Systemic diseases/ dental implant courses

SYSTEMIC DISEASES
AND
THEIR INFLUENCE
ON
GENERAL AND ORAL
HEALTH
INDIAN DENTAL ACADEMY
Leader in continuing Dental Education
www.indiandentalacademy.com

CONTENTS
 INTRODUCTION
 BLOOD DISEASES
 ENDOCRINE DISEASES
 METABOLIC DISEASES
 NUTRITIONAL DISEASES
 RESPIRATORY DISEASES
 CARDIOVASCULAR DISEASES
 GIT & LIVER DISEASES
 RENAL DISEASES
 AUTOIMMUNE DISEASES
 BONE & JOINT DISEASES
 NEUROMUSCULAR DISEASES
 SEXUALLY TRANSMITTED DISEASES
 DERMATOLOGICAL DISEASES
 REFERENCES
 CONCLUSION

INTRODUCTION

HEAMATOLOGIC DISEASES

IRON – DEFICIENCY ANAEMIA :
ETIOLOGY:
• Chronic blood loss
• Improper iron absorption
• Inadequate dietary intake
• Increased requirement – pregnancy
CLINICAL FEATURES :
• Pallor
• Lassitude , fatigue
• Headache , Insomnia
• Palpitations
ORAL MANIFESTATIONS :
• Cracks or fissures at the corners of the mouth
• Atrophic tongue www.indiandentalacademy.com

PLUMMER – VINSON SYNDROME
• Iron deficiency anemia
• Koilonychia
• Esophageal strictures or webs

PERNICIOUS ANEMIA
Deficiency of vitamin B12
CLINICAL FEATURES :
• Pallor
• Fatigue
• Headache , dizziness
• Nausea , vomiting , diarrhea , abdominal pain
• Loss of appetite , loss of weight
• Shortness of breath
• Paresthesia
• Glossitis , glossodynia , glossopyrosis ( beefy red tongue)
• Stomatitis

APLASTIC ANEMIA
Lack of bone marrow activity
CLINICAL FEATURES :
Anemia, leukemia, thrombocytopenia
Dyspnea on slight exertion
Numbness & tingling of extremities
Decreased resistance to infection
Petechiae
Spontaneous gingival bleeding
Ulcers – oral mucosa & pharynx

THALASSEMIA
Diminished synthesis of α- or β- chain
CLINICAL FEATURES :
Pallor
Fever , chills
Generalised weakness
Hepatosplenomegaly
Mongoloid face
Flaring or protrusion of max. anteriors
Oral mucosa - pale

SICKLE CELL ANEMIA
Defective hemoglobin formation
CLINICAL FEATURES :
Weakness , fatigue
Shortness of breath
Pain in joints , limbs ,abdomen
Nausea , vomiting
Systolic murmur & cardiomegaly
Pallor
Generalised osteoporosis
Loss of trabeculation of jaw bones
Delayed eruption of teeth
Enamel hypoplasia www.indiandentalacademy.com

MANAGEMENT :
Recognition of the type of anemia
Diagnosis & treatment of underlying cause
DENTAL MANAGEMENT :
Low risk patients (hematocit > 30%) - Normal dental protocol
High risk patients (hematocrit < 30%) -
• History
• Physician’s consultation
• Defer elective dental care until clinical status normalized
• Stress reduction – shorter appointment
• GA contraindicated
• Hospitalization – advanced surgical procedures

POLYCYTHEMIA
TYPES:
1. Primary
2. Secondary
CLINICAL FEATURES:
Headache, dizziness
Weakness, lassitude
Tinnitus
Mental confusion
Slurring of the speech
Digits may be cyanotic
Splenomegaly

ORAL MANIFESTATIONS:
Oral mucous membrane  deep purplish red
Commonly affected - gingiva and tongue
Gingiva  swollen and bleeds on slight provocation
Submucosal petechiae, ecchymosis, hematoma
Varicosities on the ventral surface of the tongue
MANAGEMENT :
Phenylhydrazine , Radioactive ‘P’
DENTAL MANAGEMENT :
Complete blood count prior to treatment
Special attention to local hemostasis

LEUKEMIA
Buccal mucosa mucositis with
ulceration secondary to
chemotherapy.
Acute leukemias = usually in children younger than 5 years and most often
before 25 months of age
Chronic leukemias = occurs in 5th
– 7th
decade, is rare before 25 yrs
CLINCAL FEATURES:
Lymphadenopathy
Anemia
Petechiae, ecchymosis
Splenomegaly
Hepatomegaly

Oral manifestations are not observed in edentulous patients and
very young patients
Leukemic cells infiltrate the gingiva particularly if gingivitis or
periodontitis is present.
Gingival hyperplasia
MANAGEMENT :
Chemotherapy or Radiotherapy

DENTAL MANAGEMENT :
Low risk patients (successful therapy, no malignancy evident)
- Normal dental procedures
Moderate risk pts. (remission & receiving chemotherapy)
• Treatment around chemotherapy or WBC >3500 cells/mm³ or
platelets >1,00,000/mm³
• Antibiotic prophylaxis
High risk pts. (active leukemia)
• Control of infection – hospitalization
I.V. broad spectrum antibiotics
• Control of bleeding – local hemostatics
platelets

MULTIPLE MYELOMA
CLINICAL FEATURES:
Age = 40 – 70 years
Male predilection
Pain – early feature
Bone destruction  pathologic fractures
Occasionally swelling over the area of bone involvement
Mandible commonly affected
Pain, swelling, expansion of the jaw, numbness,
mobility of the teeth
LAB FEATURES:
Bence – Jones protein www.indiandentalacademy.com

