Test – Cementogenesis (answers)

1. The coronal two-third of root surfaces is covered by this type of cementum:

• coronal cementum

• cellular fibrillar cementum

• acellullar fibrillar cementum

• MTA cement

• acellular afibrillar cementum

2. Multinuclear giant cells, responsible for cement resorption:

• osteoclasts

• cementoblasts

• cementocytes

• osteoblasts

• cementoclasts

3. The main fiber component in the extracellular matrix of the fibrillar cementum is:

• type I collagen

• oxytalan fibers

• type XII collagen

• type III collagen

• argyrophil fibers

4. Proteins synthesized by the epithelial cells of the Hertwig’s root sheath that induce cementogenesis:

• osteopontins

• enamel matrix proteins

• tenascins

• fibronectins

• sialoproteins

5. Localization of progeitor cells regulating the regeneration of cementum, PDL and alveolar bone:

• gingival epithelium

• gingival connective tissue

• alveolar bone

• dentin

• periodontal ligament

10. 1.10. Pathomechanism of bleeding and its relation to dentistry – Katalin Varnai

Many dental procedures are associated with a risk of bleeding, which in the large majority of cases is self-limiting and non-problematic. Sometimes, however, complications may arise due to inherited or acquired bleeding disorders, hemostatic defects secondary to the underlying disease or medication. A routine dental surgery may sometimes reveal a bleeding abnormality.

Before a dental procedure, it is important to ask about personal and family bleeding history (extensive bruising, frequent nosebleeds, heavy menstrual bleeding, prolonged bleeding after surgery or an invasive dental procedure), diseases affecting hemostasis (liver or kidney disease, malignant tumors) and therapies (coumarine derivatives, anti-platelet drugs).

Hemostasis is a highly regulated process that maintains the fluidity of blood in the vessels, while limits the amount of blood loss after an injury and optimizes wound healing. To fulfill this task, a highly regulated interaction is necessary between the vessel wall, platelets, coagulation factors and the fibrinolytic system.

Figure 1.109. Figure 1. – Regulation of hemostasis

Vascular defects are rarely the cause of bleeding disorders and are usually associated with mild bleeding confined to skin or mucosa.

Platelet disorders can be hereditary or acquired and may be due to decreased production, excess comsumption or altered function of platelets. The following bleeding symptoms may occur: mucocutaneous bleeding (petechiae, ecchymosis, suffusion), epistaxis, and menorrhagia. In the oral cavity, the most common clinical symptoms are petechiae, gingival hyperplasia, spontaneous gingival bleeding and ecchymosis.

Thrombocytopenia may be mild, moderate or severe. The minimun platelet level before dental procedures is 50 G/L, extensive surgery may require > 100 G/L. Inherited thrombocytopenia is rare and is often one component of a syndrome. Acquired thrombocytopenia is most commonly of immune origin such as in the case of idiopathic thrombocytopenic purpura (ITP).

Thrombocytopathy can be congenital or acquired. It is very rare in its congenital form, such as Glanzmann thrombasthenia, when mucocutaneous bleeding occurs at birth or early infancy.

Of the acquired platelet defects, the most common are drug induced in antiplatelet therapy.

During ASA therapy (100 mg/day), dental procedures can be carried out atraumatically with local hemostatic agents without cessation of the drug. Non-steroid anti-inflammatory drugs (NSAIDs) act like ASA. Two days before surgery a cessation of NSAID is proposed and the therapy can be continued a day after the operation.

Thienopyridine (clopidrogel, ticlipodin), ASA+clopidogrel or ASA+dipyridamole combination may significantly increase the risk of bleeding. In this case, a haematological concilium is mandatory.

Figure 1.110. Figure 2. – Platelet inhibitors

Among the congenital coagulation defects, haemophilia A (HA), haemophilia B (HB) and von Willebrand Factor (vWF) deficiency are the most common. Symptoms may include prolonged bleeding, ecchymosis, deep hematomas, epitaxis, spontaneous gingival bleeding and hemarthrosis. 25% of the normal level usually provides satisfatory clotting. Patients with levels of less than 5% will have symptoms of abnormal bleeding such as easy bruising. When the FVIII level is less than 1%, the condition is classified as severe, with spontaneous bleeding.

Dental treatment of haemophilic patients can be carried out only at a dedicated facility. Management of HA patients undergoing dental surgery consists of increasing FVIII levels, replacing FVIII and inhibiting fibrinolysis. Normal factor level (50-100%) has to be maintained from surgery to wound healing. DDAVP (Desmopressin) is used to achieve a transient increase of endogenous FVIII and vWF in mild forms of HA and vWD.^{1, 2, 3, 4}

Acquired coagulation defects are most often caused by antihtrombotic therapy. The use of oral anticoagulants (coumarin derivatives) inhibits the modification on the K-dependent clotting factors zymogen II, VII, IX and X.

Minor dental procedures can be carried out with local hemostasis with INR within therapeutic range (2-3 obtained within 24 hours).

INR = International Normalised Ratio, PT = prothrombin Time, ISI = International Sensitivity Index.

If the procedure is invasive, extensive or carries a large risk of bleeding, the dose of coumarin can be reduced or changed to heparin (LMWH), for which an hemostasic consilium and institutional background is indispensible.

Mild bleeding can be reduced by supplying vitamin K. In case of an emergency, it is necessary to use fresh frozen plasma (FFP), recombinant Factor VIIa (rFVIIa), and Prothrombin Complex Concentrate (PCC).

Treatment of patients with bleeding disorders is based on guidelines and agreement between different medical specialties.⁵

Figure 1.111. Figure 3. – Anticoagulant drugs

Figure 1.112. Figure 4. – Blood collection tube containing sodium citrate for coagulation

tests

Figure 1.113. Figure 5. – Blood collection tube containing K2EDTA for laboratory tests

in hematology

Figure 1.114. Figure 6. – Blood collection tube for the determination of erythrocyte sedimentation rate

10.1. Test – Pathomechanism of bleeding and its relation to