemoptysis and joint pain
 Hemorrhagic and vesicular skin eruptions common
Wegener’s granulomatosis is an
uncommon

 Gingival lesions appear friable, granular or as gingival enlargement:
“strawberry gingivitis”. There may be destruction of underlying
palatal and alveolar bone causing oral-antral fistula
 Other lesions as ulceration of palate, diffuse ulcerative stomatitis,
spontaneous exfoliation of teeth and failure of tooth sockets to heal
following extraction
 The diagnosis of Wegener’s granulomatosis is made by clinical
features of illness associated with the presence of c-ANCA + and
pathology, characterized by a vasculitis of small arteries and veins,
the presence of giant cells and epithelioid cell granulomas

 Crohn’s disease (CD) is a chronic inflammatory bowel disease characterized by
transmural granulomatous inflammation involving any part of the
gastrointestinal tract in a discontinuous manner
 The median age of presentation of CD is 7.9 years, and 4% of pediatric CD
occurs below 5 yrs
 Common GIT symptoms :abdominal pain, diarrhea, fever and weight loss
 Oral manifestations : mucosal tags ,lip swelling,fissures, buccal mucosal
swelling or cobble stoning, deep linear ulcerations and localised mucogingivitis
 Diagnosis :clinical,laboratory,endoscopic and histological finding
 Treatment : 5-aminosalicylic acid (5ASA) with or without steroids depending on
the activity of the disease . Immunosuppressive drugs like azathioprine, 6
mercaptopurine, cyclosporin A and methotrexatewww.indiandentalacademy.com

 Cancer of the soft palate accounts for approximately 2% of head
and neck mucosal malignancies. Half of all hard palate cancers are
squamous cell carcinomas; in the soft palate, 80% of cancers are
SCCs
 Etiological factors: Reverse smoking, Alcohol, constant irritation-ill-
fitting dentures
 SCCs of the palate manifest as exophylitic or ulcerative surface
lesions, Ca soft palate is usually manifests as a non healing ulcer;
advanced cases may cause perforation
 Often patients are asymptomatic in the early stages, but they may

 In persons with advanced-stage soft palate
cancers, velopharyngeal insufficiency, altered
speech, difficulty swallowing, referred otalgia,
trismus and perforations may be seen
 Diagnosis :toluedine blue staining, definitive
diagnosis by biopsy
 Treatment: for Ca hard palate-
surgery,radiotherapy
Ca soft palate- radiotherapy

 Cocaine usage has a growing incidence worldwide. The most
common route of administration is nasal that induces local
vasoconstriction and irritation on the exposed tissue due to the
effect of both the active substance and others added during its
manufacture
 The highest risk group are individuals between 18 to 30 years old
regardless of gender, socioeconomic status or occupation
 Cocaine induces vasoconstriction and might cause necrosis in the
mucosae and surrounding tissues (cartilaginous and osseous).
 Frequent contact induces nasal septal destruction, choanae,

Hard palate perforation
caused by cocaine
abuse

 Extranodal NK T-cell lymphoma (nasal type angiocentric lymphoma or midline lethal
granuloma) is a rare process that is charachterized clinically by aggressive, non relenting
destruction of the midline structures of the palate and nasal fossa.
 In the initial stages patients may report nasal stuffiness, or epistaxis with or without pain.
 Swelling of the soft palate or posterior hard palate may preced the formation of of a deep
necrotic ulcer which usually occupies a midline position.
 Later ulcerations enlarge and may lead to bone necrosis which typically creates a
oroantral fistula.
 Lesions appear clinically as aggressive necrotic ulcers that are progressive and
nonhealing.
 Secondary infection may complicate the course of the disease and life threatening
hemorrhage may occur.
 Patient dies of hemorrhage if large vessels are eroded.