MANAGEMENT :
• Chemotherapy
• Radiotherapy
• Bone marrow transplant
DENTAL MANAGEMENT :
• Oral prophylaxis
• Broad spectrum antibiotics
• Anti-bacterial mouthwashes (chlorhexidine)

HEMOPHILIA
TYPES:
1. Hemophilia A  factor VIII deficiency
2. Hemophilia B  factor IX deficiency
3. Hemophilia C  factor XI deficiency
CLINICAL FEATURES:
Persistent bleeding – either spontaneous or following slight trauma
Hemorrhage in subcutaneous tissues, internal organs and joints
Gingival bleeding
Subperiosteal bleeding with reactive new bone formation  Mandibular
Pseudo-tumor

BLEEDING DISORDERS
1. Thrombocytopenia – Idiopathic
Secondary
2. Von Willebrand’s disease – abnormal factor VIII
CLINICAL FEATURES :
• Excessive bleeding spontaneously or following trauma
• Epistaxis
• Bleeding into GIT , skin
• Profuse gingival bleeding
• Petchiae on oral mucosa

MANAGEMENT :
Depends on nature of hemostatic defect & its cause
1. Fresh frozen plasma
2. Cryoprecipitate
3. Amino caproic acid
DENTAL MANAGEMENT :
1. History
2. Physician’s consultation
3. BT, CT checked prior to treatment
4. Local hemostatic measures
5. Avoid aspirin www.indiandentalacademy.com

LYMPHOMAS
Malignancy of lymphoreticular origin that involves the lymph nodes
HODGKIN’S LYMPHOMA :
Thomas Hodgkin (1832)
CLINICAL FEATURES :
Younger adults
Unilateral painless swelling of the neck
Lymphadenopathy (well-defined , rubbery in consistency)
Mediastinal nodes – cough or breathlessness
Elderly pts. – night sweat , Pel-Ebstein fever ,weight loss
Secondarily involve mandible & overlying alveolar mucosa
MANAGEMENT :
History & physical examination
Biopsy of lymph nodes
Chemotherapy (vincristine , bleomycin , doxorubicin , decarbazine)
Radiotherapy (3500 – 4500 cGy)www.indiandentalacademy.com

NON HODGKIN’S LYMPHOMA :
Mononuclear proliferation of lymphoid cells
CLINICAL FEATURES :
Older age group
Lymphadenopathy
Weight loss , night sweat , fever , pruritis
Hepatoslenomegaly
Extra nodal involvement – GIT , bone marrow , kidney
Swelling grow rapidly & later ulcerate
Sometimes large , fungating , necrotic foul smelling masses
Jaw involvement – tooth mobility & pain
Paresthesia of mental nerve
MANAGEMENT :
Radiotherapy , chemotherapy (Vincristine , Prednisone , cyclophosphamide)
Autologous stem cell transplantation – relapsed caseswww.indiandentalacademy.com

DENTAL MANAGEMENT :
Avoid elective or complicated procedures
Increased risk of infection – periodic oral examination , antibiotics
Xerostomia – oral prophylaxis , low sucrose diet
fluoride mouth rinse , artificial saliva

ENDOCRINE DISORDERS

TYPES:
HYPERPARATHYROIDISM
CLINICAL FEATURES:
1. Age = 30 – 60 years
2. Female predilection
3. Bone pain, Joint stiffness, Pathological fractures
4. Generalized osteoporosis, Pseudocyst formationwww.indiandentalacademy.com

• Giant cell tumor or a “cyst” of the jaw
• Mobility, sudden drifting and loss of teeth
RADIOLOGIC FEATURES:
1. Demineralization of the skeleton
2. Osteitis fibrosa generalisata
3. Brown’s tumor
4. Pathologic calcifications
5. Loss of lamina dura
TREATMENT:
Excision of the parathyroid tumor.

HYPOPARATHYROIDISM
Causes hypocalcemia
CLINICAL FEATURES:
1. Tetany, carpopedal spasms
2. Neuromuscular excitability
3. Anxiety and depression
1. Enamel Hypoplasia
2. Delayed eruption
3. External root resorption
4. Root dilacerationwww.indiandentalacademy.com

HYPERTHYROIDISM
• Excess circulating thyroid hormone
• Increased BMR
• Serum protein bound iodine concentration is increased
CLINICAL FEATURES :
• Facial expression of surprise with
wide-eyed staring (exophthalmos)
• Patients are nervous and
highly emotional
• Increased sensitivity to epinephrine
and usually hypertensive
• Weight loss, intolerance to heatwww.indiandentalacademy.com

• Pretibial edema
• Early shedding of deciduous teeth
• Early eruption of permanent teeth
• Adults may show generalized decrease in bone density
• Loss of alveolar bone in edentulous areaswww.indiandentalacademy.com

MANAGEMENT :
• Anti thyoid drugs – Propyluracil
• β blockers – Propranolol
• Radioactive Iodine
• Surgery
DENTAL MANAGEMENT :
• Proper history
• Defer treatment until thyroid function tests are normal
• Minimize stress
• Minimize use of epinephrine
• Anti thyroid drugs before treatment

HYPOTHYROIDISM
Congenital  cretinism
Adults or children Myxedema
CRETINISM :
Retarded mental and physical development
Generalized edema
Base of skull shortened, retraction of bridge of the nose with flaring
Mandible underdeveloped, maxilla overdeveloped
Atrophic salivary glands
Enlarged tongue  malocclusion
Delayed shedding of deciduous teeth
Delayed eruption of permanent teeth

MYXEDEMA
Patient is lethargic
Intolerance to cold, weight gain
Sparse hair
Skin is doughy to touch
Dull expressionless face
Periorbital edema
Enlarged tongue - separation of teeth
Periodontal diseases - loss of teeth

