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MANAGEMENT OF MEDICALLY
COMPROMISED CHILDREN
KARISHMA.S
III MDS
CONTENTS
INTRODUCTION
TYPES OF MEDICALLY COMPROMISED CONDITIONS
CARDIOVASCULAR DISEASES
DENTAL TREATMENT CONSIDERATIONS
ANTIBIOTIC PROPHYLAXIS
OTHER MEDICALLY COMPROMISED CONDITIONS
REFERENCES
SYSTEMIC DISEASES INCLUDE:
1. Cardiovascular diseases
2. Respiratory diseases
3. Liver diseases
4. Endocrine diseases
5. Renal diseases
6. Sexually transmitted diseases(AIDS)
7. Blood diseases
8. Childhood cancers
INTRODUCTION
 Patients with medically compromised conditions suffers from a certain systemic condition which puts
him/her at risk from undergoing regular treatment.
 The majority of medically compromised patients need oral healthcare, a working knowledge of the
multitude of medically complex conditions is critical for dental professionals.
 This knowledge is necessary to help prevent, minimize, and alert clinicians to possiblily adverse side
effects potentially associated with procedures and drugs used in dentistry.
 Take precautions to enable the patient to undergo treatment without complications.
PREOPERATIVE MANAGEMENT:
1. Good detailed medical history of the patient should be taken and updated
during each visit.
2. The medical condition should be mentioned in the consent form.
3. Any problem in previous dental treatment should be reported precisely.
4. Report any previous hospitalization of the patient and the reason for it.
5. Early morning appointments are preferred except in cardiac patients which are
preferred to be in late morning.
6. In school oral health program, severe medically compromised patients are
treated at the program centers
THE MEDICALLY COMPROMISED PATIENT
Patient Assessment
 Category I: Healthy patient
 Category II: Medical conditions requiring schedule changes
 Category III: Medical conditions requiring significant modifications in
dental treatment
 Category IV: Medical conditions requiring major modifications in
dental treatment
 Category V: Serious medical conditions
CARDIOVASCULAR DISEASES
Cardiovascular
diseases
congenital
cyanotic
acyanotic
acquired
Rheumatic
fever
Infective
endocarditis
RHEUMATIC HEART DISEASE
 It is an acute inflammatory
condition, due to strep. A
 Rare in infancy
 Commonly appears between 6 – 15
years.
 Pharngitis infection following sore
throat, result in scaring &
calcification of valves followed by
valvular stenosis.
DENTAL TREATMENT
CONSIDERATIONS
• Careful dental evaluation and treatments have to be completed before surgery
• Preventive dental program
• Cardiologist consultation
• Antibiotic prophylaxis
• Dental treatment should be completed 3-4 weeks of the planned surgery to allow
healing and normal micro flora
DENTAL PROBLEMS AND TREATMENT
• Pulp therapy < extraction and space maintainer
• Permanent dentition – endodontic therapy after careful evalyation
• Oral sedation is beneficial
• Orthodontic treatment under antibiotic prophylaxis
• Cessation of anticoagulation therapy
• GA for severe debilitationg heart disease.
DENTAL PROCEDURES FOR WHICH ENDOCARDITIS PROPHYLAXIS IS
ADVISIBLE FOR HIGHEST RISK PATIENTS
All dental procedures that involve manipulation of gingival tissue or the
periapical region of the teeth or perforation of the oral mucosa.
CARDIAC CONDITIONS ASSOCIATED WITH HIGHEST RISK OF ADVERSE
OUTCOME FROM ENDOCARDITIS FOR WHICH PROPHYLAXIS WITH DENTAL
PROCEDURES IS ADVISIBLE
1. Prosthetic cardiac valve or prosthetic material used for cardiac repair.
2. Previous infective endocarditis
3. Congenital heart diseases (CHD)
4. Unrepaired cyanotic CHD
5. Completely repaired congenital heart defect with prosthetic material/ device
6. Repaired CHD
7. Cardiac transplantation
DENTAL MANAGEMENT OF A CHILD WITH CONGENITAL HEART
DISEASE - A CASE REPORT Arulpari Mahalingam1., Kirthivasan Vaidyanathan2., Paavai Ilango3*
Sanjay Cherian4 and Dhanapriya5
A 5-year-old old female child diagnosed with congenital heart disease soon after birth was referred for dental opinion
prior to cardiac surgery. Her medical history revealed that she had dyspnoea on exertion since birth and she was
found to have TOF (Ventricular septal defect, Patent ductus arteriosus, Supramitral membrane) with severe
pulmonary artery hypertension. On intraoral examination, she was found to have poor oral hygiene and multiple deep
carious lesions in relation to 51, 52, 54, 61, 62, 64, 73, 74, 75, 84 and 85. The patient was an uncooperative patient
with high levels of dental anxiety. The child was continued on her routine cardiac medications.
The treatment plan was divided into preventive treatment and corrective treatment procedures. In the preventive
treatment protocol, fluoride prophylaxis, diet counseling and oral hygiene instructions were given to the child and her
parents. The corrective treatment plan included pulpectomy in relation to 51,52,61,62,74,75, 84, 85, pulpotomy in
relation to 54, 64 and composite restoration in relation to 73.
A written informed consent and opinion was obtained from the parents and clearance was obtained from the pediatric
cardiologist. Antibiotic prophylaxis of Amoxicillin 50mg/kg body weight was given one hour prior to the procedure.
Hawary et al showed that CHD leads to alteration in the structure of enamel and dentin of deciduous
incisors at an ultrastructural level. It also leads to a significant decrease in mineral content (Ca and P)
of deciduous enamel and dentin when compared to healthy controls, rendering the dentition at
increased risk of dental caries.
AAPD guidelines 2011
Children:
(5–10 years)1/2 adult
(< 5 years) 1/4 adult
Special Circumstances The 2007 AHA
guidelines state that an antibiotic for
prophylaxis should be administered in a
single dose before the procedure. However, in
the event that the dosage of antibiotic is
inadvertently not administered before the
procedure, it may be administered up to two
hours after the procedure. For patients
already receiving an antibiotic that is also
recommended for IE prophylaxis, then a drug
should be selected from a different class
AAE Quick Reference Guide on Antibiotic Prophylaxis 2017 U
HAEMATOLOGICAL DISORDERS
Haematological disorders may be broadly classified into three groups;
1. Red cell disorders
2.White cell disorders
3.Disorders of homeostasis, including platelets and coagulation factors
RED CELL DISORDERS:
Anemia is defined as reduction in the volume of red blood cells (haematocrit) in the
packed cell volume (PCV) or in the concentration of hemoglobin in peripheral venous
blood. The various types of anemias are as follows:
Sickle - Cell Anemia:
It is inherited as an autosomal recessive disorder due to an abnormal hemoglobin
known as “ hemoglobin S ” hypoxia induced distortion of the erythrocytes into a
sickled shape occurs. The sickling phenomenon which occurs only in a reduced
oxygen tension causes both a chronic compensated haemolytic anemia and vaso-
occlusive crisis, resulting in pain and tissue damage caused due to infarction.
Clinical features
General features
• Anemia due to
haemolysis
• Aplastic crisis
• Impaired growth
• Skeletal deformities
Dental
• Jaw pain caused by infarction or osteomyelitis
• Labial anesthesia due to cranial neuropathies
• Mental nerve palsy due to vasoocclusive crisis
• Susceptibility to infection
• Hypomineralisation of dentin, abrupt alteration
• of dentinogenesis, calcified bodies in pulp chamber
• Hyper cementosis
• Osteoporosis of the jaw due to bone marrow hyperplasia
• Dense lamina dura
• Risk of use of local anesthesia with vasoconstrictor.
• Conservative approach to dentistry.
• Antibiotics before surgical proceedings.
• Inhalation sedation is safe provided that 100% oxygen is administered for at least 4 to 5
minutes at the end of the procedure to avoid diffusion hypoxia airway should be
maintained with, N2O-O2
• Where general anesthesia is unavoidable in hospital, maintenance of at least 30% oxygen
is mandatory, fluid maintenance is necessary and preoperative exchange transfusions may
be needed .
• Use desferrioxamine mesylate by subcutaneous infusion and hydroxyurea may be used to
raise HbF levels and reduce the frequency and severity of vaso-occlusive crisis.
• Minimize stress, because significant stress, decreases the child 's ability to oxygenate
tissues adequately.
• Emphasis on preventive dental health like brushing, fluorides, diet counselling and recall.
THALASSAEMIA:
Thalassaemia is inherited as an autosomal recessive disease and is characterized by a reduced
synthesis of one or more of the alpha/beta globin chains, leading to a decreased haemoglobin
production and a hypochromic microcytic anaemia . The thalassemias are frequently referred to
as major and minor forms, distinguished by their manifestation in either homozygous or
heterozygous state.
Thalassemia major is the most common .
Clinical features:
• Manifestation appears within the first yrear of life.
• Severe anemia, failure to thrive, poor appetite
• Hepatosplenomegaly, folate deficiency, growth
retardation, jaundice, recurrent ulcers.
• Hemosiderosis due to iron overload , following
frequent transfusion.
Oral changes:
• Hyperplasia of the marrow; leading to expansion of marrow cavity.
• Chipmunk facies with an enlargement of the maxilla and spacing of the
teeth, increased over jet protnision of the middle third of the face,
• Extreme tightness of the upper lip.
• Ocular hypertelorism, epicanthal folds and browning of the skin.
• Radiographic changes: 'chicken wire’ appearance of the alveolar bone,
delayed pneumatisation of the sinuses, hair-on-end appearance of the skull
• Large medullary cavities, thin cortices and generalized osteoporosis
• Pain and swelling of the parotid glands and atrophic candidiasis
Dental management of thalassaemia:
 Prevention of dental disease
 Avoidance of general anesthesia in the presence
of a chronic, severe anemia, cardiomyopathy and
endocrine problems
 Need for antibiotic prophylaxis
 Prevention methods against HIV and hepatitis
DISORDERS OF HEMOSTASIS:
Hemostasis is a series of events that culminates in
the spontaneous arrest of bleeding from a damaged
blood vessel. Without hemostasis, minor injuries
would be life-threatening and surgery would be
impossible.
