Blood diseases

Blood diseases

In our daily practice, the management of patients with blood disease is quite common.

These pathologies can affect one or sometimes all three blood lines, therefore the relationship between hematology and the dentist must be close in order to optimize patient care.

The odonto-stomatological manifestations of many hematological diseases are frequent and important: they can sometimes be revealing or very suggestive of a mechanism within a given hematological picture.

2. REMINDERS:
   1. Blood composition:

Blood is the largest organ (5 kg). It is made up of a suspension of cells in a complex liquid; plasma includes water, mineral salts, organic molecules.

{Carbohydrates, lipids, proteins)

• The cells:

-Red blood cells (RBCs) or erythrocytes which carry hemoglobin.

-White blood cells (WBCs) or leukocytes.

-Platelets or thrombocytes.

2-2-0origin of the blood elements:

Hematopoiesis is defined as the set of mechanisms that renew blood cells.

-Myelopoiesis{Formation of the myeloid lineage} takes place in the bone marrow and ensures the production and circulation of red blood cells, polymorphonuclear leukocytes, monocytes and platelets.

-Lymphopoiesis: takes place in the lymphoid organs from a lymphoid stem cell derived from the

bone marrow.

3. Complete Blood Count {CBC}

The table below gives the normal values:

GB (mm3}		4000 to 10000
Poly nu cl e air es	1500-8500	70 to 70%
Lymphocytes	2000-8000	20,040 %
Monocytes		608%

Platelets 150,000 to 400,000

4. Hemostasis:

“ Set of physiological phenomena which contribute to the prevention and stopping of bleeding ”

1. Physiology of hemostasis:

Hemostasis takes place in three phases SUCC ESS IV ES:

2. Primary hemostasis:

It is carried out in two stages:

-Vascular time: it corresponds to the reflex vasoconstriction of the damaged blood vessel.

• Platelet time: this corresponds to the adhesion of platelets to the endothelium of the vessel via Willebrand factor.

This phase results in the formation of the platelet plug. It is explored by:

-Bleeding time {TS} = 2 to 4 seconds (Duck Method)

= 5 to 8 seconds (Ivy’s method}

-Platelet count: Platelet rate 150,000 to 400,000 /mm3

2-4-3 – secondary hemostasis:

This stage takes place thanks to a cascade of reactions involving plasma factors (coagulation factors) allowing the transformation of fibrinogen into fibrin which allows the consolidation of the platelet plug and its transformation into a “red clot”.

The coagulation factors are:

I: Fibrinogen

II: Prothrombin V: Proaccelerin VII: Proconvertin

VIII: Antihemophilic Factor A IX: Antihemophilic Factor BX: Stuart Factor XI: Rosenthal Factor

These coagulation factors are glycoproteins synthesized by the liver. Some of these factors are vitamin K dependent {II, V/1, IX, X}

Coagulation activation occurs in two ways:

-The extrinsic (tissue) pathway:

It is explored by:

-Prothrombin rate: TP greater than 80

• Quick’s time: PT = 11 to 13 seconds

The International Normalized Rati

INR = (patient PT/control PT)

The intrinsic (plasmatic) pathway is explored by the Activated Cephalin Time = 25 to 35 seconds

2-4-4- Fibrinolysis:

It corresponds to the physiological destruction of fibrin ENSURING lysis OF THE CLOT

3. Red series disorders: 3- 1 Anemia:

Anemias are defined by a DECREASE in the level of hemoglobin per 100 ml of blood, but MOST OFTEN they are marked by a decrease in the number of RED BLOOD CELLS and/or hematocrit.

Clinical picture:

E ach form of anemia has its particular symptoms, but there are common symptoms such as dizziness, weakness, headaches and often paleness of the integument and mucous membranes. Other signs should be mentioned for each type of anemia.

3-1-1-Iron deficiency anemia :

This is the most common, following chronic digestive or genital bleeding, a low iron diet or poor absorption.

It is a hypochromic microcytic anemia. Oral manifestations are MARKED by:

-Mucous atrophy.

-A depaulized glossitis.

-Pallor of the BUCCA L E MUCOSA.

-Angular cheilitis and frequent oral candidiasis.