MANAGEMENT :
Thyroxine
Avoid drugs like Lithium ,Amiodarone
DENTAL MANAGEMENT :
History
Physician’s consultation
Defer treatment till thyroid function tests are normal

METABOLIC DISORDER

DIABETES MELLITUS
CLASSIFICATION:
1. Primary – type I – insulin dependant
type II – non-insulin dependant
2. Secondary – pancreatic, drug induced, gestational
3. Impaired glucose tolerance
CLINICAL FEATURES:
Polyuria, polydypsia and polyphagia
Increased susceptibility to infections
Xerostomia  inc. susceptibility to caries
Candidiasis
Burning tongue
Periodontal diseases – e.g. periodontal abscesswww.indiandentalacademy.com

MANAGEMENT :
Goals -
Establish optimal metabolic control
Prevent ketoacidosis
Prevent hypoglycemia
Low energy, weight reducing diet
Insulin – IDDM
Oral hypoglycemics – NIDDM

DENTAL MANAGEMENT :
• Defer treatment till metabolic status is stabilized
• Physician’s consultation & adjustment of insulin dose
• Pt should take normal diet & anti diabetic drugs before any
procedure
• Minimize stress – short , early morning appointments
adjunctive sedation technique
• Lengthy procedures – appointment interrupted with a snack
• Minimize risk of infection – recall oral prophylaxis
antibiotic prophylaxis
treat acute infections aggressively
PROTHODONTIC CONSIDERATIONS :
• Mucostatic impression technique
• Balanced occlusion
• Use of tissue conditioners

HISTIOCYTOSIS X
CONSISTS OF –
1. Hand – Schuller – Christian disease
2. Letterer – Siwe disease
3. Eosinophilic granuloma
Histiocytosis showing multiple radiolucencies of the mandible.

EOSINOPHILIC GRANULOMA
• Most Common, occurs in young adults
• Bone lesions  flat bones (posterior jaw)
• Oral ulcerations may develop on the gingiva, palate, and floor of
the mouth
• Lesions are destructive & well demarcated
• Radiologic findings demonstrate progressive alveolar bone loss
with dental extrusion and characteristic floating teeth

HAND-SCHULLER-CHRISTIAN DISEASE
Characterized by widespread skeletal and extraskeletal lesions and a
chronic clinical course
Male predilection
Age – < 5yrs, also seen in adolescents and young adults
Classic triad –
Single/multiple areas of punched-out
bone destruction in the skull
Uni-/bi-lateral exopthalmos Diabetes insipidus
Other manifestations – polyuria, dwarfism or infantilism
Facial asymmetry, otitis media
Skin may exhibit papular/nodular lesions

Sore mouth with/without ulcerative lesions
Halitosis, gingivitis and suppuration
Unpleasant taste
Loose and sore teeth with precocious exfoliation of teeth
Failure of healing of tooth sockets after extraction
Loss of supporting alveolar bone mimicking advanced
periodontal disease is characteristic

LETTERER-SIWE DISEASE
Common in infants, <2years
• Characterized by widespread involvement of the viscera,
potentially leading to death
• Skin lesions : -papules, plaques, vesicles, and
hemorrhagic nodules
• Oral symptoms: -large ulcerations, ecchymoses, gingivitis,
periodontitis, & subsequent tooth loss

NUTRITIONAL DISORDERS

VITAMIN A :
Deficiency : xerophthalmia ,night blindness, corneal
ulcers, bitot’s spots, follicular hyperkeratosis of
epithelium
Oral manifestations : hyperkeratosis of oral epithelium
metaplasia of salivary gland epithelium, change in
tooth bud affecting the crown
VITAMIN K :
Synthesis of clotting factors
Deficiency : prolonged clotting & bleeding
Oral manifestations : petechiae ,ecchymosis
Management : bleeding time & clotting time determined
avoid aspirin & NSAIDs
keratomalacia

VITAMIN D :
Rickets Osteomalacia
CLINICAL FEATURES
Change in epiphysis & metaphysis of bones
Poor mineralization of bone
Growth retardation
Bow legs
Rachitic rosary – prominence of costochondral junction
Change in development of enamel & dentin (enamel hypoplasia ,
inc. interglobular dentin)
Delayed eruption
Malaligned teeth
High caries index

OSTEOMALACIA
Clinical features :
Softening & distortion of the skeleton
Increased tendency to fracture
Oral manifestations :
Taylor & Day – inc. incidence of periodontitis
Management :
Dietary supplementation
Hormonal therapy
Fluoride administration
Osteomalacia secondary to malabsorption – reduce dietary fat intake

THIAMINE :
Deficiency – beri -beri
Dry beri-beri : chronic peripheral neuropathy with wrist &/or foot drop
Wet beri-beri :generalised edema due to ventricular heart failure with
pulmonary congestion
NIACIN :
Pellagra ( dermatitis ,diarrhea ,dementia )
PYRIDOXINE :
Mental confusion ,depression
FOLIC ACID :
Macrocytic anemia
VITAMIN B12 :
Megaloblastic anemia
Peripheral neuropathy ,demyleination of nerves
Dementia , Optic atrophy
Beri - beri
pellagra

VITAMIN C :
Deficiency – SCURVY characterised by
• Defective collagen formation
• Impaired wound healing
• Capillary hemorrhage
• Subnormal platelet adhiveness

Nutrient Oral Deficiency Signs
Biotin Geographic tongue; atrophy of lingual
papillae
Riboflavin Soreness and intraoral burning; cheilosis;
angular stomatitis: glossitis with a magenta
tongue
Niacin Intraoral burning; glossitis; tongue
swollen, with red tip and sides; swollen,
red fungiform papillae; filiform papillae
become inflamed and loose their epithelial
tufts (giving the characteristic slick red
appearance)
Pyridoxine Intraoral burning; glossitis; mucosal
ulcerations and erosions; cheilosis
Folic acid Gingivitis; glossitis with atrophy or
hypertrophy of filiform papillae; cheilosis

