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Dr. Suhail S. Kishawi
Consultant in Endocrinology and Diabetes
سهيل شريف القيشاوي. دلغدد الصماء والسكريأستشاري ا
أستشاري األمراض الباطنية
Oral Manifestations of Systemic Diseases (II)
Oral Manifestations of Systemic Diseases
Many systemic diseases are reflected in the oral mucosa, maxilla,
and mandible.
Mucosal changes may include ulceration or mucosal bleeding.
Immunodeficiency can lead to opportunistic diseases such as infection
and neoplasia.
Bone disease can affect the maxilla and mandible.
Systemic disease can cause dental and periodontal changes.
Drugs prescribed for a systemic disease can affect oral tissue.
Oral Manifestations of Systemic Diseases
Local factors may be involved in the manifestation of systemic
disease in oral mucosa.
The mucosa may be more easily injured due to a systemic disease,
and mild irritation and chronic inflammation may cause lesions that
otherwise would not occur.
These may include
Endocrine disorders, disorders of red and white blood cells, disorders
of platelets and other bleeding and clotting disorders, and
immunodeficiency disorders
Blood Disorders
Disorders of Red Blood Cells and Hemoglobin
Disorders of White Blood Cells
Bleeding Disorders
Blood Disorders
The complete blood count examines red blood cells, white
blood cells, and platelets.
It provides information about the number of each type of
cell, the ratio of types, and the appearance of the cells.
Disorders of Red Blood Cells
and Hemoglobin
Iron Deficiency Anemia
Pernicious Anemia
Folic Acid and Vitamin B12 Deficiency Anemia
Thalassemia
Sickle Cell Anemia
Celiac Sprue
Aplastic Anemia
Polycythemia
Normal CBC
Anemia
A reduction in the oxygen-carrying capacity of blood
Most often related to a decrease in the number of circulating
red blood cells
Nutritional anemias A deficiency in a substance required for the normal
development of red blood cells, commonly vitamins
Suppression of bone marrow stem cells
Infection
Lack of Concentration
Weakness
Irritability
Palpitation
Fatigue
Dizziness
Symptoms
Clinical Features
•Pallor of skin
•And m/m
Edema
Koilonychia
Glossitis
Stomatitis
Tachycardia
Soft ejection
systolic murmur
Signs
Anemia
Clinical features
Pallor of skin and oral mucosa
Angular cheilitis
Erythema and atrophy of oral mucosa
Loss of filiform and fungiform papillae on the dorsum of
the tongue
Iron Deficiency Anemia
An insufficient amount of iron is supplied to bone marrow for red
blood cell development.
May occur as a result of deficient iron intake, blood loss from heavy
menstrual bleeding or chronic gastrointestinal bleeding, poor iron
absorption, or an increased requirement for iron in situations such as
pregnancy or infancy
Plummer-Vinson syndrome may result from long standing iron
deficiency anemia.
Includes dysphagia, atrophy of the upper alimentary tract, and a
predisposition to developing oral cancer
Clinical Features and Oral Manifestations of Iron
Deficiency Anemia
Often asymptomatic, may have nonspecific symptoms such as
weakness and fatigue
In severe cases may see angular cheilitis, pallor of oral tissue,
and an erythematous, smooth, painful tongue
Clinical Features and Oral Manifestations of
Iron Deficiency Anemia
Pernicious Anemia
Probably an autoimmune disorder in most situations
May be caused by removal of the stomach, gastric cancer,
or gastritis
Caused by a deficiency in intrinsic factor
Intrinsic factor is secreted by parietal cells in the
stomach; it is necessary for absorption of vitamin B12
•There are a number of key steps in the absorption of Vitamin B12. The two key locations
are the stomach and the terminal ilium. Dietary vitamin B12 binds with intrinsic factor (IF) in the stomach, a transport protein produced by gastric parietal cells. The B12-IF complex then travels through the small intestine and is absorbed by special receptors in the distal ileum. This pathway is important when considering possible causes of Vitamin B12 deficiency.
•Vitamin B12 deficiency can take up to two years to develop as the body has sufficient stores for this period.
