bleeding disorders in periodontology

3. BLOOD
DYSCRASIAS
Presented By:
Dr. Pearl Bhardwaj
PG I year.
Guided By:
Dr H. S. Grover and
the Faculty

4. Introduction
• Dyscrasia (or dyskrasia) is a concept from ancient
Greek medicine, meaning bad mixture.

5. History
• The concept of dyscrasia was developed by the Greek
physician Galen (130–199 AD), who elaborated a model
of health and disease as a structure of elements,
qualities, humors, organs, and temperaments.
Health was understood in
this perspective to be a
condition of harmony or
balance among these
basic components,
called eucrasia.
Disease was interpreted as the
disproportion of bodily fluids
or four humours: phlegm,
blood, and yellow and black
bile. The imbalance was
called dyscrasia.

6. Blood
Blood
Plasma
Formed
Elements
RBCs
WBCs
Platelets
Blood is a bodily fluid that delivers necessary substances
such as nutrients and oxygen to the cells and
transports metabolic waste products away from the cells.

7. Erythrocytes or RBCs
• Circular, biconcave cell.
• Doesn’t contain a nucleus,
ribosomes, or mitochondria.
• Contains Hb which is
interwoven in the stroma.
• The functions of RBCs include:
• Carriage of O2 from the lungs to
peripheral tissues.
• Carriage of CO2.
• Approx. 5 x 106 /cumm
• Approx. life span- 120 days.

8. Haemoglobin • Present in RBCs.
• Required for:
• O2 transport
• Co2 transport
• Acts as a blood buffer
• Each molecule has 2
ingredients- haem and
globin.
• Haemoglobin is a
conjugated protein.

9. Leucocytes or WBCs
• Leukos= white + cytes= cells
• Their fundamental job is to:
• provide defence against:
• Bacteria
• Viruses
• Fungi
• Parasites
• Remove debris(dead cells) and foreign protein.
• Produce chemicals that produce inflammation.

10. Leucocytes
Granulocytes
Neutrophils
Eosinophils
Basophils
Agranulocytes
Lymphocytes
Monocyte
T- cell
B-
cell

11. Classification
Blood
dyscrasias
Disorders of
blood cells
Red cell
disorders
White cell
disorders
Disorders of
haemoglobin
Haem
disorders
Globin
disorders
Disorders of
hemostatic
mechanisms
Bleeding
disorders
Coagulation
disorders

12. RED CELL
DISORDERS

13. Red Cell Disorders
Disorders of RBCs numbers
Anaemias Polycythemia
Disorder
because of
defects in the
RBC membrane
Hereditary
Spherocytosis

14. Anaemia

15. Anaemias
Deficiency
Anaemias
Iron deficiency
anaemia
Vitamin B12
deficiency
anaemia
Folic acid
deficiency
anaemia
Hemolytic
Anaemias
Haemoglobino
p-athies
Thalassaemias
Erythrocyte
Membrane
Defects
Acquired
hemolytic
Anaemias
Others
Aplastic
anaemia
Fanconi’s
Anaemia
Associated
with systemic
diseases

16. Iron Deficiency Anaemia
• Most common
anaemia.
• Microcytic
hypochromic type of
anaemia.
• Women are affected 4
times more frequently
than men.
CAUSES
• Nutritional Deficiencies
• Chronic Blood loss
• Malaria

17. Systemic features
• None in the early stages
Cardiorespiratory
• Dyspnoea
• Tachycardia
• Palpitations
Cutaneous
• Pallor
• Koilonychia-
spoon shaped nails

18. Oral Manifestations
Angular
stomatitis
Atrophic
glossitis
Ulceration
Palatal
pallor
Carp
mouth

19. General Management
• Administration of 300 mg ferrous sulphate orally, 3 times
daily for 10 days.
• Mild gastrointestinal intolerance is the side effect.
• Takes 10 to 20 days for the hematocrit to normalize.
• Parenteral administration reserved for patients who do
not respond to oral therapy.

20. Dental Considerations
• Local Anesthesia
adequate for pain control.
• Atrophic glossitis –
soreness of tongue with
depapillation or colour
change- best known
effect of severe anaemia.
• Candidiasis may be a
presenting feature
caused by candida
albicans which may be
promoted by anaemia
itself.

21. Periodontal Manifestations
• IDA-CP patients exhibited a higher gingival index,
bleeding on probing, probing pocket depth, and
percentage (%) of sites with a clinical attachment
loss (CAL) of ≥6 mm than CP patients.
• In patients with significant anaemia, elective
periodontal surgical procedures should be avoided
as they may cause bleeding problems and also poor
wound healing.
Impact of iron deficiency anemia on chronic periodontitis and superoxide dismutase activity: a cross-sectional
study. Souvik Chakraborty, Shikha Tewari1, Rajinder Kumar Sharma, Satish Chander, Narula1, Pratap Singh
Ghalaut, Veena Ghalaut. Journal of Periodontal Implant Sci 2014;44:57-64.