Nutrient Oral Deficiency Signs
Vitamin B12 Intraoral burning; mucosal ulcerations
and erosions; painful glossitis with a beefy red or fiery
appearance eventually resulting in and atrophic (smooth
and shiny) tongue
Vitamin C Scorbutic gingivitis (sore and bleeding gums); gums
deep blue-red color; loose teeth; follicular
hyperkeratosis
Iron Cheilosis; atrophic glossitis; gingivitis;
candidiasis; intraoral burning or pain; mucosal
ulcerations and erosions; pallor
Zinc Marked halitosis; cheilosis; stomatitis;
discrete red, scaly plaques from short
lived vesicles; white coating on tongue
and mucosa

Common Disorders Associated with Oral Manifestations and
Nutrient Deficiencies.
Oral Manifestation Disorder
Cheilosis Crohn's disease; acrodermatitis enteropathica;
alcoholism; celiac disease; malabsorption syndrome;
iron-deficiency anemia
Gingivitis Crohn's disease; anorexia nervosa; celiac disease;
scurvy
Glossitis Crohn's disease; alcoholism; celiac disease;
malabsorption syndrome; pernicious anemia; iron-
deficiency anemia; amyloidosis; carcinoid syndrome
Intraoral burning Menopause; diabetes mellitus; esophageal reflux;
niacin deficiency
Ulcerations Crohn's disease; ulcerative colitis; celiac disease;
corticosteroid use; acrodermatitis enteropathica;
anorexia nervosa; pernicious anemia; iron deficiency
anemia; mercury poisoningwww.indiandentalacademy.com

RESPIRATORY DISEASES

TUBERCULOSIS
Caused by mycobacterium tuberculi.
Clinical features :
- chronic cough with hemoptysis.
- evening rise in temperature.
- weight loss.
- dysphagia
- malaise
- lymphadenitis
Oral manifestations :
- lesions involve gingiva , vestibular mucosa
- tongue , palate , floor of the mouth may be affected.
- lesions consist of ulcers , fissures or swelling .
- ulcers (solitary or multiple) occasionally painful involve dorsum of the
tongue
- tuberculous osteomyelitis seen in craniofacial skeleton
- intraglandular & perigandular lymph node infection

MANAGEMENT :
Antitubercular drugs
1st
line drugs - rifampicin , isoniazid , ethambutol , streptomycin , pyrazinamide
2nd
line drugs – clarithromycin , ciprofloxacin , para-aminosalicylic acid
Short therapy :
Rifampicin , isoniazid , pyrazinamide , ethambutol or streptomycin – 2 months
Rifampicin , isoniazid – 4 months
Long therapy ( 9 – 12 months ) :
Meningeal disease
HIV coinfection
2nd
line – drug intolerance

DENTAL MANAGEMENT :
Patients with active TB :
emergency dental treatment only.
gowning , double gloves , face masks, aseptic technique.
Patients with signs and symptoms suggestive of TB :
physicians consultation
emergency dental treatment
personal protection & aseptic technique
Patients with history of TB :
history of treatment & follow up
physician consultation if adequacy of treatment or follow up evaluation
is questionable
routine dental treatment
Patient with positive tuberculin test with no history of TB & no signs / symptoms of
active disease :
history
physician consultation
routine dental treatment

ASTHMA
Disorder characterized by chronic airway inflammation and increased
airway responsiveness
CLINICAL FEATURES :
Wheeze
Chest tightness
Cough
Dyspnea
Infections like candidiasis
Leukoplakia
MANAGEMENT :
Avoid precipitating factors
Corticosteroids
Acute cases – oxygen followed by high dose corticosteroidswww.indiandentalacademy.com

DENTAL MANAGENT :
Minimization of stress
Sedation technique
Avoid aspirin
Minimize use of epinephrine
Antibiotic prophylaxis – soft tissue manipulation
Severe asthma – elective dental procedures

CARDIOVACULAR DISEASES

RHEUMATIC HEART DISEASE
• Rheumatic fever
• Etiology:
– Group A beta hemolytic streptococci
– Hereditary
• C/F: Duckett Jones
– Essential Criteria: -
• Increased ASO titer, +ve Throat culture, Recent Scarlet fever
– Major Criteria:
• carditis, polyarthritis, sydenham chorea, erythema marginatum,
subcutaneous nodules
– Minor Criteria:
• previous rheumatic fever, polyarthralgia, fever
• Prolonged PR Interval in ECG, C reactive protein, leucocytosis,
increased ESR (Acute phase reactants)

BACTERIAL ENDOCARDITIS
• Bacterial infection of the endocardial surfaces & certain arteries
• Susceptibility: -
– Congenital / rheumatic heart disease
– Congenital anatomic heart defect
– Cardiac surgery
• Types of endocarditis: -
– Acute bacterial endocarditis:
• Explosive infection chr by high fever & prostration
• Prognosis is grave
• Staphylococcus aureus
• Death – infection toxicity / cardiac failure
– Subacute bacterial endocarditis: -
• More insidious & prostrating
• Pyrexia, malaise, anorexia, wt loss, arthralgia
• Petechiae on oral mucous membrane, conjunctivae & skin of the wrist &
ankles
• Streptococcus viridans

• Treatment:
– IV antibiotics
– Prevention of Septicemia
Dental Management
– Co-ordinated with medical management
– A thorough pt. background data
– Consultation with pt’s physician
– Definite Dental Treatment Plan
– Sedation premedication
– Preoperative antibiotic prophylaxis
– Anesthesia
Sedation premedication:
Reducing apprehension / anxiety
Caution – respiratory depressants
Dental procedure – short, atraumatic & pleasant
Anesthesia:
N2O & O2( O2 > 25%)
LA (adr) www.indiandentalacademy.com

