Hematologic disorders like neutropenia, leukemia, anemia, and thrombocytopenia can influence the periodontium. Neutropenia involves low levels of circulating neutrophils which are important for inflammatory reactions and defense against infection. This makes the tissues more susceptible to destruction from conditions like periodontitis. Leukemia is a cancer of the blood cells that can lead to infiltration of leukemic cells into the gingiva and increased risk of infection. Anemia reduces oxygen delivery and makes tissues more friable. Thrombocytopenia increases risk of bleeding from the gums. Antibody deficiency disorders like agammaglobulinemia compromise immune defenses and can result in early loss of teeth from period

1. BY:
Influence Of Hematologic
Disorders On The
Periodontium

2. SYSTEMIC DISEASE THAT HAVE PERIODONTAL
MANIFESTATION
Not initiate
chronic
destructive
periodontitis
But may
accelerate its
progression
And increase
tissue
destruction

3. LEUKOCYTE
DISORDERS
• Neutropenia
• Low levels of circulating neutrophils
•Absolute neutrophil count (ANC) less than
1500 cells/pL is considered Neutropenia
• Etiology:
• Genetic
• Drug Induced
• Viral infection
Normal neutrophil
1,500-8,000cells/µL

4. HEMATOLOGIC DISORDERS
BLOOD CELLS PLAY ESSENTIAL ROLE IN MAINTENANCE OF
PERIODONTIUM
RBC
• Gas Exchange
• Nutrient Supply
Platelets
• Normal Hemostasis
• Recruitment of cells
during inflammation
and wound healing
WBC
• Inflammatory reactions
• Cellular defense,
• Proinflammatory
cytokine release

5. Influence of hematologic
disorder on the periodentum
Leukocyte
disorders
Leukemia Anemia Thrombocytopenia
Antibody deficiency
disorders
(congenital/aquired)

6. • Mild : ANC 1000-1500 cells /µL
• Moderate: 500 to 1000 cells/µL
• Severe: less than 500 cells/µL
• Forms: Chronic- cyclic- benign
Clinical manifistaion:
• Generalized periodontal destruction – infection -
necrosis
• Generalized aggressive periodontitis (Cyclic
neutropenia)

7. AGRANULOCYTOSIS
Etiology Absence of all types of granulocytes (neutrophils, basophils, eosinophils)
Clinical manifestation
• The onset of disease is accompanied by fever, malaise, general ,weakness, and sore throat
•Ulceration in the oral cavity, oropharynx.
• The mucosa exhibits isolated necrotic patches that are black and gray sharply demarcated
from the adjacent uninvolved areas.
• The absence of a notable inflammatory
reaction caused by lack of granulocytes is a striking feature.
• Gingival hemorrhage, necrosis, increased salivation, and fetid odor are accompanying
clinical features.

8. People with neutrophil disorders often need to take special steps to
prevent complication and infections. These precautions include:
Good hygiene, including frequent hand washing and good dental care,
such as regular tooth brushing and flossing

9. LEUKEMIA
• Def : The leukemias are malignant neoplasm of WBC precursors that
are characterized by the following :
Diffuse
replacement of the
bone marrow with
proliferating
leukemic cells
Widespread
infiltrates
in the liver, spleen,
lymph nodes, and
other body sites.
Abnormal numbers
and forms of
immature WBCs in
the circulating
blood

10. Lymphocytic
(Malignancy occur in cells that
normally form lymphocytes)
Myelogenous
(Malignant change
occurs in cells that normally form red
blood cells (RBCs), some
types of WBCs, and platelets)
Acute chronic
Acute
chronic
Classification According to the cell type involved :

11. All leukemias
tend to displace
normal
components of
the bone
marrow elements
with leukemic
cells
reduced
production of
normal RBCs,
WBCs, and
platelets, which
leads to
anemia,
leukopenia and
thrombocytopena
1)poor tissue
oxygenation,
which makes
tissues more
friable and
susceptible to
Breakdown
2) increased
susceptibility to
infections
3) increased
bleeding
tendency