22. Vitamin B12 Deficiency
Anaemia

23. Vitamin B12 Deficiency
Anaemia
CAUSES
• Auto immune- Pernicious Anaemia (due to atrophy of
gastric mucosa).
• Poor Intake- specially in vegetarians.
• Malabsorption
• Congenital
• Gastrectomy
• Ileal disease
• Drugs (rare)
• Colchicine
• Neomycin

24. General Features
Slow to develop
because liver stores last
upto 3 years.
• Weakness
• Fatigue
• Light-headedness,
• Rapid heartbeat
• Rapid breathing
• Pale color to the skin
• In addition,
neurological symptoms
particularly
paresthesia of the
extremities may
develop.

25. Oral Manifestations
• A physically normal,
sore or burning tongue
can be caused by early
Vitamin B12 deficiency.
• Tongue may appear
fiery or beefy red and
the tip and margins
show papillary atrophy.
• Candidiasis can be
precipitated by
anaemia.
• Apthous stomatitis
occasionally presenting
feature.

26. Periodontal Manifestations
• Marked pallor of
the gingiva.

27. General Management
• Parenteral course of Vitamin B12 sufficient to provide
daily requirement of 2 to 5 µg until abnormality is
corrected.
• This regimen is followed by monthly intra muscular
injections ( 50 to 100 µg) for the rest of patients life.

28. Dental Considerations
• Local anaesthesia satisfactory.
• Conscious sedation- Nitrous oxide is contraindicated.
• General anaesthesia should be postponed until a low
haemoglobin has been remedied.

29. Folic Acid Deficiency Anaemia
• Needed by the body
to
• synthesize and
breakdown amino
acids
• Synthesize DNA / RNA
• Essential for the
maturation of
erythrocytes.
• Laboratory picture is
that of megaloblastic
anaemia.

30. Folic Acid Deficiency Anaemia
CAUSES
• Mostly dietary deficiency
• Malabsorption
• Coeliac disease and Crohn’s disease
• Increased demands
• Pregnancy
• Patients under going long term renal dialysis
• Drugs
• Alcohol- interferes with metabolism and absorption of folic
acid.
• Barbiturates
• Phenytoin

31. General Features
• Folate deficiency leads to anaemia
• fatigue
• dizziness
• feeling cold
• irritability
• headache
• difficulty breathing
• pale skin
• GI symptoms such as
• Nausea, vomiting
• Abdominal pain
• Diarrhea, especially after meals
• Anorexia also is common.
• In combination with the above symptoms, may lead
to marked weight loss.

32. Oral Manifestations
• In early deficiencies
• Soreness of tongue without depapillation or colour change
• In severe anaemia
• Atrophic Glossitis is the best known effect
• Angular Stomatitis is also a well known sign

33. General Management
• Oral folic acid (1 mg tablet daily) is effective in reversing
megaloblastic anaemia caused by folate deficiency.
• If the underlying cause of deficiency is irreversible (e.g.
intestinal disease), maintenance therapy is necessary.
• The patient should be given education emphasizing the
origin of the dietary deficiency.

34. Dental Considerations
• Local anaesthesia is satisfactory.
• Conscious sedation can be given if the haemoglobin
level is only moderately depressed and supplemental
oxygen can be given.
• General Anaesthesia should be postponed until a low
haemoglobin has been remedied.

35. Aplastic anaemia
• Pancytopenia with a non
functioning bone marrow.
• Rare disease causing
leucopenia,
thrombocytopenia and
refractory anaemia.
CAUSES
• Idiopathic
• Chemicals such as
benzene
• Drugs
• Hepatic viruses
• Irradiation

36. General features
Features of anaemia
• Purpura – usually
the first
manifestation
• Suseptibility to
infection
• Suseptibility to
bleeding

37. Oral manifestations
• Ulceration
• Haemorrhagic
tendencies
• Suseptibility to
infections
• Oral lichenoid
reactions
ulceration Bleeding tendencies
Lichenoid reaction

38. General Management
• First line treatment for aplastic anemia consists
of immunosuppressive drugs, typically either anti-
lymphocyte globulin or anti-thymocyte globulin, combined
with corticosteroids and cyclosporine.

39. Dental Considerations
• Treatment modifications need to take into consideration:
• Anaemia
• Haemorrhagic tendencies
• Susceptibility to infections
• Effects of corticosteroid therapy
• Hepatitis B and other viral infections
• Local anaesthesia is satisfactory.
• Conscious sedation and general anaesthesia should be
avoided

40. Periodontal Considerations
• Gingival
enlargement is a
complication of
cyclosporine
therapy.

41. Polycythemia
• Polycythemia may be
defined as an abnormal
increase in the
erythrocyte count in the
peripheral blood, usually
accompanied by an
increase in hemoglobin.
• Opposite of anaemia
• RBC count and Hb
concentration both rise.