Hemostasis occurs as a function of platelets,
vascular constriction, coagulation and fibrinolysis.
Coagulation occurs by the interaction of intrinsic
and extrinsic factors in the clotting cascade.
Hemophilia is a heredity blood disorder characterized by a deficiency of the plasma proteins
needed for normal clotting.
Oral Manifestations:
• Hemorrhage from many sites intraorally
• Gingival hemorrhage may be prolonged and
Massive
• Mouth lacerations,
• Presence of mandibular pseudotumor with
radiographic changes of tooth displacement
enlargement of bony structures , delicate
trabeculaes, and areas of radiolucency
• Caries and periodontal disease is high because
of poor oral hygiene
Complications:
- Inhibitors to factor VIII may develop
- Arthritis, degenerative joint disease
secondary to recurrent bleeding
- Blood borne viral infections like hepatitis
and HIV
Hemophilia:
Hemophilia A :
• 80%
• Factor viii deficiency
• X-linked recessive
Hemophilia B:
• 15%
• Factor IX deficiency
• X-linked recessive
Hemophilia C :
• Factor IX deficiency
• Autosommal recessive
Von willebrand’s disease :
• Von willebrand factor deficiency
• Autosomal dominant
• Spontaeous hemorrhage
• Hemarthrosis with pain, stiffness and
limited motion
• Chronic musculoskeletal problems
• Easy bruising
• Deep hematoma and hematuria
• Prolonged bleeding after surgery
• Epistaxis
 Normal range : 55-100%
Treatment Of Hemophilia – A:
• Replacement with plasma product containing factorVIII.
• Minor hemorrhage - 40% level of factor VIII
• Severe bleeding or major surgery - an initial level of 80% to 100%
followed by a maintenance level.
• Mild to moderate hemophilia A, l-deamino-8- D-arginine vasopressing
(DDAVP), a synthetic analog of vasopressin (antidiuretic harmone) can be
• used to raise factor VIII to hemostatic levels.
 Hemophiliacs with inhibitors of factor VIII, destroy factor VIII clotting activity, therefore
in such cases use prothrombin complex concentrates(rCC) or factor IX complex
concentrates, containing factors II, VII, IX and X can be given which can bypass factor
VIII inhibitors.
Treatment of Hemophilia – B:
Replacement with plasma product, 40%, high in factor IX as well as with prothrombin
complex concentrates (PCC). Fresh frozen plasma (FFP) is an emergency alternative.
Treatment of Hemophilia – C:
Since there is no concentrate containing factor XI, treatment requires the use of fresh
frozen or lyophilized plasma, along with local and topical measures.
Treatment of Von Willebrand’s Disease:
Treatment generally involves a Fresh frozen plasma or cryoprecipitate to increase
the factor VIII level and improve platelet adhesiveness.
DDAVP may be used to achieve hemostasis Local and topical measures
Dental Considerations:
• If the patient’s apprehension is significant, sedation is considered and also using acitomenophen,
propoxyphene hydrochloride, narcotic analgesics is required
• When general anesthesia is considered, oral intubation is preferred over nasal intubation,
• Intramuscular injections should be avoided.
• For patients who require deep scaling, initially do supra gingivally and then repeat after 7-14 days
after proper healing.
• Factor replacement before frenectomy and other periodontal surgeries.
• Eiectrosurgery is done because of the possibility of continued bleeding.
• Small carious lesions are restored without a factor concentrate replacement
• Use of 8A or 14A retainers are avoided but high speed vacuum and saliva ejectors are used.
• Use retraction cords during crown preparation
• Antibiotic prophylaxis before extraction.
• Use of topical hemostatic agents such as bovine thrombin., microfibrillar collagen hemostat,
• gelfoam, absorbable oxidized cellulose, cellulose bandage, collagen, bovine collagen bone
wax,surgicel.
• Instrumentation and filling beyond the apex should be avoided.
• Fixed appliances preferred than removable
• Careful adaptation and cementation of bands should be done but usually preformed bands and
brackets are preferred.
• DDVP increases fibrinolytic activity and should be used only in conjunction with an
antifibrmolytic agent.
PLATELET DISORDERS
• Platelet disorders can be divided into those caused by platelet dysfunction (qualitative) and those
caused by inadequate numbers of platelets (quantitative).
• Platelets normally number between 1,50,000 and 4,00.000/ cumm. of blood. Patients with counts less
than 1,00.000 have a moderate disease, and those with less than 50.000 have a severe
thrombocytopenia.
• When levels drop to 30,000 to 50,000 spontaneous bleeding occurs.
Idiopathic thrombocytopenic purpura
It is an autoimmune disorder in which there is an abnormal reduction in the normal circulating blood
platelets, affecting 4 in 100,000 children per year with a peak incidence of upto 4 years. It may be acute
in 80 – 90% of cases or chronic in 10-20%
Causes;
There are a variety of causes of
thrombocytopenia both reversible and
irreversible.
Reversible causes are:
- Drugs, transient bone marrow suppression owing
to cytotoxic chemotherapy.
- Gold salts, indomethacin, digitoxin, quinidine,
quinine, hydrochlorothiazides, alcohol, thiazine
diuretics, all these have been implicated in decreased
platelet production.
General Manifestation:
• Sudden onset of purpura
• Bruising
• Conjunctival and retinal hemorrhages
• Epistaxis
• Hemorrhages, bullae and vesicles of mucous membrane often occur
as a result of platelet count below 20,000/ cu mm
• No clinical bleeding or surgical hemorrhage is expected with greater
than 50,000/ cu mm of circulating platelets
• Spontaneous bleeding rarely occurs, until counts are below 10,000
to 20,000/ mm
Oral manifestations:
• Ecchymoses and frank hemorrhages
• Profuse gingival hemorrhages
• Petechiae also occur in the mucosa, and commonly
• palate appear with numerous, tiny, grouped clusters of
reddish spot only a millimeter or less in diameter
General and dental management:
• Elective dental treatment should be deferred until a platelet count is above 50,000/mm3
• Give steroids at a dose of 1 to 2 mg/kg to bring up the platelet level
• Splenectomy
• Replacement therapy usually involves platelet concentrate transfusion or whole blood transfusion
before oral surgical procedures, one unit of platelets usually increases a patient’s count by
6000/mm3
• Improve red cell mass, supply coagulation factors
• Use local measures of hemostasis
• Use IV immune globulin 19 kg/day twice before dental extraction
• Avoid blocks and extraction if possible during acute phase
• Avoid NSAID’s and aspirin 7 days preoperatively before any surgical procedures
RESPIRATORY DISORDERS
Approximately 33% of the chronic diseases seen in childhood are allergic
disorders.
Classification of allergic reactions might best be approached by identifying the
organ or organs attached
 Nose - Hay fever, allergic rhinitis
 Lungs - Asthama, allergic cough
 Skin and mucosa and subcutaneous tissue of mouth - urticarial, eczema, contact
dermatitis
BRONCHIAL ASTHMA
It is due to bronchospasm or hyperirritability of the trachea-bronchial tree.
 Most serious of allergic disorders in childhood.
 Often associated with specific allergen
 Predominant in URT
 Emotional stress
Patient is treated by:
1. Corticosteroids inhalators.
2. Bronchodilator.
3. Beta adrenergic stimulator.
Although destructive these are short lived and responsive to inhaled adrenergic aerosols,
epinephrine injection or theophillin given orally.
Clinical symptoms:
• Wheezing
• Hyperinflation
• Extended expiration
Narcotics have to be avoided
Chloral hydrate – safe clinical hypnotic
Chloral hydrate + hydroxyzine
Clinical management:
• Carry inhalers/nebulizers
• 1:1000 epinephrine subcutaneous
• Aminophylline with oxygen
• Upright position
• Asprin and NSAIDS are contraindicated
• Asthama attack – 100% oxygen and subcutaneous 0.3
ml of 1:1000 epinephrin
Food allergy:
Fish, crustaceans, nuts
Allergic Rhinitis:
• Pollen, dust, molds
• Hereditary component
Clinical features:
• Nasal obstruction, sneezing, itching and excessive lacrimation
• Polypoid changes of turbinates
 50% children with untreated allergic rhinitis develop asthama
Rubber dam is advocated for patients
with nasal obstruction with a
modification. With the youngs frame
this modification will shift the dam to
one side of the mouth
Strong correlation between alleries and
malocclusion: (Moyer)
- Hyper trophy of lower lip
- Hypotonicity of upper lip
- Open bite
- Flat face
- High v arch palate
- Orofacial dysfunctions
Cystic fibrosis
Cystic fibrosis is a monogenetic disorder (autosomal recessive) that presents as a multisystem
disease involving the exocrine glands not just the pancreas (micro obstruction leading to cystic
degeneration) but the sweat glands as well as the glands in the liver. It is characterized by chronic
obstruction, airway infection , maldigestion caused by pancreatic insufficiency, and other
abnormalities of the digestive tract. Sexual development is delayed and failure to thrive is
observed.
Defective gland secretions cause abnormal water and electrolyte transport across the epithelial
cells resulting in a chronic respiratory and G1 disease.
Over retention of mucus takes place in the lungs.
Oral Manifestations:
• Variable degree of discoloration of teeth due to tetracyclin therapy, enamel
hypoplasia
• Changes in salivary viscosity and composition
• High incidence of mouth breathing , open bite associated with chronic nasal
and sinus obstruction
• Dental development and eruption are delayed
• Oral ulceration
• Low incidence of dental caries due to frequent intake of antibiotics, increased
pH, buffer capacity of saliva, together with the increased levels of calcium and
phosphorus of saliva.
Dental Problems and Treatment:
• Complete medical history and consultation with the child's physician is imperative
• Patients can be treated in an upright position to enable the clearance of secretions.