Standard general
prophylaxis
Amoxicillin Adults: 2 g
Children: 50 mg per kg
Taken orally one hour before the procedure
Patient is unable to
take oral
medications
Ampicillin Adults: 2 g
IM or IV 30 minutes before the procedure
Patient is allergic
to penicillin
Clindamycin
or
Adults: 600 mg
Cefadroxil or
cephalexin or
Adults: 2 g
Azithromycin or
clarithromycin
Adults: 500 mg
Patient is allergic
to penicillin &
unable to take oral
medication
Clindamycin
or
Cefazolin
Adults: 600 mg
IV 30 min before procedure
Adults: 1 g
IM or IV 30 min before the procedure

HYPERTENSION
Abnormal elevation of resting arterial systolic blood pressure above 140
mm Hg and/or elevation of diastolic blood pressure above 90 mm Hg
Types :
Primary Secondary
Normal BP - 120/80 mm Hg
Controlled – upto 140/90mm Hg
Mild hypertension - 140/90 – 160/105 mm Hg
Moderate hypertension – 160/105 – 170/115
Severe hypertension – 170 /115 – 190/125
Target organ damage :
Blood vessels : structural changes ,ateriosclerosis
CNS : stroke ,encephalopathy
Retina : retinopathy
Heart : coronary artery diseases
Kidney : proteinuria , renal failure

MANAGEMENT :
Non drug therapy – correcting obesity , reducing alcohol intake
restricting salt intake , regular physical exercise
Drugs – diuretics
β blockers , α blockers , α & β blockers
calcium channel blockers
ACE inhibitors
angiotensin receptor antagonist
DENTAL MANAGEMENT :
History
Examine BP before any procedure
Minimize stress - early morning appointment
Patient should have taken regular dose of drug
GA avoided
Gingival retraction cords containing epinephrine avoided
Mild hypertension – normal protocol
Moderate - normal protocol +sedation
Severe - defer treatment till medical mgmt instituted

ANGINA PECTORIS
CLINICAL FEATURES :
Chest pain
Discomfort
Dyspnea on exertion
MANAGEMENT :
Identification & control of risk factors
Careful assessment of the extent & severity of the disease
Sublingual Nitroglycerine – 0.3mg
‘Ca’ channel blockers – moderate or severe angina
DENTAL MANAGEMENT :
Mild Angina – normal protocol
Moderate Angina – Physician’s consultation
normal protocol
prophylactic nitroglycerine & sedation technique
Severe Angina – treatment under hospitalizationwww.indiandentalacademy.com

MYOCARDIAL INFECTION
Irreversible myocardial damage as a result of prolonged ischemic injury
CLINICAL FEATURES :
Severe chest pain
Dyspnea
Palpitations
Tachycardia
Hypotension
Oliguria
MANAGEMENT :
History
Immediate measures – high flow oxygen
IV analgesics
ECG monitoring
Defibrillation
Aspirin (75 – 300 mg)
Thrombolytic therapy www.indiandentalacademy.com

DENTAL MANAGEMENT :
< 6 months post MI – defer the treatment
6 months - 1 yr – normal protocol
physician’s consultation
hospitalization recommended
minimization of stress
adjunctive sedation therapy

GASTROINTESTINAL
DISEASES

HEPATITIS
TYPES :
Hepatitis A – faeco-oral
Hepatitis B – saliva , parenteral , sexual contact
Hepatitis C – saliva , parenteral
Hepatitis D – parenteral , sexual contact
Hepatitis E – faeces
CLINICAL MANIFESTATIONS :
Prodromal symptoms – malaise , headache
Jaundice
Anorexia , nausea , vomiting , diarrhea
Abdominal pain , liver tenderness
Lymphadenopathy , splenomegalywww.indiandentalacademy.com

Yellowish discoloration of oral mucosa
Petechiae , ecchymosis
MANAGEMENT :
Nutritious diet
Avoid drugs
Avoid surgical procedures
DENTAL MANAGEMENT :
Proper history
Liver function tests, BT,CT
Low risk pts. (Normal LFT , no surface antigens)
Normal dental protocol
Use gloves , mouth masks ,eye wear

High risk pts. (abnormal LFT, surface antigen present)
Appointments at the end of the day
Defer elective procedures
Avoid contacting blood & oral secretions
Strict sterilization procedures
Double gloving , masks & eye wear
Draping all exposed dental equipments
Wipe all surfaces with disinfectants
Minimal use of aerosols
Disposable items
Immunoglobulin if needle stick injury

CIRRHOSIS
Loss of liver cells & progressive scarring as a result of injury
CLINICAL FEATURES :
Jaundice , ascites
Spider telengectasia , bleeding
Esophageal varices
Splenomegaly
Digital clubbing
Bleeding gums
Petechiae , ecchymosiswww.indiandentalacademy.com

MANAGEMENT :
Treatment of etiologic factor
Low protein diet
Limited salt & fluid intake
Diuretics
Platelets & fresh frozen plasma
DENTAL MANAGEMENT :
Restrict procedures causing bleeding
Avoid aspirin & NSAIDs
Non surgical procedures – normal protocol with attention to
hemostasis
Surgical procedures : hospitalization , platelet transfusionwww.indiandentalacademy.com