42. Polycythemia
• It can be:
• Primary aka
Polycythemia Vera
• Due to malignant changes in
erythrocyte producing cells.
• Secondary
• Where there is an excess
need of RBCs for survival.
Eg at high altitudes, COPD
and cyanotic heart diseases.

43. Systemic features
• Headache
• Dizziness
• Vertigo
• Tinnitus
• Hemorrhages
• Ruddy cyanotic skin
seen on the face and
extremities
• Splenomegaly is a
common finding on
physical
examination.

44. General Management
• Goal of medical therapy is to reduce erythroid over
production and to lower blood viscosity.
• When the hematocrit rises above 60%, blood is removed
usually about 500 ml initially, by phlebotomy every 2 to 3
days until hematocrit is controlled.
• Thereafter ,maintenance therapy consists of long term
phlebotomy or myelosuppressive therapy.
• Long term myelosupression by chemo therapy or
irradiation is efficient.

45. Oral manifestations
• Facial plethora (red
florid complexion)
is a cardinal sign
particularly evident
around the ears,
nose and lips.
• Oral mucosa may
have cyanotic or
purplish
appearance.

46. Oral manifestations
• Bleeding
tendencies are
evident as
• petechiae,
• hemorrhages
• or prolonged
bleeding following
extractions or
periodontal surgery.

47. Periodontal Manifestations
• The gingivae
appears congested
and edematous
and may bleed
spontaneously
because of
hyperviscosity and
hypertension.
• Gingival
enlargement may
be seen.

48. Disorder in RBC
membrane

49. Hereditary Spherocytosis
• also known
as Minkowski–
Chauffard syndrome
• Intrinsic defect in RBC
membrane that
renders it spheroidal,
less deformable and
vulnerable to spleenic
sequestration and
destruction.
• Mutations disrupt
vertical interactions
between spectrin
meshwork and intrinsic
membrane proteins.

50. Hereditary Spherocytosis

51. General features
Signs and symptoms are highly variable
• Include mild pallor
• Intermittent jaundice
• Splenomegaly.

52. Oral Manifestations
• Manifest in the
mucosa as
deposition of blood
pigments during
episodes of jaundice
or in acute infections.
• Severe dental
infection may trigger
an attack requiring
hospitalisation.

53. General Management
• Splenectomy is frequently performed and is invariably
successful in correcting the haemolysis of erythrocytes.
• Gall Bladder is also removed if symptomatic or diseased.
(affected in about half of the patients).

54. Disorders of Hb
Hb abnormalities
Hereditary
Hemoglobinopathies
Porphyrias
Thalassemias
Acquired
Carboxy
hemoglobenemia
Methemoglobenemia

55. Haemoglobinopathies
• They are genetically determined disorders of
haemoglobin production.
• Each of the haemoglobin peptide (globin) chains has a
unique amino acid sequence that can be altered as a
result of DNA mutations.
• Haemoglobinopathies are mostly seen in non –
caucasians.

56. Sickling Disorders
• It is an autosomal
recessive disorder.
• Erythrocytes distort into
cresent or sickle shape.
• HbS haemoglobin
present instead of HbA.
• 2 α chains as usual but in
the β chains, in position
6, valine instead of
glutamic acid is present.
• Sickling of RBCs leads to
stasis, hemolysis and
microthrombosis of
blood.

57. General Features
6 main problems:
• Painful Crises
• Usually due to infarction brought on by infection,
dehydration, hypoxia, acidosis or cold.
• Form mainly in spleen, bones and joints, brain, kidney,
lungs, retinae and skin.
• Haematological crises
• Caused by parvovirus infection.
• Can be: haemolytic, aplastic or sequestration.
• Chronic Anaemia
• Chronic hyperbilirubinaemia
• Infections- pnuemococci, meningococci, haemophilus
and salmonellae
• Sequestration syndromes

58. Oral Manifestations
• Pallor of the oral
mucosa.
• Slow tooth
development and
eruption.
• Hypoplasia of
enamel secondary
to anemia.

59. Radiographically,
• “Step ladder”
trabecular pattern
• Lamina Dura is
more distinct
• Calcified pulp
canals
• Hypercementosis
may be seen.

60. General Management
• Painful and febrile crises of sickle cell anemia are
managed with analgesics, sedatives, bed rest and fluids.
• When vaso- occluson develops, transfusion therapy is
advocated.
• Whole blood or packed cells are used to increase the
erythrocyte count and to promote tissue oxygenation.