•Distal ileum
•Site of B12 absorption
•Oesophagus
•Stomach
•IF Intrinsic factor
•Vitamin B12 ingested
Vitamin B12
•Pernicious anaemia: the leading cause of
B12 deficiency. IgG autoantibodies target gastric parietal cells and its product IF causing an atrophic gastritis. This results in reduced secretion of intrinsic factor and therefore reduced B12-IF complex for absorption in the distal ileum.
•Causes of vitamin B12 deficiency
1. Pernicious anaemia
2. Inadequate intake
3. Poor absorption
Clinical Features and Oral Manifestations of
Pernicious Anemia
Weakness, pallor, and fatigue on exertion,nausea, dizziness,
diarrhea, abdominal pain, loss of appetite, and weight loss
Angular cheilitis, mucosal pallor, painful atrophic and
erythematous mucosa, mucosal ulceration, loss of papillae on the
dorsum of the tongue, and burning and painful tongue
Clinical Features and Oral
Manifestations of Pernicious Anemia
Folic Acid and Vitamin B12
Deficiency Anemia
From dietary deficiencies
Can occur in association with malnutrition
May be found with alcoholism or pregnancy
Oral Manifestations of Folic Acid and Vitamin
B12 Deficiency Anemia
Oral manifestations are indistinguishable from
those of pernicious anemia.
Thalassemia
(Mediterranean Anemia)
A group of inherited disorders of hemoglobin synthesis
An autosomal dominant inheritance pattern
The heterozygous form may be mildly symptomatic or asymptomatic.
The homozygous form is associated with severe hemolytic anemia.
Clinical Features and Oral Manifestations of
Thalassemia
Yellow skin & pallor, fever, malaise, and weakness
The face includes prominent cheekbones, depression of the
bridge of the nose, a prominent maxilla, and protrusion or
flaring of maxillary anterior teeth.
Radiographs of skull may show marked vertical striation
(hair on end appearance)
Skull x-ray in a 5 year old boy with thalassemia major
Marked vertical striations give the appearance of hair standing on end
Sickle Cell Anemia
An inherited blood disorder When someone is heterozygous, it is called sickle cell trait.
When someone is homozygous, they are much more severely
affected.
Occurs before age 30 and is more common in women than in men
The red blood cells develop a sickle shape when there is
decreased oxygen.
This can be triggered by exercise, exertion, administration of a
general anesthetic, pregnancy, or even sleep.
Clinical Features and Oral Manifestations of
Sickle Cell Anemia
The person has weakness, shortness of breath, fatigue, joint
pain, and nausea.
Radiographic
There is a loss of trabeculation, and large, irregular marrow
spaces appear.
A “hair-on-end” pattern may be seen in the skull.
Clinical Features and Oral Manifestations of
Sickle Cell Anemia
Celiac Sprue
A chronic disorder due to sensitivity to wheat gluten
Ingestion causes injury to intestinal mucosa.
This injury may cause malabsorption of nutrients and a resulting
anemia.
Clinical Features and Oral Manifestations of
Celiac Sprue
Symptoms include diarrhea, nervousness, and paresthesia.
Painful, burning tongue, atrophy of papillae, and ulceration of oral
mucosa
Aplastic Anemia
A severe depression of bone marrow activity causes a decrease in
all circulating blood cells. – pancytopenia
Primary aplastic anemia – the cause is unknown
Secondary aplastic anemia – a result of a drug or chemical
agent
Aplastic Anemia
Oral Manifestations of Aplastic Anemia
Infection, spontaneous bleeding, petechiae, and purpuric
spots
Polycythemia
Characterized by an increase in the number of circulating
red blood cells
May be absolute or relative
The three forms of polycythemia are
Polycythemia Vera
Secondary Polycythemia
Relative Polycythemia
Polycythemia Vera (Primary Polycythemia)
A neoplastic proliferation of bone marrow stem cells causes
an abnormally high number of circulating red blood cells.
Unknown cause
More common in men than in women
Age of onset usually between 40 and 60 years of age
Clinical features
Headache, dizziness, and itching (pruritus)
Thrombi may form.
Secondary Polycythemia
The increase in red blood cells is caused by a physiologic
response to decreased oxygen.
A decrease in blood oxygen causes an increase in erythropoietin
by the kidneys.
May be due to pulmonary disease, heart disease, living at high
altitude, or elevation in carbon monoxide
Relative Polycythemia
Caused by a decrease in plasma volume
Causes may include diuretics, vomiting, diarrhea, or excessive
sweating.