3-1-2-A nem ie mega/ab/astic (from Biermer) :

It can be due to a vitamin B12 deficiency (most often due to an abnormality of intestinal or gastric absorption). Vitamin B12 being of great importance FOR the formation of RBCs

BUCCAL MANIFESTATIONS ARE FREQUENT AND EARLY, DOMINATED BY ” Hunter’s glossitis ” WHICH CONSTITUTES

a valuable SIGN of this disease and can SOMETIMES be revealing: The tongue IS atrophied, SMOOTH and stripped of fur with a burning sensation and loss of taste.

3. Hemolytic anemia:

It is a condition characterized by massive and abnormal destruction of blood cells. It can be hereditary or acquired.

1. hereditary forms:

-Thalassemia:

It is characterized by an imbalance between the production of the different chains of hemoglobin. They are classified according to the deficient chain into Beta and Alpha thalassemia. It occurs in different forms:

-Thalassemia minor : Asymptomatic.

-Thalassemia intermedia : REQUIRING BLOOD TRA NS FU S IO NS.

-Thalassemia major including Cooley’s disease: This is a serious form which begins in childhood and is characterized by the following clinical signs:

• Skin pallor with jaundice.
• Pale buccal mucosa.
• Mongoloid FACIES.

– DENTAL DYSCHROMISMS (SIGN OF HYPERHEMOLYSIS).

– SICKLE CELL DISEASE :

It is a constitutional abnormality of the structure of globin which results from a genetic mutation resulting in the replacement of one amino acid by another giving

“hemoglobin 5 ”, with CHARACTERISTIC deformation of the RBC (hard and curved); it is also called “sickle cell anemia ”.

The heterozygous form is practically asymptomatic.

The homozygous form manifests itself as follows on the bucco-pharyngeal plane

– Hemolytic jaundice;

-Palor of the mucous membranes

-Bone pain, sometimes in the jaws.

• Radiologically, Alignment of the risk characteristics of the interdental septa in steps and

OSTE OPOROSE OF THE MAXILLA.

2. acquired forms:

Hemolytic anemia can be caused by:

-SPLENOMEGALY

-An immunological origin

-Toxic effect of certain medications.

The same clinical manifestations are found as in hereditary forms of hemolytic anemia.

4. APLASTIC ANEMIA :

. .

Fonconi’s disease or anemia is a hereditary condition that results in bone marrow aplasia around the age of 10. In this case, all three blood lines are affected, and the anemia is accompanied by leukopenia and thrombocytopenia.

Management of a patient with anemia:

-Whatever the type of anemia, the practitioner must contact the treating hematologist in order to establish the surgical protocol.

-Request an NFS

– Any bloody act should not be performed before the hemoglobin level improves (greater than 10 g/100 ml).

Some anemias (hemolytic and aplastic) require antibiotic prophylaxis even in the case of minimal intervention.

3-2-P OLYGL OBULIE by V AQUEZ :

It is a myeloproliferative disease of unknown cause characterized by an increase in the red blood cell count above 6 million/mm3 and a hemoglobin count above 18g/100ml.

Clinically, we find:

-Facial erythrosis.

-A reddish-purple, sometimes purplish, oral mucosa.

-Bleeding gums.

-A significant risk of hemorrhage during a bloody act.

4. T RUBLES of the white series:
   1. Non –  proliferative TROUBLE :
      1. N EUTROPENIA and AGRANULOCYTOSIS:

Neutropenia is a decrease in the level of white blood cells, particularly neutrophils.

Agranulocytosis is a serious condition characterized by a significant decrease in neutrophils or a complete absence of granulocytes.

The decrease in white blood cell count may be of unknown cause, it may be encountered

in leukemia or following certain medications (antimitotic chemotherapy).

These conditions are primarily expressed by a major risk of infection. Oral manifestations are frequent, resulting in persistent, recurrent, necrotic, extensive deep and superficial, and painful ulcers.

Bacterial infections (gingivitis, periodontitis) and candidiasis are common.

2. Neutrophil dysfunction:

This is a hereditary or acquired anomaly (medications, alcohol poisoning, Down’s syndrome, etc.) affecting the phagocytic function of neutrophils.