61. Dental Considerations
• Sickle cell anaemia with Hb less than 11 gm/dl presents
a hazard for general anaesthesia.
• Local anaesthesia is the preferred mode for pain control.
• Conscious sedation can be used safely.
• Preferable to avoid Prilocaine which in overdose may
cause methaemoglobinaemia.
• Aspirin is best avoided- may cause acidosis in large
doses.
• Prophylactic antibiotics should be given and infections
may be treated vigorously.
• Elective surgery should be carried out in the hospital and
the anaemia should be corrected pre operatively with the
Hb brought upto 10gm/dl.

62. Thalassaemias
• These are autosomally dominant, inherited
disorders in which either alpha or beta globin chains
are synthesized at a low rate, thereby lessening the
production of Hb A.
• Characterized by hypochromic microcytic anaemia.
• They may be
• Severe- major thalassemia
• Mild – minor thalassemia
• May affect
• alpha chain- alpha thalassemia
• Beta chain- beta thalassemia

63. Beta- Thalassemia
• Results from depressed
production of beta
chains.
• Homozygous beta
thalassemia (Cooley’s
anaemia or thalassemia
major) is characterized
by:
• Increasingly severe
anaemia
• Hepatosplenomegaly
• Skeletal Abnormalities
• Heterozygotes for beta
thalassemia may be
asymptomatic.

64. Oral manifestations
• Marked
overdevelopment of
maxilla and mandible.
• The osseous changes
cause
• prominent cheekbones,
• sunken root of the nose,
• labial inclination of the
maxillary incisor,
• inadequate lip seal.
These lead to the
description “chipmunk”
or “rodent facies”.
• The oral mucosa may
be pale, owing to
anaemia or yellow
tinged due to jaundice.

65. General Management
• Treatment includes blood transfusions to temporarily
control anemia.
• Repeated transfusions accelerate development of
electromyocardial instability.
• Iron chelating agents have been used to improve serum
iron balance in these patients.
• In select cases, splenectomy may be helpful.
• Prognosis for thalassemia major is unfavorable and no
successful therapy is available.
• Death usually occurs early.
• Thalassemia minor often requires no specefic therapy
unless haemoglobin levels drop.

66. Dental Considerations
• Patients undergoing repeated transfusions are at a risk
of Hepatitis B, C and HIV carriage.
• Since splenectomy results in an immune defect, it is
prudent to cover surgical procedures with prophylactic
anti- microbials.
• Local anaesthesia is safe.
• Conscious sedation may be given with oxygen levels not
less than 30%.
• General anaesthesia may be complicated by
enlargement of the maxilla (difficulty in entubation).

67. Periodontal Considerations
• Severe gingivitis is
evident if the patient is
subjected to
splenectomy.
• The colour of gingiva
sometimes tends to
be dark due to high
ferritin levels in the
blood.
• Periodontitis, gingivitis
etc. are very
dangerous foci of
infection in these
immune impaired
individuals. This
situation is worsened
in the presence ofDental considerations in Thalassemic patients Dr Sakshi Madhok, Dr Saksham Madhok. (IOSR-
JDMS)Volume 13, Issue 6 Ver. IV (Jun. 2014), PP 57-62.

68. WBC DISORDERS

69. Classification
WBC
Disorders
Non-
Neoplastic
Leukopenia Leukocytosis
Neoplastic
Leukemias Lymphomas

70. Leukaemias
• Leukemias are potentially lethal diseases in which there
is neoplastic proliferation of bone marrow WBCs.
• They are classified by:
• Clinical course- acute or chronic
• Cell of origin- lymphoblast or non lymphoblast
• Dental management of such patients is often
complicated by bleeding tendencies and susceptibility to
infection.

71. Acute Lymphoblastic
Leukemia
• Most common malignant disease of children.
• Usually in childhood but can affect any age group.
CAUSES
• Ionizing radiation
• Exposure to benzene

72. Clinical features
• Anaemia
• Lymphadenopathy
• Splenomegaly
• Infections
• Fever
• Bruising
• Bleeding tendencies

73. Oral manifestations
• Oral bleeding and
petechiae are typical
manifestations
• Oral pallor
• Gingival swelling
(sometimes)
• Mucosal or gingival
ulceration
• Pericoronitis
• Cervical
lymphadenopathy
• Oral and Peri- oral
Herpetic infections
• Candidiasis caused by
Candida albicans

74. General Management
• Treatment of choice is with prednisolone.
• Other anti leukemic agents like anthracycline antibiotic
are added if needed.

75. Dental considerations
• Preventive oral health care is essential and conservative dental
treatment may be possible.
• Surgery should be deferred except in emergencies .
• Regional local anaesthetics contra indicated if there is severe
haemorrhagic tendencies.
• Conscious sedation is usually possible.
• Anaemia is a contradiction to general anaesthesia however iv
sedation may be used.
• Because of dangers of infection and hemorrhage desmopressin
or platelet or blood infusions may be needed pre operatively.
• Antibiotic coverage should be started pre operatively and
continued till the wound heals.
• Any extraction sockets should not be packed as they predispose
to infection.
• Aspirin and other NSAIDs should not be given since they can
aggravate bleeding.