12. THE PERIODONTIUM IN LEUKEMIC PATIENTS:
Leukemic
Infiltration
Oral
Ulceration
and
Infection
Bleeding

13. LEUKEMIC INFILTRATION
• Leukemic cells infiltrate the gingiva and less frequently the alveolar bone which
lead to gingival enlargement
• accumulation of immature leukemic blast cells in the gingiva adjacent to tooth
surfaces
• Leukemic gingival enlargement is not found in edentulous patients or in patients
with chronic leukemia
• Gingiva appears bluish red and cyanotic, with a rounding and tenseness of the
gingival margin

14. • Microscopic picture :
-Gingiva exhibits a dense and diffuse infiltration of predominantly immature leukocytes
in the attached and marginal gingiva.
-The normal connective tissue components of the gingiva are displaced by the leukemic
cells
-The blood vessels are distended and contain predominantly leukemic cells
-RBCs are reduced in number
-Intercellular and intracellular edema
-The inner aspect of the marginal gingiva is usually ulcerated, and marginal necrosis with
with pseudomembrane formation may also be seen.
-The periodontal ligament and alveolar bone may also be involved in acute and
subacute leukemia

15. BLEEDING
• Gingival hemorrhage is a common finding in leukemic patients
• Caused by the thrombocytopenia that results from the replacement of bone
marrow cells with leukemic cells
• petechiae are often found, with or without leukemic infiltrates in the skin and
throughout the oral mucosa
• submucosal bleeding manifests as ecchymosis
• Oral bleeding has been reported as a presenting sign in 17.7% of patients with
acute leukemia and in 4.4% of patients with chronic leukemia

16. ORAL ULCERATION AND INFECTION
• Granulocytopenia occurs which increases the host susceptibility to opportunistic
microorganisms and leads to ulcerations and infections.
• Discrete, punched-out ulcers are covered by firmly attached white slough can be
found on the oral mucosa.
• Necrotizing ulcerative gingivitis are more frequent and more severe in patients with
terminal cases of acute leukemia
• In leukemic patients , altered and degenerated tissue is extremely susceptible to
bacterial infection, which can be so severe as to cause acute gingival necrosis with
pseudomembrane formation
• In those with chronic leukemia, oral changes that suggest a hematologic disturbance
are rare

17. DENTAL MANAGEMENT
• Prior to chemotherapy :
Consultation with the
oncologist
Dental examination and
treatment planning
Treatment should be based on
the acute needs and postponing
elective treatments until clinical
and laboratory conditions of the
patient is stable
Elimination of sources of
infection
Oral hygiene measures advices
• During chemotherapy :
Preventive oral health
care
Dental treatments should
be scheduled after patient’s
blood counts have recovered

18. GINGIVAL BIOPSY
In patients with diagnosed leukemia, gingival biopsy may indicate the
extent to which leukemic infiltration is responsible for the altered clinical
appearance of the gingiva.
It is important to note that the absence of leukemic involvement in a
gingival biopsy specimen does not rule out the possibility of leukemia
BUT

19. ANEMIA :

20. Anemia is a deficiency in the quantity or quality of the blood as
manifested by a reduction in the number of erythrocytes and in the
amount of hemoglobin. Anemia may be the result of blood loss,
defective blood formation, or increased RBC destruction.

21. Anemias are classified according to cellular morphology and hemoglobin :
content as follows:
(1) macrocytic hyperchromic anemia (pernicious
anemia). decrease in red blood cells that occurs when the intestines cannot properly absorb vitamin B12.
(2) microcytic hypochromic anemia (iron deficiency anemia).
is caused by lack of iron, often because of blood loss or pregnancy.
(3) sickle cell anemia.
the hemoglobin is abnormal, which causes the red blood cells to become hard and sticky and look like a C-
shaped farm tool called a “sickle.” The sickle cells die early, which causes a constant shortage of red blood
cells. Also, when they travel through small blood vessels, they get stuck and clog the blood flow
(4) normocytic–normochromic anemia
(hemolytic or aplastic anemia)
a condition that occurs when your body stops producing enough new blood cells.

22. Pernicious anemia :
results in tongue changes in 75% of patients.
The tongue appears red, smooth, and shiny as a result of atrophy of
the papillae

23. THERE IS ALSO MARKED PALLOR OF THE GINGIVA

24. IRON DEFICIENCY ANEMIA :
induces similar tongue and
gingival changes. A syndrome that consists of glossitis and ulceration
of the oral mucosa and oropharynx and that induces dysphagia
(Plummer–Vinson syndrome) has been described in patients with
iron deficiency anemia.

