Oral medicine 2020-2021

Blood loss Anemia Inadequate production

of mature erythrocytes
Classification acc. To etiology

Chronic acute

↑↑ destruction of Impaired blood

RBCs production

Extra corpuscular Intracorpuscular

Iron
causes causes deficiency Pernicious
anemia anemia

Aplastic
anemia.
Hereditary

Cooly’s sickle cell

anemia anemia

Acquired

Hemolytic anemia
associated with lead
poisoning

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 Oral medicine 2020-2021

PERNICIOUS ANEMIA (Addison's anemia) APLASTIC ANEMIA

B12 deficiency in absorption as secondary to intrinsic factor  Primary or idiopathic: unknown origin, fatal prognosis, young
deficiency in the stomach adult
 Secondary : known origin, better prognosis, any age
1. Drugs and chemicals through:
Etiology &
 Myelosuppressive effect , Marrow depression,
Types
Hypersensitivity reaction
2. Infections: T.B, hepatitis & infectious mononucleosis
3. Radiation
4. pregnancy and thymoma
Age: (↑ in frequency with advancing age.) rare before30 years Age : at any age (common in young adults)
Sex: Males > females Symptoms due to ↓ RBCs:
Symptoms:  weakness after slight physical exertion
 triad of symptom: Generalized weakness, sore painful  pallor of skin
tongue, numbness and tingling of the extremities.
 breathlessness, headache.
Signs:
Symptoms due to ↓ WBCs: ↑ Bacterial & fungal infection
Clinical  Fatigability, headache, dizziness, nausea, vomiting,
Features diarrhea, loss of appetite, shortness of breath, loss of Symptoms due to ↓ Platelets:
weight, pallor and abdominal pain  bruising & bleeding.
Nervous system  retinal and cerebral hemorrhages.
 sensory disturbances Signs :
 tingling sensation in the fingers and toes  ankle edema & numbness and tingling of extremities.
Gastrointestinal complaint:  anginal pain &congestive cardiac failure
 Epigastric discomfort, constipation or diarrhea
Glossitis & disturbance in taste sensation 1. Pallor of oral mucosa (d.t ↓ RBCs)
 Hunter glossitis showing fiery red appearance in 2. Spontaneous hemorrhage from gingiva
megaloblastic anemia , may undergo remission but 3. Petechiae, often are present on the soft palate
recurrent attacks are common 4. In severe cases, there may be submucosal ecchymosis.
Beefy red tongue: 5. Gingival hyperplasia
Oral  entirely or in patches scattered over the dorsum and lateral 6. Large ragged ulcers covered by gray or black necrotic membrane
Manifest border of tongue (d.t ↓ resistance to infection)
Hunter glossitis or Moeller glossitis :
 similar to the bald tongue of sandwich' seen in pellagra.
Xerostomia → lobulation on tongue
Oral mucosa :greenish yellow color( junction of hard & soft palate)