76. Acute Myeloid Leukemia
• Most common leukemia in adults
CLINICAL FEATURES
• Anaemia
• Lymphadenopathy
• Splenomegaly
• Infections
• Fever
• Bruising and bleeding tendencies
• Night sweats
• Lethargy
• Weight loss

77. Oral manifestations
• Oral bleeding and
petechiae are typical
manifestations
• Mucosal pallor
• Mucosal or gingival
ulceration
• Pericoronitis
• Cervical
lymphadenopathy
• Gingival swelling
(sometimes)- occurs
due to abnormal
response to dental
plaque

78. General Management
• Less responsive to therapy and continues to be lethal for
the majority affected.
• Remission is the result of intensive treatment with
cytosine arabinoside, together with anthracycline
antibiotic, daunorubicin and sometimes methotrexate.

79. Dental considerations
• Preventive oral health care is essential and
conservative dental treatment may be possible.
• Surgery should be deferred except in emergencies .
• Antibiotic coverage should be started pre operatively
and continued till the wound heals.

80. Chronic Lymphocytic
Leukemia• Primary disease of older persons.
• The cause of CLL remains unknown.
CLINICAL FEATURES
• Many are asymptomatic.
• In others,
• Fatigue
• Fever
• Weight loss
• Anorexia
• Lymphadenopathy
• Haemorrhage

81. Oral manifestations
• Gingival bleeding
• Oral petechiae
• Oral ulceration
• Herpes simplex
infection may occur
• Candidiasis is
common
• Bleeding
tendencies
• Liability to
infections

82. General Management
• The chemotherapeutic agent used in the treatment of
CLL is the alkylating agent chlorambucil.
• This agent may be given with prednisone, especially if
autoimmune hemolytic anemia and thrombocytopenia
are present.
• This therapy reduces nodal and spleen size and
improves the quality of life.

83. Dental considerations
• Local anaesthesia is satisfactory.
• Conscious sedation may been given.
• General anaesthesia should be carried out in a hospital.

84. Chronic Myeloid Leukemia
• Most dramatic white cell disorder.
• Proliferation of myeloid cells in the bone marrow,
peripheral blood and other tissues.
CLINICAL FEATURES
• Anaemia
• Weight loss
• Joint pains
• Splenomegaly
• Hepatomegaly
• Rarely lymphadenopathy

85. Oral manifestations
• Pallor of mucosa
due to anaemia
• Disturbance of
taste
• Xerostomia
• Oral hemorrhages
• Swelling of salivary
glands

86. General Management
• Treatment of CML is with the alkylating agent busulfan or
with hydroxyurea.
• These cytotoxic drugs reduce peripheral blood counts
and spleen size, making the patient less symptomatic.

87. Dental considerations
• Treatment planning should take into consideration:
• Bleeding tendencies
• Liability to infection
• Anaemia
• Susceptibility to hepatitis B, C and HIV infection.

88. Periodontal Considerations
• Periodontal manifestations consist of leukemic infiltration,
gingival bleeding. Their expression is more common in
acute forms of leukemia than in chronic forms.
LEUKEMIC INFILTRATION
• Leukemic cells can infiltrate the gingiva and less
frequently the alveolar bone.
• Gingival infiltration results in leukemic gingival
enlargement.
• Clinically, the gingiva appears:
• Bluish red and cyanotic
• Rounding and tenseness of the gingival margin
• Increase in size, mostly in the interdental papilla & partially
covering the crowns of the teeth..

89. Periodontal Considerations
BLEEDING
• Gingival hemorrhage is a common finding in leukemic
patients.
• It is caused by the thrombocytopenia resulting from
replacement of bone marrow cells by leukemic cells and
from the inhibition of normal stem cell function by
leukemic cells

90. Leukemic gingival
enlargement• Most important oral sign
of leukemia.
• True enlargement occurs
in acute leukemia and
seldom in chronic
leukemia.
• It may be
• diffuse or marginal
• localized or generalized.
• Normal contours of
gingiva are lost.
• It may appear as
• A diffuse enlargement
• An oversized extension of
the margins
• A discrete tumor like
interproximal mass

91. Leukemic gingival
enlargement
• Stippling is replaced
by spongy, swollen
tissue that tends to
peel away from the
teeth and bleed easily.
• The consistency is
moderately firm, bit
there is a tendency
towards friability.
• Progressive disease
produces purple, shiny
and hemorrhagic
gingiva.
• Purpuric features like
petechial lesions and
ecchymosis are
common.