26. SICKLE CELL ANEMIA :
is a hereditary form of chronic hemolytic anemia that occurs almost exclusively in
blacks. It
is characterized by pallor, jaundice, weakness, rheumatoid manifestations, and leg
ulcers. Oral changes include generalized osteoporosis of the jaws, with a peculiar
stepladder alignment of the trabeculae of the interdental septa, along with pallor
and yellowish discoloration of the oral mucosa .

27. ORAL ASPECTS OF SICKLE CELL DISEASE
RADIOGRAPH DEMONSTRATING INCREASED RADIOLUCENCY
OF THE BONE IN THE INFERIOR BODY OF THE MANDIBLE

30. APLASTIC ANEMIA :
results from a failure of the bone marrow
to produce erythrocytes. The etiology is usually the effect of toxic
drugs on the marrow or the displacement of RBCs by leukemic cells.
Oral changes include pale discoloration of the oral mucosa
and increased susceptibility to infection because of the concomitant
neutropenia.

31. THESE MANIFESTATIONS INCLUDE PETECHIAL
HEMORRHAGES, GINGIVAL SWELLING AND SPONTANEOUS
BLEEDING, ULCERATION, PALLOR AND SEVERE
PERIODONTAL DISEASE

32. Case report :
44-year-old patient reported to the Department of Oral Medicine and Radiology with
complaints of bleeding of gums for the duration of 1 month. Bleeding of gums was
spontaneous and continuous. Greater frequency of bleeding was noticed in the early
mornings. Bleeding occurred from all quadrants of the mouth and the patient reported that
about one cup of blood per day was oozing from the gums. The patient reported a negative
history of rectal bleeding, hemoptysis or hematemesis. The patient had visited a local
physician 20 days back and had been prescribed antibiotics (metronidazole, albendazole),
vitamin C supplement and a multivitamin. He also gave a history of acid peptic disease for
the past 25 years. Patient reported a history of easy bruising and reported ecchymosis and
petechiae on arms, legs and buttocks. On examination, extreme pallor of lower palpebral
conjunctiva

34. INTRA-ORAL PHOTOGRAPH SHOWING ACCENTUATED
BLEEDING O GINGIVA ON MANIPULATION.

35. . INTRA-ORAL PHOTOGRAPH SHOWING ORAL HEMATOMA ON
THE RIGHT BUCCAL MUCOSA IN RELATION TO THE LINE OF
OCCLUSION IN THE MOLAR REGION WHICH IS APPROXIMATELY
2 MM IN SIZE.

36. INTRA-ORAL PHOTOGRAPH SHOWING TWO HEMATOMAS
ON THE UPPER LABIAL MUCOSA. THE LESION ON THE
SIDE IS FORMED BY COALESCING OF MULTIPLE SMALL
LESIONS.

37. INTRA-ORAL PHOTOGRAPH SHOWING THREE
HEMATOMAS ON THE DORSUM OF THE TONGUE.

38. THROMBOCYTOPENIA:
DEFINITION:
IS A TERM THAT USED TO DESCRIBE THE CONDITION OF A REDUCED
PLATELET COUNT EITHER DUE TO : - LACK OF PLATELET PRODUCTION OR
- INCREASED PLATELET DESTRUCTION
- INCREASED LOSS .
PURPURA IS
PURPLISH APPEARANCE OF SKIN OR MUCOUS MEMBRANE THAT
OCCURS AS A RESULT OF DECREASED PLATELETS .