• Anterior tooth discoloration can be treated with composite veneering or jacket crowns
• Sedation carries the risk of respiratory depression and a compromised airway
• General anesthesia should be considered , only if local anesthesia is not successful, with antibiotic
coverage when there is a significant pulmonary involvement
• Strict oral hygiene program and regular dental care if systemic conditions are under control
• Dietary' advice with sugar-free liquid antibiotic preparations.
Medical management:
• Recurrent infections are treated with antibiotics
• Regular physiotherapy with postural drainage of chest fluids.
• Advise high-calorie diet with supplemental pancreatic enzymes and vitamins with their meals
• Nasogastric intake if oral intake is not possible
DENTAL MANAGEMENT
Medical consultation.
1. Reduce stress & anxiety.
2. Local anesthesia can be administered
3. Sedation and General anesthesia can be given, if indicated
4. Drugs contraindicated: Aspirin,NSAIDS, penicillin
5. in case of asthmatic attack= administer 100% oxygen and seat the patient in upright position
6.Administer 0.3ml of 1:1000 epinephrine
LIVER DISORDERS
Advanced liver diseases include:
Liver cirrhosis - Jaundice
Potential complications:
1. Impaired drug detoxication e.g. sedative, analgesics, general anesthesia.
2. Bleeding disorders ( decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption).
3. Transmission of viral hepatitis.
DENTAL
MANAGEMENT
1) Medical consultation.
2) Avoid drugs metabolized in liver:
L.A - Lidocaine, Mepicaine
Sedatives - Valium
Antibiotics - Ampicillin
Analgesics - Aspirin
3) Vit.k ----- 10 mg/day before surgery.
4) G.A ------ cause bleeding.
ORAL
MANIFESTATION:
1. Reduced salivary flow
2. Burning mouth/tongue
3. Candidiasis
4. Altered taste
5. Progressive periodontitis
6 . Dental caries
7 . Oral neuropathies
8. Parotid enlargement
9. Sialosis
10. Delayed wound healing
11. Increased glucose content in gingival
crevicular fluid
HEPATITIS B
The main problems are: highly infective disease, bleeding tendency and drug sensitivity.
 Pure saliva does not contain HBsAg, but serum via gingival exudates does.
 Blood, plasma or serum can be infectious as little as 0.0000001 ml of HBsAg.
 Dentist should treat the patient within the current regulations for cross infection control.
 Patients with active acute hepatitis B should have dental treatment after complete recovery only,
which take about three months after symptomatic recovery.
 Needle stick injury can transmit the virus. An injection of hepatitis
B immuno- globulin (HBIG) within 24h of contact may protect from
developing hepatitis.
Patients who are hepatitis carriers. If a patient is found to be a hepatitis B carrier,
recommendations from the Center for Disease Control for avoiding transmission of infection
should be closely followed.
Some hepatitis carriers may have chronic active hepatitis, leading to compromised liver
function and interfering with hemostasis and drug metabolism. Physician consultation or
laboratory screening for liver function is advised.
Patients with signs or symptoms of hepatitis. Any patient having signs or symptoms suggesting
hepatitis should be referred to a physician, and should not be treated. If emergency care
becomes necessary, it should be provided as for the patient with acute disease.
ORAL COMPLICATIONS ASSOCIATED WITH HEPATITIS
Potential for abnormal bleeding
If surgery is required, it is advisable to:
Check the prothrombin time. If it is greater than 35 seconds, an injection of vitamin
K will usually correct the problem. This should be discussed with the patient’s
physician.
Monitor the bleeding time to check platelet function. If it is not less than 20 minutes,
the patient may require platelet replacement before surgery. This should also be
discussed with the patient’s physician. significant liver damage.
Childhood cancers
• Leading non accidental causes of pediatric mortality
• Types of childhood cancers are different from adults and are in the order of leukemia>brain and
spinal cord tumors > neuroblastoma > lymphoma > rhabdomyoma > bone cancers.
• Children diagnosed with cancer face unique oral and dental needs either as a manifestation of
underlying cause or due to cancer treatment.
• The survivors have their own set of unique oral challenges such as, xerostomia, neuropathy,
dental caries, trismus, mucosal fibrosis, graft versus host disease, microdontia, agenesis of teeth.
• Since leukemia, in particular ALL, AML are most common childhood malignancies.
Incidence
Occurs at 13 per 100,000 people per year. Acute lymphocytic leukemia is primarily a disease of children and young
adults.
Classification:
Leukemia is classified according to the morphology of the predominant abnormal w hite cells in the bone marrow.
They are further classified according to the progression of the clinical course as acute or chronic.
 Acute Lymphocytic Leukemia
 Acute Nonlymphocytic Leukemia
- Acute Myelocytic Leukemia
- Acute Monocytic or Myelomonocytic Leukemia
- Erythroleukemia
- Megakaryocytic Leukemia
 Chronic Myelocytic Leukemia
- Juvenile, Philadelphia chromosome negative
- Adult, Philadelphia chromosome positive
 Chronic Lymphocytic Leukemia
Etiology:
Cause in most patients is unknown , although both genetic and environmental factors are
important. They occur with increased frequency in children with syndromes like Down,
Bloom, Klinefelter, etc.
Ionizing radiation, chemicals like benzene, aromatic hydrocarbons are some of the
environmental factors that have been implicated in causing leukemia
Clinical manifestations:
Anemia , thrombocytopenia, increased WBC, neutropenia, abnormal bone marrow aspirate,
pallor, fever, tachycardia, adenopathy, gingival bleeding increased irritability, lethargy,
persistent fever, vague bone pain, hepatosplenomegaly, etc.
Oral Manifestations:
 Seen in 29% of children
 Regional lymphadenopathy, Gingival abnormalities, including hypertrophy and bleeding are
more common with nonlymphocytic leukemia whereas petechiae and ecchymoses are more
common in ALL.
 Gingiva is boggy, edematous, deep red and bleeds easily.
 Ulceration and pallor of oral mucosa.
 Rapid loosening of teeth due to necrosis of periodontal ligament.
 Occasionally cranial nerve palsies, lip paresthesia, jaw pain, gangrenous stomatitis.
 Manifestations in the jaw include loss of trabeculation, destruction of the crypts of developing
teeth, loss of lamina dura, widening of periodontal ligament space, and displacement of teeth
and tooth buds.
 Oral changes can be attributed to anemia, granulocytopenia and thrombocytopenia all of which
result from the replacement of the normal bone marrow elements by undifferentiated blast cells
or direct invasion of the tissue by the leukemic cells.
Dental Problems and Treatment:
 As infection is the primary cause of death in 80% of children with leukemia followed by bleeding, the primary
aim of dental treatment should be to prevent, control and remove oral infection, inflammation and
hemorrhage.
 Consult the child's physician prior to any treatment and take a complete medical history.
 Elective dental procedures are to be postponed if the child is not in first remission unless there is a nidus of
infection intraorally that could be a potential source of systemic infection.
 Avoid prescribing drugs like aspirin that can alter platelet function.
 As candidiasis is common , topical antifungals may need to be applied.
 Pain from ulcerative lesions can be relieved by application of topical obtundents.
 Deep lesions that bleed spontaneously – apply topical bovine thrombin.
 Pulp therapy on primary teeth is contraindicated and endodontic treatment on permanent teeth is
not recommended.
 If platelets are less than 20,000/ cubic mm dental treatment should not be undertaken without
prophylactic platelet transfusion .
 Managing of xerostomia through the use of sugarless sweets, sorbitol - based gum , artificial saliva
and topical fluoride
 If Absolute granulocyte count (AGC) is less than 1000/cubic mm elective dental treatment should be delayed.
 Avoid mouth brushing and substitute with moise gauze piece if platelet count is low.
DENTAL REHABILITATION OF A CHILD WITH ACUTE
LYMPHOCYTIC LEUKEMIA: A CASE REPORT RAED R GHOLMAN,1 EMTENAN
H FELEMBAN,2 AND OMAR AES EL MELIGY3
A 6-year-old Saudi male patient was presented to King Abdulaziz Medical City (KAMC) dental clinic in Jeddah,
Saudi Arabia. His father reported that he wants to treat his son's teeth since most of them are carious and currently
his son is complaining from severe pain related to his lower left teeth. The medical history showed that the child was
diagnosed with ALL one year ago and he is currently in the maintenance phase of chemotherapy taking oral
chemotherapeutic medications. Owing to his medical condition and the father's request, his treatment was planned to
be completed under general anesthesia (GA). The patient was referred to his physician (hematologist/oncologist) for
consultation and clearance for dental rehabilitation under GA. The patient's preoperative hematological parameters
revealed absolute neutrophil count (ANC) of 4,500/mm3 and platelets count of 349,000/mm3.
Caries risk assessment was performed by asking the parents about their child's diet, oral hygiene, and lifestyle
habits. The patient was classified as high-caries-risk patient based on caries-risk assessment tool (CRAT). Extraoral
examination of the patient revealed a normal symmetry of the face, pale skin, dry lips, and enlarged submandibular
lymph nodes. Intraoral examination revealed poor oral hygiene with mild plaque accumulation at the gingival
margins along with the buccal and lingual surfaces of teeth, which had resulted in marginal gingivitis in addition to
bleeding on probing.
(1) full coverage of carious teeth # 55, 64 and 65 using stainless
steel crowns (SSCs); (2) pulpotomy performed followed by SSCs
in teeth # 54 and 84 (According to AAPD, pulp therapy is a
relative contraindication in children with malignancies, but the
decision to perform pulp therapy was due to the stable laboratory
parameters of the patient during the previous three months in
addition he was in maintenance phase of chemotherapy); (3)
composite restoration in teeth # 51, 53, 61, 63, 72, and 73; (4)
extraction of badly decayed teeth # 52, 62, 74, 75, and 85
no space maintenance was planned to be done until the patient
receive the full dose of his chemotherapy, since immunity might
be compromised and the appliance might act as a source of
infection.
DIABETUS MELLITUS
It is characterized by persistent increase of blood glucose level.