92. LYMPHOMAS
• Malignant lymphomas are solid neoplastic growths of
lymphoid cells that arise in reticuloendothelial and
lymphoid tissue.
• They spread to distant lymphoid sites, such as liver,
spleen and bone marrow.
• Originate in the lymph nodes but can arise extra nodally.
• Several types of malignant lymphomas occur, however
those of primary interest are
• Hodgkin’s Lymphoma
• Non – Hodgkin’s Lymphoma
• Burkitt’s Lymphoma

93. Hodgkin’s Lymphoma
• It is a neoplastic
disorder originating in
lymphoid tissue.
• The disease classically
begins as a painless,
enlarging mass that
appears in the neck or
mediastinum of adults.
• Initially arises at a single
site and subsequently
spreads to contiguous
lymphoid structures.
• Characterized by a
neoplastic proliferation of
large multi nucleated
reticulum cells known as
Reed Stenberg Cells.

94. • Progressive
painless swelling of
the cervical lymph
nodes.
• Generalized itching
• Cyclic elevations of
body temperature
• Chills and night
sweats
• Weight loss

95. Non-Hodgkin’s Lymphoma
• Heterogenous
collection of 10
different malignant
lymphoid diseases.
• Produce numerous
atypical
lymphocytes that
obliterate normal
lymph nodal
architecture.

96. General Features
• Painless
lymphadenopathy –
presenting feature.
• Enlarged lymph
nodes are firm,
rubbery and mobile.
• Rapid nodal growth
may impair lymphatic
drainage, resulting in
lymphadema, pain,
parasthesia and skin
infiltrations

97. Oral Manifestations
• Lymphoid tissue of
Waldeyer’s Ring
frequently involved
site.
• Infiltration results in
non tender
enlargements of
tonsillar tissue or the
posterior palate.
• The surface of these
swellings may be
erythematous,
ulcerated or necrotic.

98. Oral Manifestations
• When palate is the sole
site of primary
lymphoma, it is
sometimes referred to as
lymphoproliferative
disease of the palate.
• The enlargement is slow
growing, soft, spongy
and relatively painless.
• The surface is non
ulcerated and often
lumpy, with red surface
telangiestasia.
• As the disease
progresses the colour
changes from pink to
blue purple

99. Periodontal Manifestations
• In rare cases, oral Non- Hodgkins Lymphoma can mimic
other, more common disorders and can appear as a
gingival mass.
• Lymphomas of the gingiva are frequently treated for
months as a pulpal or periodontal problem before the
correct diagnosis is made.

100. Dental Considerations
• Preventive dental measures are most important in
patients with lymphoma.
• Generally speaking, patients in a state of remission can
receive routine dental care.
• However, patients with acute signs or symptoms of
lymphoma should receive only conservative emergency
dental care.
• When invasive procedures are required in the patient
with lymphoma, a bleeding time determination and
consultation with oncologist are recommended.
• Patient undergoing chemotherapy or radiation therapy
should be observed for xerostomia or radiation caries.

101. DISORDERS OF HAEMOSTASIS

102. Haemostasis
• Normal Haemostasis
depends on a complex
interaction of the blood
vessels, platelets, fibrin
coagulation and
deposition and fibrinolytic
proteins.
• Heamostasis consists of
3 reactions:
• Primary- vascular phase
• Secondary- platelet phase
• Tertiary- coagulation phase
All of which occur at the same
time.

103. Primary Haemostasis
• Primary haemostasis is by
vasoconstriction after injury.
• This reduces the outflow of
escaping blood after injury.
• Circulating platelets are
exposed to subendothelial
collagen, which causes the
release of intra- cytoplasmic
granules that stimulate
platelet aggregation and
helps to form the soft primary
plug.
Abnormalities in primary
haemostasis
• Abnormal platelet number or
function
• Abnormal von willebrand
factor

104. Secondary Haemostasis
• The aggregation of
platelets is the second
phase of haemostasis.
• Therefore it is aka ‘the
platelet phase’.
Abnormalities in
secondary haemostasis
• Defects in the
coagulation cascade
cause more serious
bleeding than do
defects of primary
haemostasis.
• They include bleeding
into cavities (chests,
joints, cranium).

105. Tertiary Haemostasis
• It is the third and
final phase.
• It is divided into 2
pathways:
• The extrinsic
pathway
• The intrinsic
pathway

106. Bleeding Disorders
CAUSES
Defects in haemostasis, leading to bleeding disorders can
comprise:
• Platelet activation and function
• Anti – thrombin function
• The more common causes include
• Warfarin- which interferes with clotting factor production
• Vitamin K blockage
• Aspirin – one tablet of which impairs platelet function for
almost 1 week.

107. General Features
• Deep haemorrhage
into muscles, joints
or skin.
• Bleeding from and
into mucosae and
skin (‘bruising’)-
suggests purpura.