39. THROMBOCYTOPENIC PURPURA MAY BE :
- IDIOPATHIC ( WERLHORF’S DISEASE ) OR
- SECONDARY TO SOME KNOWN ETIOLOGIC FACTOR
NORMAL PLATELET VALUE :
150000- 450000 / UL

40. ETIOLOGY OF THROMBOCYTOPENIA
- APLASIA OF BONE MARROW
- DISPLACEMENT OF MEGAKARYOCYTE IN MARROW
- LEUKEMIA
- REPLACEMENT OF MARROW BY TUMOR
- DESTRUCTION OF MARROW BY IRRADIATION, RADIUM OR BY DRUGS
BENZENE, AMINOPYRENE, ARSENICAL AGENTS

41. ORAL & PERIODONTAL MANIFESTATION OF
THROMBOCYTOPENIA:
- THE GINGIVA ARE SWOLLEN, SOFT AND FRIABLE
- PETECHIAE & HEMORRHAGIC VESICLES OCCUR IN THE ORAL CAVITY,
PARTICULARLY IN THE PALATE, THE TONSILLAR PILLARS, &THE BUCCAL
MUCOSA .
- BLEEDING OCCURS SPONTANEOUSLY OR WITH THE SLIGHTEST
PROVOCATION, &IT IS DIFFICULT TO CONTROL .

42. ANTIBODY
DEFICIENCY
DISORDERS

43. ANTIBODY DEFICIENCY DISORDERS
Agammaglobulinemia
Results from a deficiency
in B cells.
T-cell function remains
normal.

44. - X –linked recessive gene
(bruton’s tyrosine kinase).
- The gene is responsible for B-
cell development so production
of antibodies is deficient.

45. • Onset of recurrent bacterial infections in the 2nd & 3rd decades of
life.
• Basic immunological defect is failure of B-lymphocytes
differentiation into plasma cells.
• Enlarged spleen and swollen glands or lymph nodes.
• Autoantibodies against their blood cells.
• Cause unknown.(Not genetic)
• Aggressive periodontitis is a common finding.

46. ORAL MANIFESTATION:
1. Acute gingival inflammation of both primary
and permanent dentitions.
2. Gingival proliferation
3. Extremely acute inflammation
4. Rapid destruction of bone
5. Recession
6. Tooth mobility
7. Pathologic migration
8. Early tooth loss

47. Cases of periodontal
disease that are
attributed to LAD are
rare. They begin
during or immediately
after the eruption of
the primary teeth.

48. GENETIC DISORDERS
CHÉDIAK–HIGASHI SYNDROME
LAZY LEUKOCYTE SYNDROME
LEUKOCYTE ADHESION DEFICIENCY
PAPILLON–LEFÈVRE SYNDROME
DOWN SYNDROME

49. CHÉDIAK–HIGASHI SYNDROME
• Rare autosomal recessive disorder that affects the production of organelles found
in almost every cell.
• It affects mostly the melanocytes, platelets, and phagocytes including
neutrophiles .

50. CHÉDIAK–HIGASHI SYNDROME
• It causes :
Partial albinism(skin and eyes),
{Melanocytes}
Mild bleeding disorders, {Platelets }
Recurrent bacterial infections(skin
abscesses,
pneumonitis, otitis media, and
sinusitis)
{Phagocytes}

51. CHÉDIAK–HIGASHI SYNDROME
• Neutrophils contain abnormal, giant lysosomes that can fuse with
the phagosome, but their ability to release their contents is
impaired
• Functional neutrophil defects include decreased chemotaxis,
degranulation, and microbicidal activity.
• As a result patients are susceptible to repeated infections that can
be serious and life threatening

52. CHÉDIAK–HIGASHI SYNDROME
• The disease reveals itself periodontally by :
 Severe gingivitis
 Aggressive periodontitis.
 Bone loss is usually generalized and severe.
 Patients do not respond to periodontal
therapy.
 Premature loss of both deciduous and
permanent dentitions.
 Oral findings include ulcerations of the
tongue and buccal mucosa.

53. LAZY LEUKOCYTE SYNDROME
• Characterized by normal bone marrow count of neutrophilis but severe neutropenia (100 - 200 /mm3)
is evident in the peripheral circulation
• Inability of the cells to migrate from the marrow to the peripheral blood or from the peripheral blood
to the site of tissue injury.
• There is loss of chemotactic functions but normal phagocytic and
bactericidal functions.

54. LAZY LEUKOCYTE SYNDROME
 Systemic signs and symptoms
 High fever,
 Cough,
 Pneumonia, and
 Purulent skin abscesses,
 Oral manifestations include
 Painful stomatitis,
 Gingivitis,
 Recurrent ulcerations of the buccal mucosa and tongue,
 Rapidly progressive bone loss, and tooth loss at an early age.