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Clinical diagnosis : same as C/P
Laboratory diagnosis:
 Histologically of Oral epith cells :
 enlarged, hyperchromatic nuclei with prominent
nucleoli and serrated nuclear membranes.
diagnosis  blood count:
 ↓ RBCs count 3 million or less/ mm3
 ↓ WBCs count & mean corpuscular hemoglobin
 Schilling test: absence of intrinsic factor.
 ↑ Gastric pH & Achlorhydria (↓ HCL secretion)
Daily subcautenous Vitamin B12 for first week.
1. If therapy is successful, doses are then administered twice
weekly for another 4-5 weeks.
2. After this 100 pg monthly by subcutaneous or intramuscular
Management
route
Diet modifications
 supplementary vit B12. oral tablet of 100-200 pg
↓ Physical activity
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Oral medicine 2020-2021
Clinical diagnosis: same as C/P
Laboratory diagnosis:
1. Pancytopenia : ↓ no. RBCs, WBCs, Platelets
 ↓ no. RBCs : 1 million cells/mm3
 ↓ no. WBCs: 2000/mm3 (↓ resistance to infection)
 ↓ no, Platelets: 20000/mm3.
 ↓ no. Reticulocyte (immature RBCs)
2. Bleeding time is prolonged and clotting time is normal.
3. normocytic or some degree macrocytic anemia
4. Bone marrow is fatty and few developing cells.
1. Removal of cause
2. antibiotics and transfusion (Supportive therapy)
3. androgenic steroid : +++ Hemopoiesis
4. Bone marrow transplantation
5. Anti-fibrinolytic agents (as aminocaproic acid or tranexamic
acid) → ↓ Gingival bleeding
6. Immunosuppressive therapy (if patient can’t take B.M
transplantation)→ Antithymocyte globulin combine with
cyclosporine
 Oral medicine 2020-2021
Iron deficiency anemia Plummer-Vinson Syndrome (Paterson Kelly syndrome)
a. of iron in the diet
Severe form of Iron deficiency anemia Ch. By: dysphagia, iron
b. of iron (hypochlorhydria & diarrhea)
deficiency anemia, dystrophy of nails (koilonychias) and
Etiology c. of iron (growing child & in pregnancy) glossitis.
d. of iron
e. Subtotal or complete
(most common anemia) Age : middle age (40-50 years)
Age: 4th and 5th decades Sex : Women
Sex : Women > Man Symptoms :
Symptoms:
 characteristic asthenic appearance
 experiences tiredness, headache, paresthesia and lack of
concentration  spasm in throat
Signs: Signs:
1. Koilonychia (brittle, flattened & spoon shape nails)  Dysphagia: d.t webs in esophagus, Muscular
C/P 2. tingling and pins and needle sensation in the extremities degeneration & stenosis of esophageal mucosa
(neuropathy)  spoon-shaped nails. (Koilonychia)
3. dysphagia (D.t pharyngeal mucosal thickening & mucosal web)
 A lemon-tined pallor of the skin.
4. Gastrointestinal symptoms: Liver and spleen may be palpable &
gastrointestinal bleeding  Splenomegaly in 20 –30% of cases
5. Knuckle pigmentation ( at dorsum of hand at
metacarpophalangeal joint)
6. Sideropenic anemia: Ch by ring sideroblasts ( iron accumulate in
mitochondria around nucleus)
1. Pallor of mucosa and gingiva : 1. mouth is narrow
 ↓ oxygenated blood & ↓levels of hemoglobin 2. Oral mucosa : Atrophy , pale & painful
2. Generalized Atrophy of oral mucosa (tongue & buccal mucosa) 3. Tongue: atrophy of filliform &fungiform papillae →sorness
3. Tongue changes & pain
 Painful (burning) & soreness sensation
4. Angular cheilitis: Vermilion borders of the lip are very thin
 Tongue papillae atrophy : filiform firstly in sever case fungiform
may disappear → waxy or glistening tongue 5. dry mouth
Oral 6. upper alimentary tract mucous membrane: Atrophy →
4. Angular cheilitis
manifest development of carcinoma
5. Ulceration:
 softening of epithelium → linear ulceration of the skin→
extending upto and beyond the mucocutaneous junction. → pain
& bleeding
 Recurrent aphthous ulceration &candidal lesions
6. Slow healing:
7. Gingival enlargement:
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 Oral medicine 2020-2021
same as C/P same as C/P

Diagnosis 1. anemia is microcytic and hypochromic  Atrophic epithelium and atrophy of lamina propria and
2. ↓ hemoglobin level: as low as 4 g/100 mL. → so ↓ serum iron muscles. + same as Iron deficiency anemia
3. normal or slightly ↓ RBC count potentially serious because pharyngeal and
4. ↓ MCV, MCH and MCHC are all reduced intraoral carcinoma are common in those patients.
The etiology of iron deficiency should be established first.
Iron supplement: Iron supplements are given to treat iron deficiency
1. oral supplements of iron(Almost patient)
anemia. It also improves mild dysphagia in patients.
 ferrousfumerate or ferrous sulphate ( 300 mg three to four
times a day for a period of 6months).
Managem. 2. parenteral route of administration 1. Diet modi fication in mildly symptomatic patients.
 unable to take iron by mouth 2. esophageal dilatation.
Long lasting
 unable to or absorb iron by mouth. 3. passage of endoscope.
dysphagia (severe
 The recommended single dose of iron sorbitol is 1.5 mg of 4. ND:YAG laser therapy
symptoms)
iron per kg of body weight, given daily. 5. Needle-knife electroincision
Dental  ↓ hemoglobin value → refer the patient to the physician.
managem.  does not perform elective oral surgical