108. Localized Oral Purpura
• Blood blisters are
occasionally seen,
typically in older
persons in the
absence of obvious
trauma.
• These blood blisters
are often in the
palate and may
sometimes be 1 cm
or more in diameter
and after rupture
may leave a sore
area for a time.

109. Platelet Disorders

110. Platelet Disorders
• Platelet disorders may be the result of
• alteration in platelet numbers,
• either decreased (thrombocytopenia)
• increased (thrombocythemia),
• altered platelet function (thrombocytopathia).
• Platelet disorders may be:
• Quantitative- Thrombocytopenic purpura
• Qualitative- Disorders of platelet function

111. Causes
• Failed platelet production
• Thrombocytopenia
• von Willebrand’s disease.
• Excessive platelet Destruction
• Idiopathic Thombocytopenic Purpura
• DIC
• Abnormal platelet Function
• Abnormal platelet Regulation

112. Thrombocytopenic Purpura
• Thrombocytopenia is a bleeding disorder characterised
by a platelet count below the normal range.
• Reduced counts may be due to:
• Failure of platelet production
• Disordered platelet distribution
• Increased platelet destruction.
• It may be:
• Auto- immune or Idiopathic
• Drug induced

113. Idiopathic Thrombocytopenic
Purpura
• Aka auto – immune
thrombocytopenic
purpura.
• ITP is one of the
most common
causes of
thrombocytopenia.
• Is auto immune and
can lead to purpura
and prolonged
bleeding.

114. Drug Induced
Thrombocytopenic Purpura
• Reactions of drugs
or toxins resulting in
a low platelet count
and bleeding
tendency.
• Common offenders
are:
• Quinidine
• Quiunine
• Sulfonamides
• Heavy alcohol
consumption.

115. General Features
• Hallmarks are:
• Abrupt appearance of
petechial hemorrhages.
• Purpura
• Bruises after trauma
• Petechiae cover
extensive surface area
appearing rash like,
but are tender and do
not itch.
• Located chiefly on
arms, lower leg, upper
chest and neck.
• In severe cases-
mucosal bleeding of
the GIT may occur.

116. Oral Manifestations
• Include petechiae
• Ecchymoses
• Post operative
haemorrhage.
• Sumucous purpura
may be conspicous
and sometimes
seen as
“blackcurrant jelly”
blood blisters.

117. Dental Considerations
• Regional local anaesthetic block injections can be given.
• Major surgery requires platelets more than 75x 10 9 /l.
• Conscious sedation can be given.
• General anaesthesia can be given in an hospital.
• Avoid aspirin and other NSAIDs.

118. Periodontal Considerations
• Gingiva is soft,
swollen and friable.
• Bleeding occurs on
the slightest
provocation and is
difficult to control.
• The severity of the
gingival condition is
dramatically
alleviated by
removal of the local
factors.

119. CONGENITAL COAGULATION
DEFECTS
Most important hereditary bleeding disorders
include:
von Willibrand’s disease
Haemophilia A and B

120. Haemophilia
• X linked disorder resulting from a deficiency in clotting
factor VIII (Hemophilia A or classic) or factor IX
(Hemophilia B or Christmas Disease) .
• Affects males, females are carriers.
• 3 forms of hemophilia are seen:
• Severe- < 1% of normal factor VIII
• Moderate – 1% - 5%
• Mild – 5% – 25%

121. General Features
• Characterized by
severe, persistent
bleeding.
• Hemorrhage into soft
tissue, muscles,
organs and joints.
Clinically these are
prominent as
hematomas and
hemarthroses.
• Excessive bleeding
after trauma.
Intractable oozing or
rapid blood loss one
hour or more after
injury.
• Sometimes
spontaneous bleeding.

122. Oral Manifestations
• Petechiae
• Ecchymoses
• Spontaneous
gingival bleeding can
occur
• Prolonged massive
bleeding even from
simple tooth
exfoliation or
extraction.
• Associated with
anaemia induced
pallor and
pseudoaphthae.

123. Dental considerations
• Local anaesthetic injections or surgery can be followed
by persistent bleeding for days.
• The hemorrhage cannot be controlled by pressure alone.
• Bleeding tendency may be aggravated by NSAIDs.
• In all but severe haemophiliacs, non surgical dental
treatment can usually be carried out under antifibrinolytic
cover.
• Extractions and dentoalveolar surgery should be
carefully planned. A factor VIII level between 50 and
75% is required.
• Mild hemophiliacs requiring such surgeries can be
managed usually without factor replacements.
Desmopressin and tranexamic acid are primary
alternative.
• Post operative suturing is desirable. Vicryl sutures are

124. Periodontal considerations
• Periodontal health is of critical importance for the
hemophiliac for 2 primary reasons:
• Hyperemic gingival contribute to spontaneous and
induced gingival bleeding.
• Periodontitis is leading cause for tooth morbidity
necessitating extractions.
• In all but severe hemophiliacs, scaling can be
carried out without LA.
• Periodontal surgery requires LA and factor VIII
replacement to a level between 50 to 75%
Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty dentistry for the hemophiliac: Is there a
protocol in place?. Indian J Dent Res 2007;18:48-54

125. von Willebrand’s disease
• Due to inherited
deficiency in vWF.
• Most common
inherited bleeding
disorders.
• Affects both males
and females.