55. LEUKOCYTE ADHESION DEFICIENCY
• Autosomal recessive disorder (localized to chromosome 21).
• Most often diagnosed at birth.
• Many children with LAD do not survive.
• LAD results from an inability to produce or a failure to normally express an
important cell surface integrin (CD18), which is necessary for leukocytes to adhere
to the vessel wall at the site of infection

56. LEUKOCYTE ADHESION DEFICIENCY
• Cases of periodontal disease that are attributed to LAD are rare.
• They begin during or immediately after the eruption of the primary
teeth.
• Extremely acute inflammation and proliferation of the gingival tissues
• Rapid destruction of the bone are found.
• Profound defects in peripheral blood neutrophils and monocytes
• Absence of neutrophils in the gingival tissues have been noted in patients with LAD.
• Both the primary and the permanent teeth are affected, often resulting in early tooth loss.

57. PAPILLON-LEFEVRE SYNDROM
• very rare autosomal-recessive disease caused by mutations
in the CTS gene, coding for the proteolytic enzyme cathepsin
C
• No gender predilection
• Prevalence : 1 to 4 cases per 1 million individuals
• The disease has both Cutaneous and Periodontal
involvements appear together when the patient is between
the ages of 2 / 4 years

58. I. Cutaneous lesions:
• Hyperkeratosis
• Ichthyosis
localized areas on the palms, soles, knees, and elbows

59. II.Periodontal Involvement :
• Patients present first clinical signs in the oral cavity as soon as the
deciduous teeth erupt .
• The oral manifestations of primary teeth are represented by
plaque accumulation, severe gingivitis, periodontitis .
• Often gingival tissues near teeth are inflamed, edematous, tender
to palpation and periodontal abscesses are noticed on teeth, while
those of edentulous regions appeared healthy.
• Premature exfoliation of all deciduous teeth by the age of 5 to 6
• After patients will loss of all deciduous teeth, gingival inflammation
inflammation disappears, and the oral mucosa takes on a healthy
appearance .

60. • The time of eruption of permanent teeth is physiological in timing and normal in shape .
• When teeth erupt the gingiva becomes Characterized by severe gingival inflammation, with high
bleeding indexes, associated with plaque accumulation, deep periodontal pockets begin to form.
• Teeth presented with high mobility, fluttering of the anterior group, and loss of the vertical
dimension and Spontaneous loss.
• At a very early age (usually 15 to 20 years), patients are often edentulous except for the third
molars .
• Tooth extraction sites heal uneventfully

61. • Radiographic investigations show generalized alveolar bone loss and migration of
teeth whit no evidence of root resorption.

64. MICROSCOPIC CHANGES
• chronic inflammation of the lateral wall of the pocket with a predominantly
plasma cell infiltrate, considerable osteoclastic activity with an apparent lack of
osteoblastic activity, and an extremely thin cementum .
• Firatli and colleagues reported depressed chemotaxis of peripheral neutrophils
and suggested that this explained the pathogenesis of the Papillon–Lefèvre
syndrome.
• Ghaffer and colleagues found significantly
depressed neutrophil function in probands with Papillon–Lefèvre syndrome.

65. MANAGEMENT
• if an early diagnosis is made nonsurgical treatment is performed :
• scaling and root planning
• antibiotic amoxicillin and metronidazole (250 mg, three times daily) for 1 week
• mouth rinse (0.2% chlorhexidine gluconate, 10 mL twice daily
• educate the patient on correct oral hygiene
• When teeth are lost, prosthetic therapy will be necessary to replace the lost
elements.
• The prosthetic treatment will be age-specific and will be made with partial or
complete dentures .

66. DOWN SYNDROME
• Mongolism, Trisomy 21
• is a congenital disease caused by a chromosomal abnormality
• characterized by mental deficiency and growth retardation
• The prevalence of periodontal disease is high, occurring in almost 100% of patients
who are younger than 30 years of age.

67. Periodontal disease in those with Down syndrome is
characterized by:
• Deep periodontal pockets
• Substantial plaque accumulation
• Moderate gingivitis
• Moderate recession

68. • The disease progresses rapidly.
• The high prevalence and increased severity of periodontal
destruction associated is most likely explained by poor PMN
chemotaxis, phagocytosis, and intracellular killing .