CROHN’S DISEASE
Granulomatous inflammation of the intestine of unknown etiology
ETIOLOGY:
Genetics, infective agents, smoking, immunological
CLINICAL FEATURES:
Pain, Nausea, Vomiting and Diarrhea
Steatorrhea and malabsorption of nutrients
Pyostomatitis vegetans - broad based papillary projections, tiny abscesses or
vegetations developing in the area of intense erythema
Tiny pustule  ulceration  coalesce  necrosis
Buccal mucosa  ‘cobblestone’ appearance
Glossitis , angular chelitis www.indiandentalacademy.com

MANAGEMENT :
Corticosteroids
Sulfasalazine
Metronidazole
DENTAL MANAGEMENT :
Minimize stress – shorter appointment
sedation
Steroid supplements for adrenal insufficiency
Periodontal therapy

RENAL DISEASES

CHRONIC RENAL FAILURE
Etiology :
Renal artery stenosis
Interstitial diseases
Polycystic kidney disease
Diabetes
CLINICAL FEATURES :
Anemia
Hypertension
Renal osteodystrophy
Myopathy
Neuropathy

Mucosal ulcerations
Bleeding gums , petechaie , ecchymosis
Periodontitis
Opportunistic infections – candida
MANAGEMENT :
Identify underlying cause & its management
Institute renal replacement therapy – dialysis , transplantation
DENTAL MANAGEMET :
Recall oral prophylaxis
Avoid aspirin, tetracycline

AUTOIMMUNE DISEASES

SJOGREN’S SYNDROME
TYPES :
1. Primary
2. Secondary
CLINICAL FEATURES :
1. Age = Above 40 yrs
2. Female predilection
3. Xerostomia
4. Dryness of the eyes
5. Enlarged salivary glands
6. Lymphadenopathy
7. Secondary – rheumatoid arthritis
Characteristic fissuring of
tongue and loss of papillae as
seen in xerostomia.
Sialogram
Parotid-Sjogren's
syndrome

MANAGEMENT :
Oral prophylaxis
Salivary substitutes (salivart , mouthkote)
Pilocarpine hydrochloride 2%
Sodium carboxymethylcellulose
Chlorhexidine mouthwash
Fluoride toothpaste – caries prevention

LUPUS ERYTHEMATOSUS
Exists in two forms –
1. Systemic lupus erythematosus (SLE)
2. Discoid lupus erythematosus (DLE)
ETIOLOGY:
1. Genetic predisposition and immunologic abnormality
2. Mediated by a viral infection
CLINICAL FEATURES:
Marked predilection for females
Age = 30yrs (females) / 40yrs (males) / also reported in children
Generalized manifestations  involvement of multiple organs

SYSTEMIC LUPUS ERYTHEMATOSUS :
Erythematous patches on the face  coalesce to form symmetrical
pattern over the cheeks & across the bridge of the nose – butterfly
distribution
Kidney  ‘wire loops’ (glomerular capillaries)  renal insufficiency
Heart  atypical endocarditis, fibrinoid degeneration

DISCOID LUPUS ERYTHEMATOSUS –
• Common sites – face, oral mucous membrane, chest, back
and extremities
• Cutaneous lesions  elevated red/purple macules 
covered by gray/yellowish adherent scales  forceful
removal reveals ‘carpet tack’ extensions dipped into enlarged
pilosebaceous canals
• Appearance - lesions red or pink (periphery) and atrophic &
scarred with characteristic central healing

Discoid form – oral lesions begin as erythematous areas, often depressed
without induration and typically with white spots
Margins of the lesion are not sharply demarcated
Central healing  depressed scarring
Common site – buccal mucosa, palate, tongue,
vermillion border of the lips (especially lower lip)
Systemic form – lesions are similar to discoid form except that
hyperemia, edema and extensions of the lesions are sometimes more
pronounced.
Greater tendency for bleeding, petechiae and superficial ulceration
surrounded by a red halo.
Superimposed oral moniliasis and xerostomia have also been reported

MANAGEMENT :
Corticosteroids
DENTAL MANAGEMENT :
Hematologic profile (CBC, PT, PTT, BT)
Antibiotic prophylaxis for procedures involving bleeding
Avoid aspirin & NSAIDs

DISEASES OF BONES

PAGET’S DISEASE
Occurs predominantly over 40 years of age
Chronic disease symptoms develop slowly
CLINICAL FEATURES:
Bone pain
Severe headache
Deafness
Blindness
Facial paralysis
Dizziness
Weakness
Involved bones become warm to touch because of increased vascularity.
Increased tendency for pathological fracture.www.indiandentalacademy.com

Progressive enlargement of maxilla.
Alveolar ridge becomes widened and palate is flattened.
Teeth become loose and migrate.
Mouth may remain open exposing the teeth.
MANAGEMENT:
Bisphosphonates (reduce bone turnover rate )
Calcitonin www.indiandentalacademy.com

FIBROUS DYSPLASIA
Chronic disorder of the skeleton  Causes expansion of one or more bones
due to abnormal development of the fibrous, or connective tissue within
the bone.
One bone may be affected (monostotic), or numerous bones affected
(polyostotic)
Most common sites  femur (thigh bone), tibia (shin bone), ribs, skull,
facial bones, humerous (upper arm), and pelvis

CLINICAL FEATURES :
Deformity , thickening or bowing of long bones
Bone pain
Pathologic fractures
Skin lesions – café-au-lait spots
Expansion & deformity of the jaw
Eruption pattern of teeth altered
MANAGEMENT :
Mild cases – surgical correction
Severe cases - radiation

NEUROMUSCULAR
DISORDERS

EPILEPSY
Types :
Grand mal
Petit mal
Simple partial
Complex partial
CLINICAL FEATURES :
Generalized seizures
Loss of consciousness
Abnormal motor activity may be seen
ORAL MANIFESTATION :
Gingival hyperplasia