Body does not produce sufficient amount of insulin or the patient does not respond
to the insulin that is produced.
Types :
1. IDDM(Type1) : failure to produce insulin by the body
2. NIDDM(Type 2) : Insulin resistance
3. GDM ( Gestational DM) : pregnant women with a previous history of diabetes.
May preceed development of type 2 diabetes
Oral manifestation:
1. Gingivitis
2. Alveolar bone resorption
3. Xerostomia
4. Delayed wound healing
5. Pulpitis in non carious tooth
6. Burning sensation in tongue
7. Acetone smell in breath
Dental management:
 Comprehensive history, screening
 Appointment –early mornings, stress free, atraumatic as possible
 Premeditation
 Local anesthesia- use of vasoconstrictors
 vital pulp therapy – preferred to extractions
 Use of pulp capping and pulpotomy is questionable
in a child with uncontrolled diabetes.
• Dietary control is often difficult to enforce which encourages frequent snacking , the elevated
salivary glucose, decreased salivary flow may be responsible for promoting dental caries in
the uncontrolled patient.
• In children with poorly controlled diabetes, the levels of severe gingivitis and periodontitis are
higher due to decreased salivary flow or elevated salivaiy glucose in these patients.
• The incidence of periodontitis increases among diabetic subjects after puberty which has been
suggested due to disturbed local polymorphic neutrophil chemotaxis, combined with increased
plaque, and phagocytosis compromise may explain the increased levels of gingivitis found in
children with poorly controlled diabetes.
RENAL FAILURE
Progressive and irreversible decline in the total number of functioning
nephrons, with a conconmitant decline in glomerular filtration rate.
Classification:
 Acute
 Chronic
 Acquired
 Congenital
CHRONIC RENAL FAILURE
Causes:
Congenital abnormalities of kidney and urinary tract to produce before 5 years. A fter 5 years
glomerular and hereditary renal diseases become more prominent.
Clinical manifestation:
 Facial puffiness
 Muscle weakness and wasting
 Itching
 Growth retardation
 Uraemic breath
ORAL MANISFESTATIONS
1. Mucosal pallor
2. Candidiasis & oral petechae
3. Extrinsic discoloration of teeth
4. Enamel hypoplasia
5. Tooth mobility & premature tooth loss
6. Oral calcifications
7. Total/partial loss of lamina dura
8. Pulp calcifications
9. Root resorptions
Dental management:
1. Consultation with the patient’s physician
2. When surgical procedures are considered- assess bleeding time
3. Avoid hypertension drugs
4. Optimal treatment time is 1 day before dialysis
5. Increased need for oral prophylaxis
6. Acute renal diseases – postpone elective procedures
7. Fluid/electrolyte imbalance should be maintained by managing those oral
diseases like herpetic stomatitis, severe caries, cellulitis that can compromise a
child’s fluid intake.
8. Antibiotic prophylaxis before dental treatment to prevent bacteremia
AIDS
Definition: Presence of antibodies to HIV and opportunistic infections.
Etiology: Caused by human immunodeficiency virus(HIV), RNA retro virus
2 groups:
 Human T lymphotrophic retrovirus (HTLV I and HTLV III)
 Human immune deficiency virus (HIV I and HIV II)
HIV I- commonest cause of HIV throughout the world.
Popovic identified HTLV III as the causative agents if AIDS.
MODES OF TRANSMISSION
A) Parenteral
1. Needle sharing among drug abusers
2. HIV infected patient to health care worker
3. Patients with haemophilia, haematologic disorders, major
surgeries requiring blood transfusions
4. Tissue or organ transplants from HIV infected doners
5. Household contacts without establishing sexual or drug
related behavoiurs
6. Health care workers to the patients
B) Perinatal transmission
Occurs before, during or shortly after birth
1. Prenatal and postnatal transfer from HIV infected mother to the baby during 8-
12 weeks of gestation
2. during blood transfusion from infected mother during or shorty after birth
3. mother was infected during unsafe sex with an infected partner or during breast
feeding
4. Transmission during cesarean delivery
C) Sexual transmission
1. Infants born to mothers who are prostitutes
2. Unprotected homosexual and heterosexual intercourse
3. Frequent foreign travel with sexual contacts
D) Body fluid transmission
Blood, Semen, breast milk, tears, sweat, urine, vaginal or cervical secretions –
implicated in the transmission
ORAL MANIFESTATIONS OF HIV INFECTION
Bacterial Infections: Gingivo-perodotal diseases
Fungal Infections:
 Epstein –Bar virus
 Herpes simplex virus
 Varicella- Zoster virus
 Cytomegalovirus
Neoplasms
Kaposi’s sarcoma
Lymphoma
Other neoplasm
Other oral lesions
Oral ulcers
Salivary gland enlargement
Diagnosis:
Diagnosis of pediatric AIDS is by clinical screening and serologic confirmation. World Health
Organization has defined pediatric AIDS as an infant or child presenting with at least a major
criterion along with at least 2 minor criteria in the absence of any immunosuppression.
Major signs
• Chronic diarrhoea for more than one month
• Prolonged fever for more than one month
• Weight loss
Minor Signs:
• Oropharyngeal conditions
• Repeated cough for more than one month
• Generalized lymphadenopathy
• Generalized dermatitis
• Maternal HIV infection
Typical pediatric findings (Rubenstein , 1986):
• Pulmonary lymphoid hyperplasia
• Salivary gland enlargement
• Pyogenic bacterial infection such as otitis media
• Developmental craniofacial features
• Chronic recurrent diarrhoea
• Hepatosplenomegaly
• Chronic pneumonitis
• Failure to thrive
• Progressive encephalopathy
Candidiasis:
Recurrent candidiasis, which is persistent for long
periods and often resistant to conventional antifungal
therapy, is a frequent oral manifestation in pediatric HIV
infection/AIDS. Oral candidiasis in HIV infected children
is variable and is manifested as pseudomembranous plaques,
erythematous patches, angular cheilitis , hyperplastic
plaques.
Angular cheilitis appears as fissures or cracks at
the commissures of the lips.
Treatment
The lesions may subside or disappear with treatment,
but relapse is common. The treatment can be
either topical or systemic
Viral Infections:
In HIV - infection, several viruses are able to colonize or react, producing lesions in the mouth.
These
include herpes - group viruses and papillomaviruses.
Herpes simplex
Herpes simplex is caused by herpes simplex virus I (HS V) and it recurs frequently in children
with advanced HIV disease. The virus become latent in trigeminal ganglion and any sort of
stimulation to the sensory nerve may reactivate the virus along the sensory' nerves to the mucosal
or the epithelial surfaces interrelated by the reactivated ganglion leading to recurrent oral herpes
lesions.
Herpes Zoster
Herpes zoster is caused by varicella zoster virus (HVZ) due to reactivation of the virus along the
cutaneous surface ganglion becauseof immunosuppression
Treatment of viral infections:
Herpetic lesions may be treated with systemic doses of acyclovir ranging from 1 to 2 gm
daily taken, orally or IV in individuals with more severe oropharyngeal lesions or in those
unable to swallow.
Bacterial Infection:
Oral lesions of bacterial origin may include mycobacterium aviumintracellulare and Klebsiella
pneumoniae.
HIV associated gingivitis ( HFV-G ) and HIV associated periodontitis (HIV-P)
Linear gingival erythema (LGE) and ANUG like lesion called as necrotizing ulcerative
periodontitis have been reported in children
Treatment:
• Aggressive curratage
• Peridex (0.12% chlorhexidine digluconate)rinses three times daily
• Antibiotic treatment
Recurrent apthous ulcers in HIV infected persons:
They appear as a well circumscribed ulcers with an erythematous margin. The ulcers of a minor
form appear as 0.5 to 1 cm, herpetiform appear in clusters of small ulcers usually on soft palate and
oropharynx major ulcers appear as large necrotic ulcers of 2-4cm which are painful and last
for several weeks.
Treatment:
Fluconomide ointment (0.5%)
Orabase 3-6 times/day
Dexamethasone 0.5 mg/ml
Petechiae:
20 -30% of HIV infected patients may develop thrombocytopenic purpura
at any age. oral lesions appear as small blood filled purpuric lesions.
Causes:
HIV induced autoantibodies
Megakaryocyte infection
Aplasia
AZT therapy which may suppress the bone marrow
MANAGEMENT OF AIDS
PREVENTION
 Barrier techniques
 Proper sterilization
- HIV is sensitive to autoclaving at 121⁰C for 15min at 1 atm pressure
- Dry heat Sterilization upto 170⁰C
- Viruses can be inactivated by heating lyophilized factor
Disinfection of innate objects:
- Calcium hypochlorite
- 0.2% Na hypochlorite
- 10 min at room temperature in 10% bleach, 50% ethanol and 3% hydrogen peroxide.
DRUGS USED FOR AIDS
 Acyclovir 1-2 g daily once orally or IV
 Zidovudine(AZT) – attacks the virus through the enzyme reverse transcriptase
Other drugs:
1. Dideoxycytoxine(ddc)
2. Dideoxyinosis (ddI)
3. Stavudine (d4T)
 Use of protese inhibitors- Saquinavir, Indinavir & Ritonivir
 Triple drug therapy:
AZT combination with indinavir and 3 TC(lamivudine) to reduce HIV copies in the plasma
of infected patients(to treat not to cure)
AIDS VACCINE
A lot of research – not successful
Due to continuous mutation of genes of the virus
Moreover HIV viruses varies across regions as well as individuals.
Practically not feasible to develop vaccine for each individual
CONCLUSION
REFERENCES
 Pediatric dentistry – scientific foundations and clinical practice – Stewart and Barber
 Textbook of Pedodontics. Shobha Tandon. 2nd edn.
 Dentistry for the child and adolescence. 9th edition. Mc Donald Avery and Dean
AAE Quick Reference Guide on Antibiotic Prophylaxis 2017 Update
Arulpari Mahalingam et al., Dental Management of A Child With Congenital Heart Disease
- A Case Report
Gholman RR, Felemban EH, El Meligy OAES. Dental Rehabilitation of a Child with
Acute Lymphocytic Leukemia: A Case Report. Int J Clin Pediatr Dent 2019;12(6):582–586.