126. General Manifestations
• Generally, bleeding
manifestations are
mild.
• Epistaxis
• Bleeding from the
mucous membrane
• Purpura of mucous
membrane and skin
• Menorrhagia in
females

127. Oral Manifestations
• Gingival bleeding is
the most common
finding- in about 30
– 40% of the
diseased.
• Uncontrollable
bleeding during
dental procedures
like gingival
manipulation and
pulpectomy.

128. Dental Considerations
• Aspirin and NSAIDs should be avoided.
• Local infilteration anaesthesia should generally be used.
• Nerve block anaesthesia is generally contra indicated
because injections delivered into loose alveolar tissue
(highly vascular regions) may produce bleeding or a
dissecting hematoma that could obstruct the patient’s
airway.
• Conscious sedation can be given, but care must be
taken not to damage the vein.
• General anaesthesia must be given in hospital.
• Intubation is a possible hazard because of the risk of
submucosal bleeding in the airway.

129. Periodontal Considerations
• Gingival haemorrhage
is more common than
in haemophilia.
• Even minor gingival
manipulation can lead
to uncontrollable
bleeding.
• Cryoprecipitate or
other anti fibrinolytic
agents shoulld be
administered to
minimize bleeding.
• Post operative diet
should be soft and
semi solid to minimize
trauma to the gingiva.

130. GUIDELINES FOR ORAL
HEALTH CARE OF PATIENTS
WITH HEMATOLOGIC DISEASE

134. Guidelines for Hemorrhagic
Dental Procedures
• Should be avoided when patients conditions are poorly
controlled.
• Provide prophylactic antibiotics to prevent infection when
open wounds are present.
• Obtain pre operative CBC, DLC, platelet count, bleeding
time, PT and APTT. Any abnormal values mandate a
consultation.
• Oral surgical procedures should be done only if
absolutely necessary and in a hospital setting.
• Single dental extractions should be performed as
opposed to multiple extractions.
• Pay meticulous attention to good technique and primary
closure.

135. Guidelines for Dental
Emergencies
• Pallative emergency treatment only.
• Dental infections should be treated aggressively with
antibiotics and drainage.
• Surgical procedures should be avoided until control of
disease can be assessed with blood profiles.
• Non – Aspirin or Non- NSAID containing drugs should be
prescribed as post operational analgesics.
• If the patient comes back with bleeding-
• Debride the wound site and remove any clot.
• Control the bleeding by packing the socket with absorbable
microfibrillar collagen or thrombin soaked gauze.

136. Conclusion
• Recording a proper history including past medical and
dental history and family history of the patient goes a
long way in helping the clinician in managing patients
with bleeding disorders.
• It not only helps in reaching to a proper diagnosis of the
patient’s condition but also in forming a holistic treatment
plan that is beneficial for the patient.
• Knowledge of the signs and symptoms, both oral and
systemic of these diseases enable the clinician in
diagnosing cases in which the patient does not have any
information about the presence of such disease.

137. References
1. Concise medical physiology, Chaudhuri, IV edition.
2. Robbin’s Basic Pathology, Seventh Edition.
3. Medical Problems in Dentistry; Crispian Scully, Roderick A. Cawson; V
edition.
4. Carranza’s Clinical Periodontology, X edition.
5. Color Atlas of Oral Diseases; George Laskaris; III edition
6. Oral Diagnosis, Oral Medicine and Treatment Planning, Bricker,
Langlais, Miller, II edition.
7. Impact of iron deficiency anemia on chronic periodontitis and
superoxide dismutase activity: a cross-sectional study. Souvik
Chakraborty, Shikha Tewari1, Rajinder Kumar Sharma, Satish Chander,
Narula1, Pratap Singh Ghalaut, Veena Ghalaut. Journal of Periodontal
Implant Sci 2014;44:57-64.
8. Naveen Kumar J, Anil Kumar R, Varadarajan R, Sharma N. Specialty
dentistry for the hemophiliac: Is there a protocol in place?. Indian J
Dent Res 2007;18:48-54
9. Dental considerations in Thalassemic patients Dr Sakshi Madhok, Dr
Saksham Madhok. (IOSR-JDMS)Volume 13, Issue 6 Ver. IV (Jun.
2014), PP 57-62.