MANAGEMENT :
History & physical examination
Eliminate causative factors
Drugs – Phenytoin , Carbamazepine , Ethosuximide
DENTAL MANAGEMENT :
Pts with poor control – dental therapy contraindicated
NSAIDs preferred
Opoids – dose reduced
Gingival hyperplasia – recall oral prophylaxis
surgical correction
alternate anticonvulsant
Minimize aspiration – rubber dam & clamp with floss
fixed prosthesis
metal reinforced crowns preferredwww.indiandentalacademy.com

MANAGEMENT OF SEIZURES :
Place pt. in supine position
Gently restrain the patient
Maintain airway patency
Place towel or padded tongue depreesor
Remove sharp objects from patient’s vicinity
Recurrent seizures – medical assisstance
Diazepam i.v. slowly

BELL’S PALSY
Etiology :
Ischemia of facial nerve near stylomastoid foramen
Trauma – VII n.
Surgery – parotid gland
CLINICAL FEATURES :
Unilateral paralysis of facial muscles
Mask like appearance
Drooping of corner of the mouth
Drooling of saliva
When pt. smiles, forehead does not wrinkle nor does the eyebrow raise
Difficulty in speech & eating
Altered taste sensation
TREATMENT :
No specific treatment
Vasodialators – histamine
Permanent paralysis – surgical anastomosis of nerveswww.indiandentalacademy.com

TRIGEMINAL NEURALGIA
Etiology :
Circulatory insufficiency
Compression of Gasserian ganglion by carotid a. pulsations
CLINICAL FEATURES :
Unilateral (right side of the face)
Pain – sharp , lancinating or stabbing
Trigger zones – vermillion border of lip, alae of nose, cheek,
around the eyes
Attack lasts for few sec to min
TREATMENT :
LA – block the onset of pain
Carbamazepine , Phenytoin sodium
Injection of alcohol or boiling water – Gasserian ganglion
Surgical sectioning of the nervewww.indiandentalacademy.com

PARKINSON’S DISEASE
Degenerative disease affecting the basal ganglia
Etiology :
Unknown , depletion of dopaminergic receptors
CLINICAL FEATURES :
Tremors
Rigidity of limbs
Bradykinesia
Slow mentation
Slow shuffling gait
ORAL MANIFESTATION :
Expressionless face
Difficulty in swallowing & mastication
Drooling of saliva
Labored speech www.indiandentalacademy.com

MANAGEMENT :
Levodopa + carbidopa
Dopamine receptor agonist – bromocriptine
Physiotherapy
Speech therapy
DENTAL MANAGEMENT :
Minimize stress
Rubber dam – prevent aspiration & maintain a dry field
Xerostomia - Regular oral prophylaxis

MYASTHENIS GRAVIS
Chronic disease characterised by weakness of skeletal muscles,
particularly those innervated by cranial nerves
Etiology :
Defect in the neuromuscular transmission of acetylcholine
CLINICAL FEATURES:
Middle aged women
Abnormal fatiguable weakness of muscles
Intermittent ptosis or diplopia
Loss of weight
Difficulty in mastication & deglutition
Speech slowed & slurred

TREATMENT :
Maximize the activity of Ach at the remaining receptors
Anticholinesterase – Physostigmine , Pyridostigmine (30 – 120 mg qid)
Corticosteroids
Thymectomy
DENTAL MANAGEMENT :
Endotracheal intubation to prevent respiratory crisis
Airway should be kept clear
Adequate suction & use of rubber dam
Avoid narcotics , tranquilizers

SEXUALLY TRANSMITTED
DISEASES

First reported in USA in 1981
• Caused by HIV
• Modes of transmission
– Sexual contact
– Sharing of needles and syringes among IV drug users
– Mother to child (transplacental, perinatal, breast feeding)
– Blood transfusion
– Transplantation of infected organs
HIV infection is divided into –
• Group I – acute infection
• Group II – asymptomatic infection
• Group III – persistent generalized lymphadenopathy
• Group IV – ARC (AIDS related complex)
ACQUIRED IMMUNODEICIENCY SYNDROME

Oral manifestation of HIV infection
• Group I – lesions strongly associated with HIV
– Candidiasis, hairy leukoplakia, NUG, NUP, Kaposi’s sarcoma
• Group II – lesions less commonly associated with HIV
– Mycobacterium avium intracellulare, necrotizing stomatitis,
ulcerations, xerostomia, thrombocytopenic purpura, HSV, HPV,
Herpes zoster
• Group III – lesions seen in HIV
– Bacterial – actinomycosis, K. pneumoniae
– Fungal – cryptococcus, histoplasma
– Viral – cytomegalovirus
– Parasitic – pneumocystitis carnii
– Drug reactions – Lichenoid reactions, recurrent aphthous stomatitis
– Neoplasms – Non-Hodgkin’s lymphomawww.indiandentalacademy.com

MANAGEMENT :
Treatment of virus &prevention of opportunistic infections
Drugs –
Nucleoside reverse transcriptase inhibitors – Zidovudine
Non nucleoside reverse transcriptase inhibitors – Nevirapine
Protease inhibitors – Indinavir
DENTAL MANAGEMENT :
Render only immediate treatment
Double gloving , mouth masks ,eye wear
Meticulous sterilization & disinfection of apparatus , impressions
Pts. with severe thrombocytopenia – platelet replacement before surgery
Prophylactic antibiotics
Treatment of opportunistic infections

ANUG Ulcers
candidiasis
Wart (HPV) Kaposi’s sarcoma Hairy leucoplakia
Herpes labialis Hemorrhagic tongue (HSV)

SYPHILIS
• Cause :Treponema pallidum
• Primary mode of transmission
- Sexual
- Mother --- fetus
- Blood transfusion
• Pt highly infectious – first 2 stage
• maternal transmission  1st ,2 stage
miscarriage, still birth,infant with
congenital malformations