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 Oral medicine 2020-2021

Thalassemia SICKLE CELL ANEMIA

‘Cooley’s anemia’, ‘Mediterranean anemia’ and ‘erythroblastic anemia’
1. Absence of alpha or beta chains → Reduces hemoglobin →
shortened lifespan of RBCs Glutamic Substitution on position 6 valine Formation of
2. Excess unpaired α chains inside cells (in case absence of β deoxygenated
hemoglobin S tactoids distort the
chain) → Alteration in structure of cells → Hemolysis of RBCs
Patho- in spleen. RBCs membrane Sickle shaped cells ↑ blood
genesis 3. ↑ hematopoiesis to maintain adequate oxygenation.→ Bone
marrow hyperplasia viscosity Thrombosis and infarction

 Patients may develop severe folic acid deficiency due to ↑

erythropoiesis
reduction or absence of α chain synthesis. homozygous individuals, whole Hb A is
 α chains are required for HbA but HbF, which is the main replaced by Hb S ‘sickle cell anemia’
hemoglobin type in fetal life. heterozygous individuals, only 50% of HbA is
 results in hydrops fetalis and intrauterine death of fetus.
replaced by HbS ‘sickle cell trait’.
reduction or absence of β chains.
 Hemolysis of RBCs due to β-globin chains but & Excess
unpaired α chains inside cells → insoluble aggregates that
precipitate within the RBCs → damage to the cell memb.
3. (

a. Occur in homozygous (severe form). In this case two

Types defective gene is affected. (90% is Hb F, 10% Hb).
b. It can be differentiated from iron deficiency anemia by
serum iron level (serum iron is higher in those patients due to
decreased Hb production that resultrom deficiency of Beta
globin chain synthesis)
 Hemoglobin H disease: It is very mild form of the disease
in which the patient may live relatively normal life.
 Hemoglobin Bart disease: infants are stillborn or die
shortly after birth.
4. clinical manifest. ( ) major & minor.
5. Occurs in
heterozygous, one defective gene is affected.
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 Oral medicine 2020-2021
 : between the ages of 6 and 24 months and after the age of 6-  Age: before the age of 30 years (Most of persons expire before
8 months. the age of 40 years.)
 :  Sex and age: females > Male

pallor of skin, fever, chills, malaise, generalized weakness,
prominent cheek bone and mild hepatosplenomegaly.
 :
Bone marrow hyperplasia & frontal head bossing & marked
overdevelopment of malar bone which is associated with a
short nose having a depressed bridge
 :
Due to deposition of iron in various organs (due to
multiple transfusions).

Most patients die in childhood due to anemia and cardiac
failure.
 Incubation period: Clinical manifestations begin only after
several months ( as Hb F protects against sickling phenomenon)
 Precipitating factors: dehydration, chills, hypothermia and
infection (may occurs spontaneously)
 Signs & Symptoms:
 fatigue, weakness and shortness of breath.
 When associated with folate deficiency, there may be growth
retardation & delayed puberty
Large heart
and murmur

C/P  : severe alveolar bone loss, pronounced

spacing of maxillary anterior teeth and mongoloid appearance. (painless)