This condition is characterized by severe bacterial and fungal infections of the skin and mucosa. The eruption of baby teeth leads to gingivitis or periodontitis, which progresses to alveolar bone loss, leading to tooth loss.

3. Bone marrow aplasia:

This is a global quantitative bone marrow failure affecting the three lines, characterized by the existence of an infectious syndrome and/or a hemorrhagic syndrome and/or anemia.

Support:

The practitioner must be concerned about the risk of infection

-Work in collaboration with the attending physician.

-Antibiotic prophylaxis is necessary pre- and postoperatively.

-Prohibit hematotoxic drugs (Aspirin, etc.)

2. Proliferative syndrome:
   1. Leukemia:

These are malignant neoplastic diseases of hematopoietic tissues characterized by an abnormal and intense proliferation of leukocytes to the detriment of healthy white blood cells, red blood cells and platelets.

1. Acute leukemia:

It involves the presence of myeloblasts or lymphoblasts, immature forms of white blood cells, in the blood. It mainly affects children and young adults.

Clinical:

– Specific leukemic lesions:

They are due to the infiltration of tissues by leukemic cells and are manifested by:

-Cervical adenomegaly.

-Infiltration of the parotid glands.

-Necrotic ulcerations.

-Gingival infiltration results in hypertrophic gingivitis which can mask the teeth .

-Lesions indirectly linked to leukemia:

These are signs of bone marrow failure:

-Anemia.

-Thrombopenia.

– Neutropenia.

2. Chronic leukemia:

They are classified into myeloid and lymphoid depending on the proliferation of mature myeloid or lymphoid cells. They mainly affect adults and the elderly.

The MUCOSA OF THE BUCCOLE is less often affected than in ACUTE LEUKEMIA; it is then pale with

petechiae and superficial ulcers.

Management of patients with LEUKEMIA :

Patients with leukemia experience hemorrhagic and

INFECTIOUS :

-Collaborate with the attending physician

-Preparation of the oral cavity before chemotherapy.

• Request an NFS:

-ANY bloody act will ONLY be considered if the WHITE BLOOD CELL RATE is GREATER than 2000/mm3 and the PLATELET RATE is GREATER than 50,000/mm3. Otherwise and in case of EMERGENCY, intervene ONLY AFTER BLOOD TRANSFUSION.

• Provide LOCAL means of hemostasis.
• Antibiotic prophylaxis is the rule.

4-2-2 – MULTIPLE Myelomas (Kahler’s Disease):

Malignant disease DUE to the uncontrolled proliferation of plasma cells. It is most often revealed by BONE PAIN linked to TUMOR invasion. Sometimes there is involvement of the jaws with BONE PAIN, BONE SWELLING and tooth mobility.

3. Lymphomas:

-Hodgkin’s disease

Malignant hemopathy characterized by the ^{proliferation} of Sternberg-Reed cells within a lymph node.

Clinical:

The disease manifests itself by the appearance of lymph nodes. The lower cervical lymph nodes are most often affected first and in the absence of treatment, proliferation occurs towards other lymph nodes.

4. Non-Hodgkin’s malignant lymphomas:

They designate a GROUP of malignant hemopathies developed from T or B lymphocytes.

Clinical:

-Cervical lymphadenopathy

-In the oral cavity, lymphomas can be located on the palate on the gum in the form of a soft, smooth, erythematous or purplish swelling, sometimes ulcerated.

-At the level of the jaw, Burkitt’s lymphoma; often simulates an infection of dental origin,

which in the next stage is characterized by swelling with lysis of the cortices.

5. histiocytosis X {Langerhansian histiocytosis}:

A condition of unknown cause characterized by the proliferation of histiocytic cells, their abnormal multiplication causing invasion of the viscera and bones.

It brings together

-Eosinophilic granuloma of the bones:

Bone gaps affecting the pelvis often affect the skull and long bones. In its maxillary location, we can find gingival swelling and dental mobility with osteolysis which can simulate periodontal disease.

