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 .
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.
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 is the oxygen carrying pigment
of the erythrocytes. It is formed by the developing
erythrocytes in the bone marrow.
an iron compound of protoporphyrin. It is the pigment
portion of hemoglobin molecules. It has oxygen carrying
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
Hemoglobin S- variation seen in the beta
chain. Seen in sickle cell anemia.
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.
·In the globin
fraction of hemoglobin there is alteration in the amino acid
structure of the polypeptide chain. Eg: sickle cell anemia
·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,
Drepanocytes- sickle cells
Drepanocytosis- occurance of drepanocytes
or sickle cells in the blood.
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.
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.
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
Dactylitis (painful osteitis in the
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
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
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
Patient's race- Blacks are more
susceptible than other races.
Family history to know sickle cell anemia
status of the parents.
Peripheral blood smear- shows sickle
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
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
CT scan or MRI may show strokes at
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.
Amniotic fluid can be tested at 14-16
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
Painful infarcts of the jaw mistaken for
toothache or osteomyelitis.
Orofaial radiographic features
Step ladder trabecular pattern.
Osteomyelitis of the mandible- moth eaten
Bone marrow hyperplasia leading to
enlarged maxilla with increased overjet and overbite.
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
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).
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.
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
FDA’s Northwest District:
Dentist of the Year, Dr.
James Walton III
Leadership Award, Dr. George
Dentists Care Award, Jean Woo
School Resource Dentist of
the Year, Dr. John Wilson