Most patients are middle-aged white men under physiologic stress,
mildly overweight, hypertensive, and heavy smokers.
Oral Manifestations of Polycythemia
The oral mucosa may appear deep red to purple; the
gingiva may be edematous and bleed easily.
Submucosal petechiae, ecchymosis, and hematoma
formation may be present.
Disorders of White Blood Cells
Agranulocytosis
Leukemia
Disorders of White Blood Cells
Three groups of white blood cells are found in
circulation.
Granulocytes • Neutrophils (PMNs), eosinophils, and basophils
Lymphocytes
Monocytes
Agranulocytosis
A significant reduction in circulating neutrophils
Leukopenia – an abnormally low white blood cell count
Neutropenia – a reduction in the number of circulating
neutrophils
Agranulocytosis
Can result from a problem in development of neutrophils or
accelerated destruction of neutrophils
Primary – the cause is unknown, may be an immunologic
disorder
Secondary – a result of chemicals or drugs
Clinical Features and Oral Manifestations of
Agranulocytosis
Sudden onset of fever, chills, jaundice, weakness, and sore
throat
Oral infection
AGRANULOCYTOSIS
(White Blood Cell disorder)
A marked reduction in circulating neutrophils.
A sudden onset of a severe sore throat.
A marked presence of infection in the mouth:
Necrotizing ulcerations
Excessive bleeding from the gingiva
Rapid destruction of supporting tissue of the teeth
Regional lymphadenopathy
Excessive bleeding from the gingiva
Necrotizing ulcerations
Regional lymphadenopathy
Leukemia
Malignant neoplasms of hematopoietic stem cells
Characterized by an excessive number of abnormal white
blood cells in circulating blood
Unknown cause; may be due to oncogenic viruses
There are many different types categorized as to whether
they are acute or chronic.
Acute Leukemias
Characterized by very immature cells and a rapidly fatal
course if not treated
Acute lymphoblastic leukemia – involves immature
lymphocytes • Primarily affects children and young adults
• Good prognosis
Acute myeloblastic leukemia – involves immature
granulocytes • Primarily affects adolescents and young adults.
• Prognosis is not as good as lymphatic.
Clinical and Oral Features of Acute Leukemias
Weakness, fever, enlargement of
lymph nodes, and bleeding
Gingival enlargement
Oral infection
Bleeding gums, petechiae and
ecchymosis
Chronic Leukemias
Slow onset
Primarily affect adults
Clinical Features and Oral Manifestations of Chronic Leukemias
Easy fatigability, weakness, weight loss, anorexia
Pallor of lips and gingiva, gingival enlargement, petechiae
and ecchymosis, gingival bleeding
Bleeding Disorders
Hemostasis
Purpura
Hemophilia
Hemostasis
A cessation of bleeding
Circulating platelets adhere to a damaged surface and
aggregate to form a temporary clot.
Fibrin binds the platelets • Fibrin is converted from fibrinogen by a cascade of circulating
proteins.
Defects may be caused by abnormalities of either platelets
or coagulation factors. These may be determined with laboratory tests.
Hemostasis
Coagulation Cascade
•(aPTT) •(PT)
•(aPTT, PT, TT)
Hemostasis
Platelet Count
To determine the number of platelets
Normal is 150,000 to 400,000/mm3
Spontaneous gingival bleeding may occur if the count is less
than 20,000/mm3
Bleeding Time
The adequacy of platelet function
Normal is between 1 and 6 minutes.
Prolonged is greater than 5 or 10 minutes.
Prothrombin Time (PT)
The ability to form a clot
Normal is usually between 11 and 16 seconds.
INR is the ratio of PT to thromboplastin activity.
Values less than 3 are considered normal.
Patients on anticoagulants may have INR values of 4 to 5.
Partial Thromboplastin Time (PTT)
Measures the other way by which clot formation occurs
A normal PTT is usually 25 to 40 seconds.
Prolongation to 45 or 50 seconds may be associated with
bleeding problems.
Over 50 seconds may be severe
Purpura
A reddish-blue or purplish discoloration of skin or mucosa
from spontaneous extravasation of blood
May be due to a defect or deficiency in blood platelets
Blood may ooze from gingival margins.