–

5. Hemostasis disorders
   1. Pathologies of primary hemostasis:
      1. Hemostasis disorders due to platelet abnormalities :

Primary hemostasis disorders are manifested by:

• Petechiae;
• Bruises;
• Hemorrhagic vesicles on the oral mucosa;
• Spontaneous or slight contact gingivitis…

Platelet disorders result in an increase in bleeding time. These disorders are classified according to whether they are due to an abnormality in number (thrombocytopenia) or function (thrombopathy).

1. Thrombocytopenia

It corresponds to a reduction in the number of platelets which is then less than 150,000/mm3.

It manifests itself by an increase in bleeding time. This decrease in the number of platelets can result

• of central origin: insufficient production (platelet production disorder and/or altered maturation) by: bone marrow aplasia of toxic, infectious, idiopathic origin: by bone marrow invasion or by constitutional anomaly;
• OF A PERIPHERAL ORIGIN

Peripheral platelet destruction is the most common cause of thrombocytopenia. It can be:

• of autoimmune origin (anti-platelet autoantibodies).
• Of idiopathic origin.

2. Thrombopath ie:

The platelet count is normal but their functions are impaired. This results in prolonged bleeding time and functional abnormalities.

The most common cause of these dysfunctions is due to certain medications: acetylsalicylic acid, ticlopidine and other non-steroidal anti-inflammatory drugs.

It can be constitutional: Glanzmann’s thrombobasthenia, Bernard Soulier syndrome.

2. Hemostasis disorders due to vascular anomaly:

Their diagnosis is essentially clinical, confirmed by the negativity of laboratory tests.

{TS is normal or isolated elongated, platelet count and function are normal). Only a decrease in capillary resistance is noted; this is a common cause of bleeding in current medical practice, they are generally moderate.

This could be:

Rheumatoid purpura. Rendu Osier disease.

Hemorrhage due to capillary fragility.

2. Coagulation disorders:
   1. Hereditary coagulopathy:
      1. Willebrand disease:

This is the most common hereditary coagulopathy. This coagulopathy results from the qualitative or quantitative decrease of Willebrand factor. Transmission is most often autosomal dominant.

The diagnosis is suggested by:

Hemorrhagic manifestations (mucosal bleeding, menorrhagia) Prolongation of bleeding time (linked to the decrease in Willebrand factor) Prolongation of activated cephalin time (ACT) (linked to the decrease in factor VIII).

The treatment consists of compensating for the deficit by providing Willebrand factor concentrates.

2. Hemophilia

This pathology corresponds to a deficiency in anti-hemophilic factor of recessive transmission linked to sex.

There are three types of hemophilia:

• Hemophilia A (Factor VIII deficiency): 80% of cases
• Hemophilia B (Factor IX deficiency): 20% of cases
• Hemophilia C (Factor XI deficiency): very rare

In terms of odontostomatology, we find:

Bleeding from the oral cavity due to a simple bite that does not respond to compression; Bleeding from spontaneous loss of baby teeth, sometimes revealing the disease;

Serious oral hematomas due to the risk of asphyxia. They can be lateropharyngeal following truncal anesthesia at the Spix spine, sometimes at the level of the floor of the mouth following an instrument slippage.

On the biological level

Normal TS.

Normal TQ and TP.

Isolated prolongation of the TCA (the antihemophilic factor involved in the endogenous pathway) Decrease in factor VIII or IX

When the rate is less than 1%: Severe hemophilia

When the rate is between 1% and 5% / Moderate hemophilia When the rate is between 5% and 25% Minor hemophilia

Treatment consists of transfusion of missing factor concentrates.

3. Other constitutional deficiencies in coagulation factors:

Apart from von Willebrand disease and hemophilia, they are rare:

-Factor V deficiency

– Factor VII deficiency;

2. Acquired coagulopathies:

– Medication modifying hemostasis: Some patients at risk of vascular thrombosis require anticoagulant medication to prevent clot formation (e.g., heart rhythm disorder, myocardial infarction, etc.)

Antivitamin K: Four coagulation factors, prothrombin (IF), VII, IX and I X are synthesized by the liver cell but a vitamin K-dependent enzyme system is necessary to complete the coagulant properties of these molecules.

Hypocoagulability is monitored by PT or INR

Heparin: Intervening in the endogenous coagulation pathway, hypocoagulability is controlled by TCA.

