DentistryUnited.com Newsletter

 


                    D e n t a l    F o l l i c l e               

             The        Monthly     E-newsletter                   Vol - I V    Number-  I          July  2009

In this Issue:

  • Editorial

  • News

  • DentistryUnited @ Rank 7 on GOOGLE

  • Laughter - The best Medicine

  • HEMOGLOBINOPATHIES A Review

  • Scientists link Oral Bacteria to Obesity

  • Florida Dental Association Recognitizes 2009 Award Recipients                                              

  • Harvard's New Dental School - The NewYork Times , May/6/1902
    The Institution that stands at Number 1 today was opened on this day in History!


     

WWW.DENTALFOLLICLE.COM  - coming soon !

Editorial :

      Dear Fellow Dentist,

As we enter the fourth year of publication of Dental Follicle - The E-Journal , I thank all the people behind it. The people who send me links to news articles to people who send me cases to people who read it . One thing I have realized is , the more time I spend in with dental follicle the more things I learn about .

The quest to use more and more of common sense and do greater jobs does not end . I read a news article recently on the web  that has made me no less than "excited 'n ' shocked" .

Martin Jones, 42, had been blind for 12 years after a tub of white hot aluminium exploded in his face as he worked at a scrapyard.To restore his lost sight  his canine was used.The procedure began when one of Mr Jones' canine teeth was removed and converted into a holder for a special optical lens by drilling a hole in it. The tooth was then inserted into his cheek for three months to enable it to grow new tissue and blood vessels. Finally , the delicate operation to insert the tooth, complete with the fitted lens into Mr Jones' right eyeball. Within two weeks of the final operation to implant the tooth in his eyeball his sight returned and he was told he had almost perfect vision in his right eye................

I hope we will have someone to write in detail bout this from dental point of veiw in our next edition..

As I always say , Dentistry has a bigger horizon than we have imagined.

 

Click here to join DentistryUnited
Click to join DentistryUnited

Yours truly

Dr. Syed  Nabeel

Editor of Dental Follicle & WebMaster www.DentistryUnited.com

News :

         

                        DentistryUnited Ranks 7 on Google  for key word "Dentistry"

Laughter - The Best Medicine :

A suspected car thief was tracked down by police after he left his false teeth at the crime scene. Police say Wojtek Lekowsky, 54, broke into a car in Czarna Dabrowka in northwest Poland and stole a stereo, but lost his teeth when he tried to make a quick getaway after the car alarm went off reports the Digital Journal.

He was tracked down using dental records and police charged him with robbery. Police spokesman said, 'He tried to tell us that while the false teeth were his, they had been stolen from him. He had not been anywhere near the car at the time of the theft, but we knew he was lying through his dentures.'


 

                                         

 

 

HEMOGLOBINOPATHIES   A Review

By Dr.Ghazala Danish MDS

Oral Diagnostitian & Radiologist

 

Hemoglobin

Hemoglobin is the oxygen carrying pigment of the erythrocytes. It is formed by the developing erythrocytes in the bone marrow.

Heme is an iron compound of protoporphyrin. It is the pigment portion of hemoglobin molecules. It has oxygen carrying capacity.

Globin is the protein portion of hemoglobin.

 

Synthesis of hemoglobin

Heme is synthesized in the mitochondria of immature red blood cells.

Globin is synthesized in the ribosomes.

Each complex molecule of hemoglobin contains four globin chains. Each globin chain carries a heme fraction in its fold. Each heme fraction carries one molecule of oxygen. Therefore each hemoglobin molecule can carry four oxygen molecules.

Hemoglobin A- normal adult hemoglobin. Has two alpha chains and two beta chains.

Hemoglobin F- Fetal hemoglobin. Has two alpha chains and two gamma chains. It declines in level between 1-2 yrs.

Hemoglobin A2- forms 2-3% of adult hemoglobin. Has two alpha chains and two delta chains.

Variants of hemoglobin

Hemoglobin H- has four beta chains. Seen in thalassemia

Hemoglobin S- variation seen in the beta chain. Seen in sickle cell anemia.

Hemoglobin C- variation in beta chain gene. Causes chronic hemolytic anemia. 

Hemoglobinopathy

Hematological disorder due to alteration in the genetically determined molecular structure of hemoglobin. Mutations in the genes of hemoglobin produce hemoglobin variants. These diseases often produce anemia.

Example- sickle cell anemia, thalassemia.