Primary syphilis
• less than 2% -other locations
- most common oral cavity
↓
lips, tongue, palate, gingiva, tonsils
 oral lesion - pain less,clean –based ulceration
 Regional lymphadenopatny –unilateral /bilateral
♦ Initial lesion heals ---- 3-8weeks

• Secondary/disseminated
- 4-10 wks after infection
- Systemic symptoms – lymphadenopathy,sore throat
malaise,headache,wt.loss,fever.
- Mucous patches, multiple painless grayish white plaques
surrounded by erythematous zone – called snail track ulcers –
puched out border

• Tertiary Syphilis / latent syphilis
– free of lesions & symptoms
♦1-30 yrs
♦serious complications
Gumma
↓
Skin,mucosa,soft tissues,bones,
& internal organs, palate, tongue
↓
indurated,nodular or ulcerated lesion
↓
extensive tissue destruction

• Congenital syphilis
Sir Jonathan Hutchinson ( 1858 ) – hutchinsons traid.
- hutchinsons teeth
- interstitial keratitis
- 8th
nerve deafness
- frontal bossing
- short maxilla
- high arched palate
- rhagades
- saber shin
- clutton’s joint
MANAGEMENT :
Penicillin
Erythromycin or tetracycline ( in allergy )

DERMATOLOGICAL DISEASES

LICHEN PLANUS
Most common dermatologic disease
Types :
Bullous Atrophic
Erosive Hypertrophied
CLINICAL FEATURES :
Lesions bilaterally symmetrical
Severe pruritis
Skin lesions – small , angular , flat - topped papules (few mm in diameter)
Coalesce – large plaques covered by wickham’s striae
Arms , thighs , knee & trunk
Lesions – white or gray velvety , thread like papules in a linear , annular ,
retiform arrangement
Buccal mucosa > lips > tongue

PEMPHIGUS
Chronic skin disease characterised by vesicles , bullae , small or large fluid
filled blisters that develop in cycles
Etiology :
Unknown , Autoimmune
Types :
Pemphigus vulgaris , P. vegetans , P. foliaceous , P.erythematous
CLINICAL FEATURES :
Vesicles , bullae on the skin raw eroded areas
Nikolsky’s sign present
Bullae rupture as soon as they are formed leaving raw eroded areas
Lesions covered with white or blood tinged exudate
Severe pain – difficulty in eating
Increased salivation seen www.indiandentalacademy.com

PEMPHIGOID
Vesiculo – bullous disease of unknowm etiology
Types :
Bullous Cicatricial
CLINICAL FEATURES :
Vesicles & bullae – conjunctiva , Nose , larynx , pharynx
Ocular lesions – conjunctivitis
palpebral & bulbar conjuctiva adhere – blindness
Vesicles & bullae rupture to leave raw ,eroded areas
Gingiva most commonly affected
Gingiva – erythematous for months after healing

ERYTHEMA MULTIFORME
Acute dermatitis of unknown etiology
Etiology :
Infections (HSV , bacterial , fungal)
Drugs (Phenylbutazone, barbiturates , Digitalis)
Radiation
CLINICAL FEATURES :
Young adults
Asymptomatic erythematous macules & papules – symmetrical pattern
Sites - hand , arms , feet , legs , face & neck
Target , iris ,bull’s eye lesions
Lesions characterised by pain & discomfort
Macules , papules , vesicles – erosions or ulcers
Tongue , palate , buccal mucosa , gingiva affected

ORAL SUBMUCOUS FIBROSIS
Insidious chronic disease affecting any part of the oral cavity & sometimes
pharynx , occasionally preceded by and/or associated with vesicle formation ,
associated with juxta – epithelial inflammatory reaction followed by
fibroelastic change of lamina propria ,with epithelial atrophy leading to
stiffness of oral mucosa and causing trismus & inability to eat
Etiology :
Betel nut chewing , nutritional deficiency
CLINICAL FEATURES :
Burning sensation of mouth particularly on eating spicy food
Vesicles , ulcers or recurrent stomatitis , with xerostomia or sialorrhea
Stiffness of mucosa
Reduced mouth opening
Difficulty in swallowing & speech
Mucosa – blanched or opaque with fibrotic bands ; buccal mucosa , tongue ,lipswww.indiandentalacademy.com

TREATMENT :
Systemic or local corticosteroids
Hyaluronidase
Topical vitamin A
Oral iron prep.
Severe cases – surgical intervention

CONCLUSION

REFERENCES :
 BURKET’S oral medicine, diagnosis & treatment planning . 10th
ed.
 Dental management of medically compromised patients . 6th
ed.
LITTLE , MILLER .
 Principles & practice of oral medicine . 2nd
ed. SONIS , FAZIO.
 Medical problems in dentistry. CAWSON.
 DAVIDSONS principles and practice of medicine. 19th
ed.
 J Prosthet Dent 2001; 86(6) : 569-73
 Oral Surg Oral Med Oral Pathol Oral Radiol Endod 2000; 89(5) : 570-6
 Dent Clin North Am. 2005 Jan;49(1):15-29
 Oral Surg Oral Med Oral Pathol. 1988 Feb;65(2):167-71.
 Dent Clin North Am. 2003 , vol 47 ( 3,4)

 Acta Odontol Scand. 2005 Oct;63(5):284-93
 J Endod. 2003 Nov;29(11):720-3.
 Br Dent J. 2003 Oct 25;195(8):439-45.
 Gen Dent. 2004 Mar-Apr;52(2):107-14
 Dent Clin North Am. 2005 Jan;49(1):127-41

Next Journal club on Saturday 15/4/06
Dr. Bhuvaneshwari

Systemic diseases/ dental implant courses

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