 Dental Management of Medically Compromised Patients. Operational Guide for School
Oral Health Program
THANK YOU

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Management of medically compromised patients

  • 1. MANAGEMENT OF MEDICALLY COMPROMISED CHILDREN KARISHMA.S III MDS
  • 2. CONTENTS INTRODUCTION TYPES OF MEDICALLY COMPROMISED CONDITIONS CARDIOVASCULAR DISEASES DENTAL TREATMENT CONSIDERATIONS ANTIBIOTIC PROPHYLAXIS OTHER MEDICALLY COMPROMISED CONDITIONS REFERENCES
  • 3. SYSTEMIC DISEASES INCLUDE: 1. Cardiovascular diseases 2. Respiratory diseases 3. Liver diseases 4. Endocrine diseases 5. Renal diseases 6. Sexually transmitted diseases(AIDS) 7. Blood diseases 8. Childhood cancers
  • 4. INTRODUCTION  Patients with medically compromised conditions suffers from a certain systemic condition which puts him/her at risk from undergoing regular treatment.  The majority of medically compromised patients need oral healthcare, a working knowledge of the multitude of medically complex conditions is critical for dental professionals.  This knowledge is necessary to help prevent, minimize, and alert clinicians to possiblily adverse side effects potentially associated with procedures and drugs used in dentistry.  Take precautions to enable the patient to undergo treatment without complications.
  • 5. PREOPERATIVE MANAGEMENT: 1. Good detailed medical history of the patient should be taken and updated during each visit. 2. The medical condition should be mentioned in the consent form. 3. Any problem in previous dental treatment should be reported precisely. 4. Report any previous hospitalization of the patient and the reason for it. 5. Early morning appointments are preferred except in cardiac patients which are preferred to be in late morning. 6. In school oral health program, severe medically compromised patients are treated at the program centers
  • 6. THE MEDICALLY COMPROMISED PATIENT Patient Assessment  Category I: Healthy patient  Category II: Medical conditions requiring schedule changes  Category III: Medical conditions requiring significant modifications in dental treatment  Category IV: Medical conditions requiring major modifications in dental treatment  Category V: Serious medical conditions
  • 9. RHEUMATIC HEART DISEASE  It is an acute inflammatory condition, due to strep. A  Rare in infancy  Commonly appears between 6 – 15 years.  Pharngitis infection following sore throat, result in scaring & calcification of valves followed by valvular stenosis.
  • 10. DENTAL TREATMENT CONSIDERATIONS • Careful dental evaluation and treatments have to be completed before surgery • Preventive dental program • Cardiologist consultation • Antibiotic prophylaxis • Dental treatment should be completed 3-4 weeks of the planned surgery to allow healing and normal micro flora DENTAL PROBLEMS AND TREATMENT • Pulp therapy < extraction and space maintainer • Permanent dentition – endodontic therapy after careful evalyation • Oral sedation is beneficial • Orthodontic treatment under antibiotic prophylaxis • Cessation of anticoagulation therapy • GA for severe debilitationg heart disease.
  • 11. DENTAL PROCEDURES FOR WHICH ENDOCARDITIS PROPHYLAXIS IS ADVISIBLE FOR HIGHEST RISK PATIENTS All dental procedures that involve manipulation of gingival tissue or the periapical region of the teeth or perforation of the oral mucosa. CARDIAC CONDITIONS ASSOCIATED WITH HIGHEST RISK OF ADVERSE OUTCOME FROM ENDOCARDITIS FOR WHICH PROPHYLAXIS WITH DENTAL PROCEDURES IS ADVISIBLE 1. Prosthetic cardiac valve or prosthetic material used for cardiac repair. 2. Previous infective endocarditis 3. Congenital heart diseases (CHD) 4. Unrepaired cyanotic CHD 5. Completely repaired congenital heart defect with prosthetic material/ device 6. Repaired CHD 7. Cardiac transplantation
  • 12. DENTAL MANAGEMENT OF A CHILD WITH CONGENITAL HEART DISEASE - A CASE REPORT Arulpari Mahalingam1., Kirthivasan Vaidyanathan2., Paavai Ilango3* Sanjay Cherian4 and Dhanapriya5 A 5-year-old old female child diagnosed with congenital heart disease soon after birth was referred for dental opinion prior to cardiac surgery. Her medical history revealed that she had dyspnoea on exertion since birth and she was found to have TOF (Ventricular septal defect, Patent ductus arteriosus, Supramitral membrane) with severe pulmonary artery hypertension. On intraoral examination, she was found to have poor oral hygiene and multiple deep carious lesions in relation to 51, 52, 54, 61, 62, 64, 73, 74, 75, 84 and 85. The patient was an uncooperative patient with high levels of dental anxiety. The child was continued on her routine cardiac medications. The treatment plan was divided into preventive treatment and corrective treatment procedures. In the preventive treatment protocol, fluoride prophylaxis, diet counseling and oral hygiene instructions were given to the child and her parents. The corrective treatment plan included pulpectomy in relation to 51,52,61,62,74,75, 84, 85, pulpotomy in relation to 54, 64 and composite restoration in relation to 73. A written informed consent and opinion was obtained from the parents and clearance was obtained from the pediatric cardiologist. Antibiotic prophylaxis of Amoxicillin 50mg/kg body weight was given one hour prior to the procedure.
  • 13. Hawary et al showed that CHD leads to alteration in the structure of enamel and dentin of deciduous incisors at an ultrastructural level. It also leads to a significant decrease in mineral content (Ca and P) of deciduous enamel and dentin when compared to healthy controls, rendering the dentition at increased risk of dental caries.
  • 14. AAPD guidelines 2011 Children: (5–10 years)1/2 adult (< 5 years) 1/4 adult Special Circumstances The 2007 AHA guidelines state that an antibiotic for prophylaxis should be administered in a single dose before the procedure. However, in the event that the dosage of antibiotic is inadvertently not administered before the procedure, it may be administered up to two hours after the procedure. For patients already receiving an antibiotic that is also recommended for IE prophylaxis, then a drug should be selected from a different class AAE Quick Reference Guide on Antibiotic Prophylaxis 2017 U
  • 16. Haematological disorders may be broadly classified into three groups; 1. Red cell disorders 2.White cell disorders 3.Disorders of homeostasis, including platelets and coagulation factors RED CELL DISORDERS: Anemia is defined as reduction in the volume of red blood cells (haematocrit) in the packed cell volume (PCV) or in the concentration of hemoglobin in peripheral venous blood. The various types of anemias are as follows:
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  • 22. Sickle - Cell Anemia: It is inherited as an autosomal recessive disorder due to an abnormal hemoglobin known as “ hemoglobin S ” hypoxia induced distortion of the erythrocytes into a sickled shape occurs. The sickling phenomenon which occurs only in a reduced oxygen tension causes both a chronic compensated haemolytic anemia and vaso- occlusive crisis, resulting in pain and tissue damage caused due to infarction.
  • 23. Clinical features General features • Anemia due to haemolysis • Aplastic crisis • Impaired growth • Skeletal deformities Dental • Jaw pain caused by infarction or osteomyelitis • Labial anesthesia due to cranial neuropathies • Mental nerve palsy due to vasoocclusive crisis • Susceptibility to infection • Hypomineralisation of dentin, abrupt alteration • of dentinogenesis, calcified bodies in pulp chamber • Hyper cementosis • Osteoporosis of the jaw due to bone marrow hyperplasia • Dense lamina dura
  • 24. • Risk of use of local anesthesia with vasoconstrictor. • Conservative approach to dentistry. • Antibiotics before surgical proceedings. • Inhalation sedation is safe provided that 100% oxygen is administered for at least 4 to 5 minutes at the end of the procedure to avoid diffusion hypoxia airway should be maintained with, N2O-O2 • Where general anesthesia is unavoidable in hospital, maintenance of at least 30% oxygen is mandatory, fluid maintenance is necessary and preoperative exchange transfusions may be needed . • Use desferrioxamine mesylate by subcutaneous infusion and hydroxyurea may be used to raise HbF levels and reduce the frequency and severity of vaso-occlusive crisis. • Minimize stress, because significant stress, decreases the child 's ability to oxygenate tissues adequately. • Emphasis on preventive dental health like brushing, fluorides, diet counselling and recall.
  • 25. THALASSAEMIA: Thalassaemia is inherited as an autosomal recessive disease and is characterized by a reduced synthesis of one or more of the alpha/beta globin chains, leading to a decreased haemoglobin production and a hypochromic microcytic anaemia . The thalassemias are frequently referred to as major and minor forms, distinguished by their manifestation in either homozygous or heterozygous state. Thalassemia major is the most common .
  • 26. Clinical features: • Manifestation appears within the first yrear of life. • Severe anemia, failure to thrive, poor appetite • Hepatosplenomegaly, folate deficiency, growth retardation, jaundice, recurrent ulcers. • Hemosiderosis due to iron overload , following frequent transfusion. Oral changes: • Hyperplasia of the marrow; leading to expansion of marrow cavity. • Chipmunk facies with an enlargement of the maxilla and spacing of the teeth, increased over jet protnision of the middle third of the face, • Extreme tightness of the upper lip. • Ocular hypertelorism, epicanthal folds and browning of the skin. • Radiographic changes: 'chicken wire’ appearance of the alveolar bone, delayed pneumatisation of the sinuses, hair-on-end appearance of the skull • Large medullary cavities, thin cortices and generalized osteoporosis • Pain and swelling of the parotid glands and atrophic candidiasis
  • 27. Dental management of thalassaemia:  Prevention of dental disease  Avoidance of general anesthesia in the presence of a chronic, severe anemia, cardiomyopathy and endocrine problems  Need for antibiotic prophylaxis  Prevention methods against HIV and hepatitis
  • 28. DISORDERS OF HEMOSTASIS: Hemostasis is a series of events that culminates in the spontaneous arrest of bleeding from a damaged blood vessel. Without hemostasis, minor injuries would be life-threatening and surgery would be impossible. Hemostasis occurs as a function of platelets, vascular constriction, coagulation and fibrinolysis. Coagulation occurs by the interaction of intrinsic and extrinsic factors in the clotting cascade.