 

Classification

         In the globin fraction of hemoglobin there is alteration in the amino acid structure of the polypeptide chain. Eg: sickle cell anemia (Qualitative disorder)

         In the globin fraction of hemoglobin amino acid sequence is normal, but polypeptide chain production is impaired or is absent. Eg: thalassemia (Quantitative disorder)

 

  • Sickle cell anemia

Synonyms: sickle cell disease, drepanocytosis

Drepanocytes- sickle cells

Drepanocytosis- occurance of drepanocytes or sickle cells in the blood.

 

Epidemiology

It is prevalent in the tropical and sub-tropical regions of Africa. In these area malaria is or was endemic. Persons with sickle cell triat are resistant to the lethal effects of Plasmodium falciparum. In normal individuals the parasite derived proteins adhere to the cell membrane of the red blood cells, endothelial cells and placental cells to gain entry into the cells. Sickling of cells prevents the infestation of the malarial plasmodium. However patients with sickle cell disease donot have greater resistance to the malarial plasmodium as the individuals with sickle cell triat have.

 

Pathogenesis

When HbS is deoxygenated the molecules of HbS polymerize to form a psuedocrystalline structures called as tactiods. These tactoids distort the red blood cell membrane and produce characteristic sickle shaped cells. Polymerization is reversible when re-oxygenation occurs, however the distortion of the cell membrane is permanent and therefore the cell becomes permanently sickled.

The greater the concentration of HbS in the individual cell, the more easily tactoids are formed. This process of tactoid formation can be enhanced or retarded by the presence of other hemoglobins.HbC participates in polymerization more readily than HbA. HbF strongly inhibits polymerization. Persistence of fetal hemoglobin in such individuals is beneficial.

 

Pathophysiology

Normal RBCs are quite elastic, which allows them to deform to pass through capillaries. In SCA the RBCs are changed to the shape of a sickle and there is loss of elasticity. The rigid blood cells are unable to deform as they pass through narrow capillaries. Sickled cells further increase the blood viscosity, reducing and eventually stopping the blood flow. This leads to thrombosis and tissue infarction, causing severe pain, swelling and tenderness. (Infarction crisis). Infarction leads to secondary osteomyelitis and secondary growth defects. As a result of splenic infarction there is hypospenism (reduced splenic functioning), thus making the patient susceptible to bacterial sepsis (as white pulp of the spleen provides lymphocytes, plasma cells and hence antibodies for the cellular and humoral specific immune defense). Infarction also leads to intermittent severe painful crisis.

Due to the mis-shape, the RBCs are destroyed in the spleen leading to hemolysis and anemia (Hemolytic anemia). In addition the cells are phagocytosed in large numbers by the mononuclear-phagocyte system further reducing their life span and increasing hemolysis. Life span of healthy RBCs is 90-120 days, whereas that of sickle cells is only 10-20 days.

Hemolysis leads to icterus, due to the breakdown of hemoglobin to produce bilirubin. Excess of bilirubin changes the bile components leading to cholelithiasis (Gall stones).

Bone marrow attempts to compensate by creating new cells, but the rate of destruction is greater than the rate of production. Thus there is bone marrow hyperplasia leading to skull bossing, especially the parietal area is bulged to give a tower skull appearance. The diploic space is markedly widened due to marrow hyperplasia. There is thinning of cortices. Trabaculae are oriented perpendicular to the inner table giving a hair on end appearance clearly visible on lateral skull radiographs. In addition there is decreased density of the skull.

 Premature epiphyseal closure results in short stature- impaired growth and development. There is kyphoscoliosis.

Dactylitis (painful osteitis in the hands)

Bone deformity- shortening of metacarpals and phalanges due to partial or complete early fusion of the growth plates and due to osteonecrosis in infancy.

Folic acid (Vitamin B9) is required to properly form RBCs. Following compensatory bone marrow hyperplasia there is folic acid deficiency. Folic acid is especially important during periods of rapid cell division and growth. Its deficiency therefore adds on to the stunted growth.

Leg ulcers are the most common cutaneous manifestation of SCD. Trauma predisposes sickle cell ulcers by promoting sickling of RBCs. These ulcers are characterized by their indolent nature and intractable course. They typically heal 16 times slower than venous ulcers (varicose ulcers). Due to their recalcitrant nature, these ulcers lead to significant disfigurement and social isolation.