 Oro-Antral Communication (OAC) is a communication between the
maxillary sinus/antrum and the oral cavity / mouth. If an OAC is not
treated, this can become lined with epithelium (skin).
 Hence, an oro-antral fistula is an epithelised tract linking the
maxillary sinus to the mouth; the tract becomes 'permanent'.
 When an OAC is created, it allows the flow of food, smoke or fluid
from the mouth into the nose - not just these but also bacteria, fungi
and viruses.
 This can set upa maxillary sinusitis, which depending on how long
thecommunication lasts for, may either yield an acute /chronic

Causes of OAC’s:
 The vast majority of OAC's are created when upper molars and premolars
are removed (almost 50%),
 tumours (18.5%),
 bone infections (osteomyelitis) (11%),
 operations to access the maxillary sinus (Caldwell-Luc procedures) (7.5%),
 trauma (7.5%),
 dentigerous cysts(3.7%),
 correction of septal perforations (3.7%),
 perforation of the sinus floor from the tooth socket when trying to remove an
upper tooth
 chronic apical infectionwww.indiandentalacademy.com

 Retention suction cups produces negative pressure on the mucosa
which it contacts. This negative pressure induced by them has a
destructive effect on the palatal tissues.
 This negative pressure reduces the blood circulation in the
underlying tissues , which causes hypoxia in the affected area and
necrosis of tissue. The underlying bony part may also be affected by
this leading to tissue perforation.

 One of the most serious complications of radiation to the head and neck but is seen
less frequently today because of better treatment modalities and prevention.
 The current prevalence rate is less than 4%, whereas the frequency approached
15% less than 20 years ago.
 Although the risk is low, it increases dramatically if a local surgical procedure is
performed within 21 days of therapy initiation or between 4 and 12 months after
therapy.
 Radiation of bone results in permanent damage to the osteocytes and
microvasculature system. The altered bone becomes hypoxic, hypovascular, and
hypocellular.
 Osteoradionecrosis is the result of nonhealing, dead bone; infection is not
necessarily present.
 The mandible is involved most frequently, although a few cases have involved thewww.indiandentalacademy.com

 Intractable pain, cortical perforation, fistula formation, surface ulceration,
and pathologic fracture may be present.
 The radiation dose is the main factor associated with bone necrosis,
although the volume of bone irradiated and the proximity of the maximal
dosing both exert an effect.
 The risk of bone necrosis increases in the presence of the following:Teeth,
Bone trauma, Periodontal disease, Concurrent chemotherapy
 Postradiation dental extractions should be avoided and are a known risk
factor for Osteoradionecrosis. Surgery performed during the first 4 months
after radiationtherapy (the so-called "golden" period) is usually associated
with normal healing.

 SURGICAL
 NON SURGICAL:
 Functional
 Non functional
 Made of acrylic + metal denture base
 Hollow bulb
 Adequate nutrition and hydration
 Appropriate antibiotics

• Palatal perforations can occur due to a number of reasons such
as developmental, infectious,granulomatous diseases, drug
abuse etc
• The lesions on the hard palate may invade into the bone or
occasionally the nasal cavity.
• The lesions of the soft palate may extend into the nasopharynx.
• The prognosis of the malignancies of the palate is not
particularly good
• Thus careful evaluation of all the patients should be done.

 Burket’s oral medicine, diagnosis and tratement. 8th edition, J.B Lippincott company
 Norman Wood ,Paul Goaz ,Differential diagnosis of oral and maxillofacial lesions,5th
ed,mosby 1997
 Shafer,Hine & Levy,Textbook of Oral Pathology,4th Ed,W.B.Saunders Company,1983
 Neville Damm Allen Bouquet, Oral and Maxillofacial Pathology,2nd edition,Saunders
2005
 Robert P Langlais,Craig S Miller,Colour Atlas of common Oral diseases, library of
Congress cataloging,1992
 Peter A. Reichart,Peter Philipsen,Colour Atlas of Dental Medicine Oral Pathology,
Thieme, Stuttgart – New York, 2000
 Vitor Alexandre Oliveira Fonseca et al. A rare case of co-infection with pulmonary
tuberculosis and oronasal actinomycosis. J. bras.pneumol. vol.35 no.11 São
Paulo Nov. 2009 www.indiandentalacademy.com

Palatal perforations/ dental implant courses

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Palatal perforations/ dental implant courses