  • 29. Hemophilia is a heredity blood disorder characterized by a deficiency of the plasma proteins needed for normal clotting. Oral Manifestations: • Hemorrhage from many sites intraorally • Gingival hemorrhage may be prolonged and Massive • Mouth lacerations, • Presence of mandibular pseudotumor with radiographic changes of tooth displacement enlargement of bony structures , delicate trabeculaes, and areas of radiolucency • Caries and periodontal disease is high because of poor oral hygiene Complications: - Inhibitors to factor VIII may develop - Arthritis, degenerative joint disease secondary to recurrent bleeding - Blood borne viral infections like hepatitis and HIV Hemophilia:
  • 30. Hemophilia A : • 80% • Factor viii deficiency • X-linked recessive Hemophilia B: • 15% • Factor IX deficiency • X-linked recessive Hemophilia C : • Factor IX deficiency • Autosommal recessive Von willebrand’s disease : • Von willebrand factor deficiency • Autosomal dominant • Spontaeous hemorrhage • Hemarthrosis with pain, stiffness and limited motion • Chronic musculoskeletal problems • Easy bruising • Deep hematoma and hematuria • Prolonged bleeding after surgery • Epistaxis
  • 31.  Normal range : 55-100%
  • 32. Treatment Of Hemophilia – A: • Replacement with plasma product containing factorVIII. • Minor hemorrhage - 40% level of factor VIII • Severe bleeding or major surgery - an initial level of 80% to 100% followed by a maintenance level. • Mild to moderate hemophilia A, l-deamino-8- D-arginine vasopressing (DDAVP), a synthetic analog of vasopressin (antidiuretic harmone) can be • used to raise factor VIII to hemostatic levels.  Hemophiliacs with inhibitors of factor VIII, destroy factor VIII clotting activity, therefore in such cases use prothrombin complex concentrates(rCC) or factor IX complex concentrates, containing factors II, VII, IX and X can be given which can bypass factor VIII inhibitors.
  • 33. Treatment of Hemophilia – B: Replacement with plasma product, 40%, high in factor IX as well as with prothrombin complex concentrates (PCC). Fresh frozen plasma (FFP) is an emergency alternative. Treatment of Hemophilia – C: Since there is no concentrate containing factor XI, treatment requires the use of fresh frozen or lyophilized plasma, along with local and topical measures. Treatment of Von Willebrand’s Disease: Treatment generally involves a Fresh frozen plasma or cryoprecipitate to increase the factor VIII level and improve platelet adhesiveness. DDAVP may be used to achieve hemostasis Local and topical measures
  • 34. Dental Considerations: • If the patient’s apprehension is significant, sedation is considered and also using acitomenophen, propoxyphene hydrochloride, narcotic analgesics is required • When general anesthesia is considered, oral intubation is preferred over nasal intubation, • Intramuscular injections should be avoided. • For patients who require deep scaling, initially do supra gingivally and then repeat after 7-14 days after proper healing. • Factor replacement before frenectomy and other periodontal surgeries. • Eiectrosurgery is done because of the possibility of continued bleeding. • Small carious lesions are restored without a factor concentrate replacement • Use of 8A or 14A retainers are avoided but high speed vacuum and saliva ejectors are used. • Use retraction cords during crown preparation
  • 35. • Antibiotic prophylaxis before extraction. • Use of topical hemostatic agents such as bovine thrombin., microfibrillar collagen hemostat, • gelfoam, absorbable oxidized cellulose, cellulose bandage, collagen, bovine collagen bone wax,surgicel. • Instrumentation and filling beyond the apex should be avoided. • Fixed appliances preferred than removable • Careful adaptation and cementation of bands should be done but usually preformed bands and brackets are preferred. • DDVP increases fibrinolytic activity and should be used only in conjunction with an antifibrmolytic agent.
  • 36. PLATELET DISORDERS • Platelet disorders can be divided into those caused by platelet dysfunction (qualitative) and those caused by inadequate numbers of platelets (quantitative). • Platelets normally number between 1,50,000 and 4,00.000/ cumm. of blood. Patients with counts less than 1,00.000 have a moderate disease, and those with less than 50.000 have a severe thrombocytopenia. • When levels drop to 30,000 to 50,000 spontaneous bleeding occurs.
  • 37. Idiopathic thrombocytopenic purpura It is an autoimmune disorder in which there is an abnormal reduction in the normal circulating blood platelets, affecting 4 in 100,000 children per year with a peak incidence of upto 4 years. It may be acute in 80 – 90% of cases or chronic in 10-20% Causes; There are a variety of causes of thrombocytopenia both reversible and irreversible. Reversible causes are: - Drugs, transient bone marrow suppression owing to cytotoxic chemotherapy. - Gold salts, indomethacin, digitoxin, quinidine, quinine, hydrochlorothiazides, alcohol, thiazine diuretics, all these have been implicated in decreased platelet production.
  • 38. General Manifestation: • Sudden onset of purpura • Bruising • Conjunctival and retinal hemorrhages • Epistaxis • Hemorrhages, bullae and vesicles of mucous membrane often occur as a result of platelet count below 20,000/ cu mm • No clinical bleeding or surgical hemorrhage is expected with greater than 50,000/ cu mm of circulating platelets • Spontaneous bleeding rarely occurs, until counts are below 10,000 to 20,000/ mm Oral manifestations: • Ecchymoses and frank hemorrhages • Profuse gingival hemorrhages • Petechiae also occur in the mucosa, and commonly • palate appear with numerous, tiny, grouped clusters of reddish spot only a millimeter or less in diameter
  • 39. General and dental management: • Elective dental treatment should be deferred until a platelet count is above 50,000/mm3 • Give steroids at a dose of 1 to 2 mg/kg to bring up the platelet level • Splenectomy • Replacement therapy usually involves platelet concentrate transfusion or whole blood transfusion before oral surgical procedures, one unit of platelets usually increases a patient’s count by 6000/mm3 • Improve red cell mass, supply coagulation factors • Use local measures of hemostasis • Use IV immune globulin 19 kg/day twice before dental extraction • Avoid blocks and extraction if possible during acute phase • Avoid NSAID’s and aspirin 7 days preoperatively before any surgical procedures
  • 40. RESPIRATORY DISORDERS Approximately 33% of the chronic diseases seen in childhood are allergic disorders. Classification of allergic reactions might best be approached by identifying the organ or organs attached  Nose - Hay fever, allergic rhinitis  Lungs - Asthama, allergic cough  Skin and mucosa and subcutaneous tissue of mouth - urticarial, eczema, contact dermatitis
  • 41. BRONCHIAL ASTHMA It is due to bronchospasm or hyperirritability of the trachea-bronchial tree.  Most serious of allergic disorders in childhood.  Often associated with specific allergen  Predominant in URT  Emotional stress Patient is treated by: 1. Corticosteroids inhalators. 2. Bronchodilator. 3. Beta adrenergic stimulator.
  • 42. Although destructive these are short lived and responsive to inhaled adrenergic aerosols, epinephrine injection or theophillin given orally. Clinical symptoms: • Wheezing • Hyperinflation • Extended expiration Narcotics have to be avoided Chloral hydrate – safe clinical hypnotic Chloral hydrate + hydroxyzine Clinical management: • Carry inhalers/nebulizers • 1:1000 epinephrine subcutaneous • Aminophylline with oxygen • Upright position • Asprin and NSAIDS are contraindicated • Asthama attack – 100% oxygen and subcutaneous 0.3 ml of 1:1000 epinephrin
  • 43. Food allergy: Fish, crustaceans, nuts Allergic Rhinitis: • Pollen, dust, molds • Hereditary component Clinical features: • Nasal obstruction, sneezing, itching and excessive lacrimation • Polypoid changes of turbinates  50% children with untreated allergic rhinitis develop asthama Rubber dam is advocated for patients with nasal obstruction with a modification. With the youngs frame this modification will shift the dam to one side of the mouth Strong correlation between alleries and malocclusion: (Moyer) - Hyper trophy of lower lip - Hypotonicity of upper lip - Open bite - Flat face - High v arch palate - Orofacial dysfunctions
  • 44. Cystic fibrosis Cystic fibrosis is a monogenetic disorder (autosomal recessive) that presents as a multisystem disease involving the exocrine glands not just the pancreas (micro obstruction leading to cystic degeneration) but the sweat glands as well as the glands in the liver. It is characterized by chronic obstruction, airway infection , maldigestion caused by pancreatic insufficiency, and other abnormalities of the digestive tract. Sexual development is delayed and failure to thrive is observed. Defective gland secretions cause abnormal water and electrolyte transport across the epithelial cells resulting in a chronic respiratory and G1 disease. Over retention of mucus takes place in the lungs.
  • 45. Oral Manifestations: • Variable degree of discoloration of teeth due to tetracyclin therapy, enamel hypoplasia • Changes in salivary viscosity and composition • High incidence of mouth breathing , open bite associated with chronic nasal and sinus obstruction • Dental development and eruption are delayed • Oral ulceration • Low incidence of dental caries due to frequent intake of antibiotics, increased pH, buffer capacity of saliva, together with the increased levels of calcium and phosphorus of saliva.