– Hemorrhagic syndromes of liver diseases

Liver diseases (viral, infectious, toxic hepatitis) and cirrhosis cause deficiencies due to a lack of synthesis.

All the factors synthesized by the liver will therefore be affected to varying degrees. The symptoms include hematomas, bruises, and oral bleeding.

3. Action to take in the event of a hemostasis disorder 5-3-1- The preventive role of the odonto-stomatologist:

Regardless of the hemostasis pathology, it should always be remembered that poor oral hygiene is responsible for the worsening of periodontal disease and therefore aggravation of hemorrhage. Emphasize the need to maintain rigorous oral hygiene, by regularly and methodically removing bacterial deposits using a soft brush.

It is important that brushing begins very early (2 years) in order to minimize periodontal damage aggravated by blood disease.

Children with bleeding disorders should have periodic check-ups.

to the dentist to screen and assess their oral health.

5-3-2- The actual conduct to be adopted:

Close collaboration must exist between the hematologist and the dental surgeon for better management of these patients.

In all cases, local hemostasis methods must be applied in all cases.

Patients with any hemostasis disorder. These methods help promote the formation and protection of the blood clot.

We distinguish

Intrinsic means :

They consist of placing products with local hemostatic action at the bottom of the alveolus.

-Gelatin sponges (Spongel*): Sterile and absorbable in 4 to 6 weeks. They provide mechanical hemostasis and serve as a supply of hemostatic products.

-Biological glues.

-Fibrin sponges (Hemofibrin*)

Extrinsic means :

– Bi-digital compression

-The sutures of the banks with a hermetic rapprochement of these

-Compression splints: These protect the clot. They are made beforehand (resin splint) or made preoperatively (silicon splint).

– What to do when faced with a patient presenting a platelet abnormality:

If the platelet count is between 50,000 and 150,000/mm3:

Apply local hemostasis measures.

If the platelet count is less than 50,000/mm3:

A prior blood transfusion is essential, combined with local hemostasis methods.

-How to deal with a patient with a coagulation factor deficiency (Hemophilia,

von Willebrand disease):

12

2 and 3

The patient must receive a preoperative transfusion of a dose of missing factor when the procedure may cause bleeding (denture extraction, scaling)

A serological assessment is required beforehand in polytransfused patients (HBV, HCV, HIV) due to the risk of contamination.

Truncal anesthesia at the Spix spine is contraindicated due to the risk of lateropharyngeal hematoma formation.

Perform a tooth extraction that is as minimally traumatic as possible.

Drugs that potentiate hemostasis disorders (acetylsalicylic acid) are contraindicated.

Intramuscular injections are also contraindicated {Risk of formation

of hematoma)

– What to do when dealing with a patient taking anticoagulants: During anti-vitamin K treatment:

Check hypocoagulability biologically by:

• TP: defining the safety zone between 25 and 35%
• I.tf.R: which allows the results to be standardized and a therapeutic zone to be defined between

INR Above 3 (TP less than 20%), there is a significant risk of bleeding.

It is necessary to emphasize the need for collaboration with the attending physician, who alone is capable

to modify the treatment. The surgical protocol is similar to that for hemophiliacs.

– Coagulopathies and liver damage

All phases of hemostasis can be affected.

Most coagulation factors are synthesized in the liver, so the risk of bleeding is increased. It will then be necessary to explore all stages of hemostasis.

We will ask:

A time of bleeding.

A platelet count.

TCA for the endogenous pathway

TP or INR for the exogenous route.

When the platelet count is > 50,000/mm ³ , with a TP in the therapeutic zone : Apply local hemostasis techniques and avoid hepatotoxic drugs . Otherwise, a prior blood transfusion is necessary .

Blood diseases

  Untreated cavities can cause painful abscesses.
Untreated cavities can cause painful abscesses.
Dental veneers camouflage imperfections such as stains or spaces.
Misaligned teeth can cause digestive problems.
Dental implants restore chewing function and smile aesthetics.
Fluoride mouthwashes strengthen enamel and prevent cavities.
Decayed baby teeth can affect the health of permanent teeth.
A soft-bristled toothbrush protects enamel and sensitive gums.
 

Blood diseases