Pallor of
palm

Skull changes:
 Hyperplasia of marrow in first year of life → prominent malar
bones & protuberant teeth
Sickle cell crisis:
 Def.: severe sickling after long quit spell of hemolytic
latency→ severe pain, Each episode occasionally punctuated
by exacerbations called as sickle cell crisis
 Precipitate factor: same as above.
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Acute chest syndrome:
 serious complication of sickle cell crisis (pulmonary
involvement)
Infarction:
 Infarction can only occur in bone and spleen but, other
tissues may also be involved. In infants, fingers and toes are
commonly affected
Thrombosis:
 in brain → severe neurologic disorders like
 smaller vessels → headache & paresthesia
 a. show pallor and jaundice
1. excessive overgrowth of maxilla → excessive lacrimation and b.
nasal stuffiness  delayed eruption and hypoplasia of the dentition, secondary
2. hyperplasia of alveolar process to their general development
3. anterior open bite & maxillary teeth are protrudes → upper c.
lip is retracted
 due to hypovascularity of the bone marrow 2ry to thrombosis
4. discoloration of dentin and enamel (d.t ↑iron deposition)
Oral d.
5. prominent malar bone → prominent cheek bone
manifest  paresthesia of mental nerve which may be secondary to
 :
occlusion involving the nerves and blood supply
 color : pale & lemon yellow tint (chronic jaundice).
e.
 Site: at the termination of hard palate & floor of mouth.
 Mongoloid facies with high cheek bones and bimaxillary
 : after dental treatment
prognathism. It is due to marrow hyperplasia resulting in an
 : increase in hard palate length and palate alveolar ridge angle.
I. Patient may be having pigmentation in oral cavity
II. in some cases persistence of mamelon
1. Hair on end appearance: trabeculae joining the inner and outer 1. ↑ R.O of Lamina dura
table of the skull are readily arranged calcified spicules 2. Thinning of inferior border of mandible (↑ R.L)
2. compensatory lamellar striation 3. Step ladder effect between roots of teeth
3. spike shaped mandibular molar Skull
R/F  Hair-on-end appearance
4. antra is reduced in size by the encroachment of the bone
formation  There is thickening of the frontal and parietal bones.
 ↑ width of the dipole space (absent of outer table)

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 Oral medicine 2020-2021
Due to osteoporosis: Osteoporosis:
Teeth:  chronic ↑ erythropoietic activity & marrow hyperplasia →
 Thin Lamina dura loss of trabeculation
 Thin Crypt of developing teeth Ground glass appearance:
 Circular R.L in lower anterior region  diminution of fine trabeculae as there is replacement of
Alveolar bone: marrow by compensatory hyperplasia
 Shows osteoporosis and blurring of trabeculae.
Due to ↑ bone marrow space (↑ hematopoiesis) :
Long bones:
 generalized radiolucency, ↑ width of shaft
 narrowing of cortices
 pathological fracture
Skull: thickened
 ↑ width of the dipole space
 Generalized granular appearance

Bone marrow:  RBCs:

 Cellular hyperplasia due to ↑ erythropoietic activity.  typical sickle shaped
RBCs:  reach level of 10 lac cells or less per cu mm
 anemia is hypochromic and microcytic.
 count about 1,000,000/mm3
 Variation in shape of RBCs:
 sickle shaped cells then ‘logjam’ and produce stasis within
1. RBCs appear pale with coloring material in the center.
Diagnosis the microvasculature.
2. safety pin cells in the circulation.
 Damage leading to fragmentation & intravascular hemolysis
 shortened life span
 ↑ Reticulocyte  Haemoglobin:
Haemoglobin:  hemoglobin is ‚S‛ Hb (abnormal).
 ↑ Hbf (90% HbF and 10% HbA.)  undergoes gelation or crystallization when deoxygenated
 Hb levels from 5 to 12 gm/ dl.
↑WBCs, Serum iron, serum Bilirubin
 good prognosis

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1. Bone marrow transplantation for young individuals → Due to
osteoporosis
2. Splenectomy if ↑ anemia severity → due to splenomegaly
3. Repeated blood transfusion → Due to ↓ RBCs
4. Chelating agent (desferrioxamine) → Due to ↑ serum iron may
lead to hemochromatosis
5. Surgical correction → in case surgical correction
Manage-
ment
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Oral medicine 2020-2021
by avoiding the precipitating factors (chilled, dehydrated
or exposed to hypoxia (high altitude)
(5 mg/daily) , ↑ erythropoietin
 Young patient with hyposplenism should be given
phenoxymethyl penicillin
 nonaddictive analgesics like aspirin, paracetamol should be
given because the episodes are recurrent pain due to tissue
infarction
 indicated in adult patients in severe cases.
 Mechanism : ↑ fetal form of hemoglobin → inhibits the
polymerization of hemoglobin S and reduce adherence of
erythrocytes to vessels walls.
should be given during crisis only. Routinely it should be
avoided, because it increases the viscosity of blood
for patient who has sickle cell trait.

 there are always chances that any infection might precipitate an
aplastic crisis

 Avoid using general anesthesia (to avoid episodes of hypoxia
because of the cerebral or myocardial thrombosis which
might result.