  • 46. Dental Problems and Treatment: • Complete medical history and consultation with the child's physician is imperative • Patients can be treated in an upright position to enable the clearance of secretions. • Anterior tooth discoloration can be treated with composite veneering or jacket crowns • Sedation carries the risk of respiratory depression and a compromised airway • General anesthesia should be considered , only if local anesthesia is not successful, with antibiotic coverage when there is a significant pulmonary involvement • Strict oral hygiene program and regular dental care if systemic conditions are under control • Dietary' advice with sugar-free liquid antibiotic preparations. Medical management: • Recurrent infections are treated with antibiotics • Regular physiotherapy with postural drainage of chest fluids. • Advise high-calorie diet with supplemental pancreatic enzymes and vitamins with their meals • Nasogastric intake if oral intake is not possible
  • 47. DENTAL MANAGEMENT Medical consultation. 1. Reduce stress & anxiety. 2. Local anesthesia can be administered 3. Sedation and General anesthesia can be given, if indicated 4. Drugs contraindicated: Aspirin,NSAIDS, penicillin 5. in case of asthmatic attack= administer 100% oxygen and seat the patient in upright position 6.Administer 0.3ml of 1:1000 epinephrine
  • 48. LIVER DISORDERS Advanced liver diseases include: Liver cirrhosis - Jaundice Potential complications: 1. Impaired drug detoxication e.g. sedative, analgesics, general anesthesia. 2. Bleeding disorders ( decrease clotting factors, excess fibrinolysis, impaired vitamin K absorption). 3. Transmission of viral hepatitis.
  • 49. DENTAL MANAGEMENT 1) Medical consultation. 2) Avoid drugs metabolized in liver: L.A - Lidocaine, Mepicaine Sedatives - Valium Antibiotics - Ampicillin Analgesics - Aspirin 3) Vit.k ----- 10 mg/day before surgery. 4) G.A ------ cause bleeding. ORAL MANIFESTATION: 1. Reduced salivary flow 2. Burning mouth/tongue 3. Candidiasis 4. Altered taste 5. Progressive periodontitis 6 . Dental caries 7 . Oral neuropathies 8. Parotid enlargement 9. Sialosis 10. Delayed wound healing 11. Increased glucose content in gingival crevicular fluid
  • 50. HEPATITIS B The main problems are: highly infective disease, bleeding tendency and drug sensitivity.  Pure saliva does not contain HBsAg, but serum via gingival exudates does.  Blood, plasma or serum can be infectious as little as 0.0000001 ml of HBsAg.  Dentist should treat the patient within the current regulations for cross infection control.  Patients with active acute hepatitis B should have dental treatment after complete recovery only, which take about three months after symptomatic recovery.  Needle stick injury can transmit the virus. An injection of hepatitis B immuno- globulin (HBIG) within 24h of contact may protect from developing hepatitis.
  • 51. Patients who are hepatitis carriers. If a patient is found to be a hepatitis B carrier, recommendations from the Center for Disease Control for avoiding transmission of infection should be closely followed. Some hepatitis carriers may have chronic active hepatitis, leading to compromised liver function and interfering with hemostasis and drug metabolism. Physician consultation or laboratory screening for liver function is advised. Patients with signs or symptoms of hepatitis. Any patient having signs or symptoms suggesting hepatitis should be referred to a physician, and should not be treated. If emergency care becomes necessary, it should be provided as for the patient with acute disease.
  • 52. ORAL COMPLICATIONS ASSOCIATED WITH HEPATITIS Potential for abnormal bleeding If surgery is required, it is advisable to: Check the prothrombin time. If it is greater than 35 seconds, an injection of vitamin K will usually correct the problem. This should be discussed with the patient’s physician. Monitor the bleeding time to check platelet function. If it is not less than 20 minutes, the patient may require platelet replacement before surgery. This should also be discussed with the patient’s physician. significant liver damage.
  • 53. Childhood cancers • Leading non accidental causes of pediatric mortality • Types of childhood cancers are different from adults and are in the order of leukemia>brain and spinal cord tumors > neuroblastoma > lymphoma > rhabdomyoma > bone cancers. • Children diagnosed with cancer face unique oral and dental needs either as a manifestation of underlying cause or due to cancer treatment. • The survivors have their own set of unique oral challenges such as, xerostomia, neuropathy, dental caries, trismus, mucosal fibrosis, graft versus host disease, microdontia, agenesis of teeth. • Since leukemia, in particular ALL, AML are most common childhood malignancies.
  • 54. Incidence Occurs at 13 per 100,000 people per year. Acute lymphocytic leukemia is primarily a disease of children and young adults. Classification: Leukemia is classified according to the morphology of the predominant abnormal w hite cells in the bone marrow. They are further classified according to the progression of the clinical course as acute or chronic.  Acute Lymphocytic Leukemia  Acute Nonlymphocytic Leukemia - Acute Myelocytic Leukemia - Acute Monocytic or Myelomonocytic Leukemia - Erythroleukemia - Megakaryocytic Leukemia  Chronic Myelocytic Leukemia - Juvenile, Philadelphia chromosome negative - Adult, Philadelphia chromosome positive  Chronic Lymphocytic Leukemia
  • 55. Etiology: Cause in most patients is unknown , although both genetic and environmental factors are important. They occur with increased frequency in children with syndromes like Down, Bloom, Klinefelter, etc. Ionizing radiation, chemicals like benzene, aromatic hydrocarbons are some of the environmental factors that have been implicated in causing leukemia Clinical manifestations: Anemia , thrombocytopenia, increased WBC, neutropenia, abnormal bone marrow aspirate, pallor, fever, tachycardia, adenopathy, gingival bleeding increased irritability, lethargy, persistent fever, vague bone pain, hepatosplenomegaly, etc.
  • 56. Oral Manifestations:  Seen in 29% of children  Regional lymphadenopathy, Gingival abnormalities, including hypertrophy and bleeding are more common with nonlymphocytic leukemia whereas petechiae and ecchymoses are more common in ALL.  Gingiva is boggy, edematous, deep red and bleeds easily.  Ulceration and pallor of oral mucosa.  Rapid loosening of teeth due to necrosis of periodontal ligament.  Occasionally cranial nerve palsies, lip paresthesia, jaw pain, gangrenous stomatitis.  Manifestations in the jaw include loss of trabeculation, destruction of the crypts of developing teeth, loss of lamina dura, widening of periodontal ligament space, and displacement of teeth and tooth buds.  Oral changes can be attributed to anemia, granulocytopenia and thrombocytopenia all of which result from the replacement of the normal bone marrow elements by undifferentiated blast cells or direct invasion of the tissue by the leukemic cells.
  • 57. Dental Problems and Treatment:  As infection is the primary cause of death in 80% of children with leukemia followed by bleeding, the primary aim of dental treatment should be to prevent, control and remove oral infection, inflammation and hemorrhage.  Consult the child's physician prior to any treatment and take a complete medical history.  Elective dental procedures are to be postponed if the child is not in first remission unless there is a nidus of infection intraorally that could be a potential source of systemic infection.  Avoid prescribing drugs like aspirin that can alter platelet function.  As candidiasis is common , topical antifungals may need to be applied.  Pain from ulcerative lesions can be relieved by application of topical obtundents.  Deep lesions that bleed spontaneously – apply topical bovine thrombin.  Pulp therapy on primary teeth is contraindicated and endodontic treatment on permanent teeth is not recommended.  If platelets are less than 20,000/ cubic mm dental treatment should not be undertaken without prophylactic platelet transfusion .  Managing of xerostomia through the use of sugarless sweets, sorbitol - based gum , artificial saliva and topical fluoride  If Absolute granulocyte count (AGC) is less than 1000/cubic mm elective dental treatment should be delayed.  Avoid mouth brushing and substitute with moise gauze piece if platelet count is low.
  • 58. DENTAL REHABILITATION OF A CHILD WITH ACUTE LYMPHOCYTIC LEUKEMIA: A CASE REPORT RAED R GHOLMAN,1 EMTENAN H FELEMBAN,2 AND OMAR AES EL MELIGY3 A 6-year-old Saudi male patient was presented to King Abdulaziz Medical City (KAMC) dental clinic in Jeddah, Saudi Arabia. His father reported that he wants to treat his son's teeth since most of them are carious and currently his son is complaining from severe pain related to his lower left teeth. The medical history showed that the child was diagnosed with ALL one year ago and he is currently in the maintenance phase of chemotherapy taking oral chemotherapeutic medications. Owing to his medical condition and the father's request, his treatment was planned to be completed under general anesthesia (GA). The patient was referred to his physician (hematologist/oncologist) for consultation and clearance for dental rehabilitation under GA. The patient's preoperative hematological parameters revealed absolute neutrophil count (ANC) of 4,500/mm3 and platelets count of 349,000/mm3. Caries risk assessment was performed by asking the parents about their child's diet, oral hygiene, and lifestyle habits. The patient was classified as high-caries-risk patient based on caries-risk assessment tool (CRAT). Extraoral examination of the patient revealed a normal symmetry of the face, pale skin, dry lips, and enlarged submandibular lymph nodes. Intraoral examination revealed poor oral hygiene with mild plaque accumulation at the gingival margins along with the buccal and lingual surfaces of teeth, which had resulted in marginal gingivitis in addition to bleeding on probing.
  • 59. (1) full coverage of carious teeth # 55, 64 and 65 using stainless steel crowns (SSCs); (2) pulpotomy performed followed by SSCs in teeth # 54 and 84 (According to AAPD, pulp therapy is a relative contraindication in children with malignancies, but the decision to perform pulp therapy was due to the stable laboratory parameters of the patient during the previous three months in addition he was in maintenance phase of chemotherapy); (3) composite restoration in teeth # 51, 53, 61, 63, 72, and 73; (4) extraction of badly decayed teeth # 52, 62, 74, 75, and 85
  • 60. no space maintenance was planned to be done until the patient receive the full dose of his chemotherapy, since immunity might be compromised and the appliance might act as a source of infection.
  • 61. DIABETUS MELLITUS It is characterized by persistent increase of blood glucose level. Body does not produce sufficient amount of insulin or the patient does not respond to the insulin that is produced. Types : 1. IDDM(Type1) : failure to produce insulin by the body 2. NIDDM(Type 2) : Insulin resistance 3. GDM ( Gestational DM) : pregnant women with a previous history of diabetes. May preceed development of type 2 diabetes
  • 62. Oral manifestation: 1. Gingivitis 2. Alveolar bone resorption 3. Xerostomia 4. Delayed wound healing 5. Pulpitis in non carious tooth 6. Burning sensation in tongue 7. Acetone smell in breath
  • 63. Dental management:  Comprehensive history, screening  Appointment –early mornings, stress free, atraumatic as possible  Premeditation  Local anesthesia- use of vasoconstrictors  vital pulp therapy – preferred to extractions  Use of pulp capping and pulpotomy is questionable in a child with uncontrolled diabetes.