Cardiomegaly- pressure in the pulmonary arteries increases probably because of thrombi and occlusion, which causes pulmonary hypertension. Due to pulmonary hypertension the work load on the right side of the heart increases, causinf ardiomegaly and right heart failure. As the blood flowing to the lung decreases, the left side of the heart also receives less amount of blood. This makes it harder for the heart to pump blood to the rest of the body to meet its need. This leads to heart failure. Severe heart  failure causes blood to back up from the heart into the inferior vena cava. This increases the pressure in the veins causing congestion in the organs like congestive hepatomegaly, congestive spleenomegaly etc.

Renal failure can result from renal hypertension. This causes proteinuria, hematuria (worsening anemia).

 

Diagnosis

 Patient's race- Blacks are more susceptible than other races.

Family history to know sickle cell anemia status of the parents.

 

Clinical findings

Hematological investigations

Peripheral blood smear- shows sickle cells

Complete blood count- Hemoglobin percentage of blood is reduced Hb% decreased normal RBC count, increased white blood cell count as patient is susceptible to bacterial sepsis.

Hemoglobin electrophoresis- a blood test that can detect different types of Hb. It uses the principle of gel electrophoresis to separate out various types of Hb. Different hemoglobins have different charges, according to those charges and amount they move at different speeds in the gel.

Sickle cell test / Sickledex test / HbS test- it is a screening test for sickle cell disease / anemia. It looks for the presence or absence of abnormal Hb in the blood that causes sickle cell disease. The test is positive if 10% HbS is present. Therefore it cannot separate sickle cell triat from individuals with disease. In sickle cell triat 20-40% of Hb is HbS. In sickle cell disease it is 80-100%.

CT scan or MRI may show strokes at certain circumstances.

Elevated bilirubin due to hemolysis.

High serum creatinine level- it is a renal function test, used as an indicator for glomerular filtration rate. In sickle cell anemia due to renal failure there is increase in serum creatinine level.

High serum potassium level- due to renal failure, nephrons are unable to excrete potassium.

Hematuria- due to renal failure.

DNA analysis- this test is used to investigate alterations and mutations in the genes responsible for production of Hb components. It determines whether a patients has one or two copies of HbS gene or copies of different Hb variants.

 

Prenatal testing

Amniotic fluid can be tested at 14-16 weeks.

Genetic councelling if one or both parents are screened positive for sickle cell test. It can be done on individuals to confirm diagnosis or sickle cell triat.

 

Orofacial manifestations

Painful infarcts of the jaw mistaken for toothache or osteomyelitis.

Pulpal necrosis

Orofaial radiographic features

Step ladder trabecular pattern.

Osteomyelitis of the mandible- moth eaten appearance.

Bone marrow hyperplasia leading to enlarged maxilla with increased overjet and overbite.

 

Dental considerations

In patients with sickle cell anemia local anesthesia is preferred over general anesthesia.

Local anesthetic agent prilocaine should be avoided as its overdose causes methemoglobinemia.

Aspirin should be avoided as its high dose may cause acidosis and precipitate crisis.

Elective surgery should be carried out in a hospital set-up.

Anemia should be corrected pre-operatively. Hb should atleast be 10gm%.

Blood should be available for transfusion.

If crisis develops oxygen should be given and bicarbonate should be administered.

Packed red cells will be required if Hb% falls below 50%.

Prophylactic antibiotics should be given (Penicillin or clindamycin).

.........................to be continued in next issue

 

Scientists link Oral Bacteria to Obesity

J. Max Goodson and colleagues from Boston-based Forsyth Institute reported Wednesday in the Journal of Dental Research that the salivary bacterial composition of overweight women differs from non-overweight women.The researchers collected saliva samples from 313 overweight women and 232 healthy individuals, and used DNA analysis to measure the two groups' salivary bacterial populations.They found significant differences in seven of the 40 species studied in the salivary bacteria of subjects in the overweight group. In addition, more than 98 percent of the overweight women could be identified by the presence of a single bacterial species called Selenomanas noxia.

VIDEO OF THE MONTH

 

 

TRI HAWK is the only 100% bur................the best in the world

 

 

 

 

Florida Dental Association Recognitizes 2009 Award Recipients

The Florida Dental Association (FDA) at the annual Florida National Dental Convention (FNDC) on June 18 through 20 recognized several dentists. These industry leaders have gone above and beyond the call of duty in the current year or during the course of their lifetime.

The following 2009 award recipients are located in the FDAs Northwest District:

Dentist of the Year, Dr. James Walton III

Leadership Award, Dr. George Dorris

Dentists Care Award, Jean Woo

School Resource Dentist of the Year, Dr. John Wilson

Harvard's New Dental School - The NewYork Times , May/6/1902

The Institution that stands at Number 1 today was opened on this day in History!