Thrombocytopenic Purpura
A bleeding disorder that results from a severe reduction in
circulating platelets
Idiopathic thrombocytopenic purpura • If the cause is unknown
Immune thrombocytopenia • An autoimmune type of process
Secondary thrombocytopenic purpura • Often associated with drugs
Clinical and Oral Manifestations of
Thrombocytopenic Purpura
Spontaneous purpuric or hemorrhagic lesions on the skin
Patients bruise easily, may have blood in urine, and have
frequent nosebleeds.
Nonthrombocytopenic Purpura
Bleeding disorders that can result from either a defect in
capillary walls or disorders of platelet function
Vitamin C deficiency and infections or chemicals and allergy
may be the cause of alterations in vascular walls.
Drugs, allergy, and autoimmune disease may cause disorders
of platelet function.
Von Willebrand disease is an autosomal dominant disorder
of platelet function.
Oral Manifestations of Nonthrombocytopenic
Purpura
Spontaneous gingival bleeding, petechiae, ecchymoses,
and hemorrhagic blisters
Hemophilia
A disorder of blood coagulation
Results in severely prolonged clotting time
Due to a deficiency in plasma proteins involved in
coagulation
Types of Hemophilia
The two most common types are type A and type B.
Transmitted as X-linked diseases through an unaffected
carrier daughter to a son
• Type A Caused by a deficiency of plasma thromboplastinogen or
factor VIII
• Type B Christmas disease
Less common, the clotting defect is plasma thromboplastin or
factor IX
Oral Manifestations of Hemophilia
Spontaneous gingival bleeding, petechiae, and ecchymosis
After an injection on person with hemophilia
Diagnosis and Treatment of Hemophilia
The bleeding time and PT in hemophilia are normal; the
PTT is prolonged.
Diagnosis involves identifying the missing factor; treatment
involves replacing it.
Immunodeficiency
Can involve the different parts of the immune system either
alone or together
May involve a deficiency in cell-mediated or humoral immunity
May involve deficiency in phagocytosis
Divided into Primary immunodeficiency of genetic origin
Secondary immunodeficiency from another underlying disorder
Primary Immunodeficiencies
Of genetic origin May involve B cells, T cells, or both
Very rare Bruton disease (X linked congenital
agammaglobulinemia)
DiGeorge syndrome (thymic hypoplasia)
Severe combined immunodeficiency
Secondary Immunodeficiencies
Secondary Immunodeficiencies
Occur as the result of an underlying disorder
May be malnutrition, viral infection, cancer, renal disease
and Hodgkin’s disease
May occur with immunosuppressive drugs, drugs used
along with radiation, chemotherapy
Oral Manifestations of Therapy for Oral Cancer
Radiation Therapy
Chemotherapy
Oral Manifestations of Therapy for Oral
Cancer
Oral cancer can be treated with surgery, radiation therapy, or
chemotherapy, or a combination.
Radiation Therapy
The patient often experiences mucositis
during radiation therapy.
Mucositis begins about the second week
of therapy and subsides a few weeks
after its completion.
It is painful and appears as an
erythematous and ulcerated mucosa.
The patients may have difficulty eating,
pain on swallowing, and loss of taste.
Radiation Therapy
Destruction of major salivary glands may result in xerostomia
The patient is prone to rampant caries and oral candidiasis.
They also are prone to osteoradionecrosis.
Radiation Therapy
Patients should have an oral evaluation before radiation therapy of the head and neck.
Potential sources for oral infection and teeth with a
questionable prognosis should be removed.
The hygienist can help with
Fluoride application Patient education Frequent follow-up appointments
Chemotherapy
Drugs used for cancer chemotherapy affect basal cells of
the epithelium.
Mucositis and oral ulceration are common complications.
A decrease in all blood cells may occur
Lowered RBC counts can lead to anemia.
Lowered WBC counts can lead to infections.
Lowered platelets can lead to bleeding problems.