  • 64. • Dietary control is often difficult to enforce which encourages frequent snacking , the elevated salivary glucose, decreased salivary flow may be responsible for promoting dental caries in the uncontrolled patient. • In children with poorly controlled diabetes, the levels of severe gingivitis and periodontitis are higher due to decreased salivary flow or elevated salivaiy glucose in these patients. • The incidence of periodontitis increases among diabetic subjects after puberty which has been suggested due to disturbed local polymorphic neutrophil chemotaxis, combined with increased plaque, and phagocytosis compromise may explain the increased levels of gingivitis found in children with poorly controlled diabetes.
  • 65. RENAL FAILURE Progressive and irreversible decline in the total number of functioning nephrons, with a conconmitant decline in glomerular filtration rate. Classification:  Acute  Chronic  Acquired  Congenital
  • 66. CHRONIC RENAL FAILURE Causes: Congenital abnormalities of kidney and urinary tract to produce before 5 years. A fter 5 years glomerular and hereditary renal diseases become more prominent. Clinical manifestation:  Facial puffiness  Muscle weakness and wasting  Itching  Growth retardation  Uraemic breath
  • 67. ORAL MANISFESTATIONS 1. Mucosal pallor 2. Candidiasis & oral petechae 3. Extrinsic discoloration of teeth 4. Enamel hypoplasia 5. Tooth mobility & premature tooth loss 6. Oral calcifications 7. Total/partial loss of lamina dura 8. Pulp calcifications 9. Root resorptions
  • 68. Dental management: 1. Consultation with the patient’s physician 2. When surgical procedures are considered- assess bleeding time 3. Avoid hypertension drugs 4. Optimal treatment time is 1 day before dialysis 5. Increased need for oral prophylaxis 6. Acute renal diseases – postpone elective procedures 7. Fluid/electrolyte imbalance should be maintained by managing those oral diseases like herpetic stomatitis, severe caries, cellulitis that can compromise a child’s fluid intake. 8. Antibiotic prophylaxis before dental treatment to prevent bacteremia
  • 69. AIDS Definition: Presence of antibodies to HIV and opportunistic infections. Etiology: Caused by human immunodeficiency virus(HIV), RNA retro virus 2 groups:  Human T lymphotrophic retrovirus (HTLV I and HTLV III)  Human immune deficiency virus (HIV I and HIV II) HIV I- commonest cause of HIV throughout the world. Popovic identified HTLV III as the causative agents if AIDS.
  • 70. MODES OF TRANSMISSION A) Parenteral 1. Needle sharing among drug abusers 2. HIV infected patient to health care worker 3. Patients with haemophilia, haematologic disorders, major surgeries requiring blood transfusions 4. Tissue or organ transplants from HIV infected doners 5. Household contacts without establishing sexual or drug related behavoiurs 6. Health care workers to the patients
  • 71. B) Perinatal transmission Occurs before, during or shortly after birth 1. Prenatal and postnatal transfer from HIV infected mother to the baby during 8- 12 weeks of gestation 2. during blood transfusion from infected mother during or shorty after birth 3. mother was infected during unsafe sex with an infected partner or during breast feeding 4. Transmission during cesarean delivery
  • 72. C) Sexual transmission 1. Infants born to mothers who are prostitutes 2. Unprotected homosexual and heterosexual intercourse 3. Frequent foreign travel with sexual contacts D) Body fluid transmission Blood, Semen, breast milk, tears, sweat, urine, vaginal or cervical secretions – implicated in the transmission
  • 73. ORAL MANIFESTATIONS OF HIV INFECTION Bacterial Infections: Gingivo-perodotal diseases Fungal Infections:  Epstein –Bar virus  Herpes simplex virus  Varicella- Zoster virus  Cytomegalovirus Neoplasms Kaposi’s sarcoma Lymphoma Other neoplasm Other oral lesions Oral ulcers Salivary gland enlargement
  • 74. Diagnosis: Diagnosis of pediatric AIDS is by clinical screening and serologic confirmation. World Health Organization has defined pediatric AIDS as an infant or child presenting with at least a major criterion along with at least 2 minor criteria in the absence of any immunosuppression. Major signs • Chronic diarrhoea for more than one month • Prolonged fever for more than one month • Weight loss Minor Signs: • Oropharyngeal conditions • Repeated cough for more than one month • Generalized lymphadenopathy • Generalized dermatitis • Maternal HIV infection Typical pediatric findings (Rubenstein , 1986): • Pulmonary lymphoid hyperplasia • Salivary gland enlargement • Pyogenic bacterial infection such as otitis media • Developmental craniofacial features • Chronic recurrent diarrhoea • Hepatosplenomegaly • Chronic pneumonitis • Failure to thrive • Progressive encephalopathy
  • 75. Candidiasis: Recurrent candidiasis, which is persistent for long periods and often resistant to conventional antifungal therapy, is a frequent oral manifestation in pediatric HIV infection/AIDS. Oral candidiasis in HIV infected children is variable and is manifested as pseudomembranous plaques, erythematous patches, angular cheilitis , hyperplastic plaques. Angular cheilitis appears as fissures or cracks at the commissures of the lips. Treatment The lesions may subside or disappear with treatment, but relapse is common. The treatment can be either topical or systemic
  • 76. Viral Infections: In HIV - infection, several viruses are able to colonize or react, producing lesions in the mouth. These include herpes - group viruses and papillomaviruses. Herpes simplex Herpes simplex is caused by herpes simplex virus I (HS V) and it recurs frequently in children with advanced HIV disease. The virus become latent in trigeminal ganglion and any sort of stimulation to the sensory nerve may reactivate the virus along the sensory' nerves to the mucosal or the epithelial surfaces interrelated by the reactivated ganglion leading to recurrent oral herpes lesions. Herpes Zoster Herpes zoster is caused by varicella zoster virus (HVZ) due to reactivation of the virus along the cutaneous surface ganglion becauseof immunosuppression
  • 77. Treatment of viral infections: Herpetic lesions may be treated with systemic doses of acyclovir ranging from 1 to 2 gm daily taken, orally or IV in individuals with more severe oropharyngeal lesions or in those unable to swallow. Bacterial Infection: Oral lesions of bacterial origin may include mycobacterium aviumintracellulare and Klebsiella pneumoniae. HIV associated gingivitis ( HFV-G ) and HIV associated periodontitis (HIV-P) Linear gingival erythema (LGE) and ANUG like lesion called as necrotizing ulcerative periodontitis have been reported in children Treatment: • Aggressive curratage • Peridex (0.12% chlorhexidine digluconate)rinses three times daily • Antibiotic treatment
  • 78. Recurrent apthous ulcers in HIV infected persons: They appear as a well circumscribed ulcers with an erythematous margin. The ulcers of a minor form appear as 0.5 to 1 cm, herpetiform appear in clusters of small ulcers usually on soft palate and oropharynx major ulcers appear as large necrotic ulcers of 2-4cm which are painful and last for several weeks. Treatment: Fluconomide ointment (0.5%) Orabase 3-6 times/day Dexamethasone 0.5 mg/ml Petechiae: 20 -30% of HIV infected patients may develop thrombocytopenic purpura at any age. oral lesions appear as small blood filled purpuric lesions. Causes: HIV induced autoantibodies Megakaryocyte infection Aplasia AZT therapy which may suppress the bone marrow
  • 79. MANAGEMENT OF AIDS PREVENTION  Barrier techniques  Proper sterilization - HIV is sensitive to autoclaving at 121⁰C for 15min at 1 atm pressure - Dry heat Sterilization upto 170⁰C - Viruses can be inactivated by heating lyophilized factor Disinfection of innate objects: - Calcium hypochlorite - 0.2% Na hypochlorite - 10 min at room temperature in 10% bleach, 50% ethanol and 3% hydrogen peroxide.
  • 80. DRUGS USED FOR AIDS  Acyclovir 1-2 g daily once orally or IV  Zidovudine(AZT) – attacks the virus through the enzyme reverse transcriptase Other drugs: 1. Dideoxycytoxine(ddc) 2. Dideoxyinosis (ddI) 3. Stavudine (d4T)  Use of protese inhibitors- Saquinavir, Indinavir & Ritonivir  Triple drug therapy: AZT combination with indinavir and 3 TC(lamivudine) to reduce HIV copies in the plasma of infected patients(to treat not to cure)
  • 81. AIDS VACCINE A lot of research – not successful Due to continuous mutation of genes of the virus Moreover HIV viruses varies across regions as well as individuals. Practically not feasible to develop vaccine for each individual
  • 83. REFERENCES  Pediatric dentistry – scientific foundations and clinical practice – Stewart and Barber  Textbook of Pedodontics. Shobha Tandon. 2nd edn.  Dentistry for the child and adolescence. 9th edition. Mc Donald Avery and Dean AAE Quick Reference Guide on Antibiotic Prophylaxis 2017 Update Arulpari Mahalingam et al., Dental Management of A Child With Congenital Heart Disease - A Case Report Gholman RR, Felemban EH, El Meligy OAES. Dental Rehabilitation of a Child with Acute Lymphocytic Leukemia: A Case Report. Int J Clin Pediatr Dent 2019;12(6):582–586.  Dental Management of Medically Compromised Patients. Operational Guide for School Oral Health Program

Notas do Editor

  1. *IM—intramuscular; IV—intravenous **Or other first or second generation oral cephalosporin in equivalent adult or pediatric dosage. †Cephalosporins should not be used in an individual with a history of anaphylaxis, angioedema or urticaria with penicillins or ampicillin.