Hematologic diseases
Leukemia
Gingival hypertrophy
Petechiae
Mucosal ulcers
Hemorrhage
Treatment of leukemia
Reactivation of herpes simplex virus – oral mucosistis
Summary of oral manifestations of gastrointestinal
and hematologic diseases
Angular cheilitis
Iron-deficiency anemia
Hemorrhage
Scurvy
Ulcerative colitis
Aphthous ulcers
Crohn's disease
Pernicious anemia
Ulcerative colitis
Intraoral burning
• Iron-deficiency anemia
• Pernicious anemia
Candidiasis
• Crohn's disease (steriod therapy)
• Iron-deficiency anemia
• Pyostomatitis vegetans (steriod
• therapy)
• Ulcerative colitis (steroid therapy
Summary of oral manifestations of
gastrointestinal and hematologic diseases
Labial swelling
Crohn's disease
Erosion of enamel and dentin
Anorexia nervosa/bulimia
Gastroesophageal reflux
Gingivitis
Anorexia nervosa/bullimia
Crohn's disease
Scurvy
Glossitis
Crohn's disease
Iron-deficiency anemia
Pernicious anemia
Ulcerative colitis
Ulcerations and erosions
Crohn's disease
Iron-deficiency anemia
Pernicious anemia
Ulcerative colitis
Sjögren syndrome autoimmune disease
men : women - 1 : 9, 50 years and older
Main signs
sicca syndrome
keratoconjuctivitis sicca
xerostomia
Oral signs
decrease in saliva
• xerostomia
dry, red, wrinkled mucosa
• difficulty in swalloving and eating
• disturbance in taste and speech
• increased dental caries
• infections
• atrophy of the papilae
• candidiasis
Connective-tissue diseases
Kawasaki disease
vasculitis of medium and large arteries
Oral signs
swelling of papilae on the surface of the
tongue (strawbery tongue)
intense erythema of the mucosal surfaces
cracked, cherry red, swolen and hemorrhagic
lips
Connective-tissue diseases
Scleroderma
diffuse sclerosis of the skin, GIT, heart
muscle, lungs, kidney
Oral signs
pursed lips – dificult to open the mouth
esophafeal sclerosis
gastroesophageal reflux – damage of
enamel
pale, rigid mucosa
teleangiectasias
decreased mobility of tongue
salivary hypofunction
Connective-tissue diseases
Limited mouth opening and decreased tongue mobility
Gingival retraction
Lupus erythematosus
autoimmune disease
Oral signs
ulcerations
oral lesions of lichen planus –
petechiae
damage of salivary glands - xerostomia
Connective-tissue diseases
ulcer
lichen planus lesions
Behcet’s Disease
Vasculitis with triad
oral, genital ulcers,
uveitis or iritis
oral
• aphthous-like
• painful, clusters on lips,
gingiva, buccal, tongue
• less often palate,
oropharynx
genital
• similar in appearance
Behcet’s Disease
occular
• uveitis, iritis
• hypopyon
healing in days to
weeks some scarring
symptoms
simultaneously,
months apart
Cystic fibrosis
Oral signs
disorder of salivary
glands
swelling lips
gingivitis
dryness
Pulmonary diseases
Sarcoidosis
Sarcoidosis, also called sarcoid (from the Greek 'sark' and 'oid' meaning "flesh-like")
An immune system disorder characterised by non-caseating granulomas (small inflammatory nodules) that most commonly arises in young adults.
The cause of the disease is still unknown.
Any organ can be affected; however, granulomas most often appear in the lungs or the lymph nodes.
Symptoms can occasionally appear suddenly but usually appear gradually.
The clinical course varies and ranges from asymptomatic disease that resolves spontaneously to a debilitating chronic condition that may lead to death.
Pulmonary Sarcoidosis
Oral signs
Multiple, nodular, painles ulcerations of the gingiva, bucal mucosa, labial mucosa and palate
Tumor like swelling of salivary glans
Swelling of the tongue
Xerostomia
Facial nerve palsy
Psoriasis
Oral signs
Fissured tongue
Small white papules
Red and white plagues
Bright red patches
Acantosis nigricans
Hyperpigmentation, papillomatosis
Oral signs
Gingival hyperplasia
Gingiva, tongue, lips - papilomas
Cutaneous diseases
Discussion Questions
What oral manifestations of systemic diseases
may be observed within the oral cavity?
What disorders of blood cells may be observed
within the oral cavity?
What effects may immunodeficiency have
upon the oral cavity?
What oral manifestations may be observed
during therapy for oral cancer?
What effects of drugs may be observed within
the oral cavity?
THANK YOU