7;9704431]thanx uabsfm & sekhon
👍
1.In a flouridated toothpaste with 0.304% monoflourophospate the ampont of
flouride ions
A.400ppm>>>>>>>>>>>@@@@@@@@@@@@@@
B.1000ppm
c.1500ppm
D.4000ppm.........wrong answer dear🙁
For the purpose of enhancing the safe use of fluoride dentifrices by children, several measures should be taken to minimise the risk of developing dental fluorosis. Parents should be advised to supervise tooth cleaning closely using only small (pea-size) quantities of
toothpaste.
Manufacturers should be encouraged to market a low fluoride dentifrice (e.g. 400-500 ppm fluoride) for infant use. This level of fluoride in
toothpaste, given that all other sources are constant and low, should result in a total fluoride intake which does not exceed the recommended upper limit of 0.07 mg/kg of body weight for a child between 2 and 7 years of age.
10 A low fluoride, sorbitol-based
toothpaste designed specifically for children is available (Colgate Junior
Toothpaste) and contains
0.304% MFP (400 ppm fluoride). Data from several independent studies indicate that, although a dose-response relationship does exist for fluoride levels in
toothpaste and caries, use of a 400 ppm fluoride-containing paste by children under 7 years of age instead of the standard 1000 ppm fluoride paste should not increase their caries risk. There is currently no glycerol-based, 400-500 ppm fluoride
toothpaste available in Australia.
2.Patient with sickle cell anaemia which is not true
A. Abnormal cell type...........true🙂
B. Be more prone to infarct...............true🙂
C.Have wide bone marrow spaces with narrow trabeculae in the alveolar bone
in oral caivity
D.Resistant to malaria parasites.................true🙂
so c) is answer of exclusion as others r true
The skeletal manifestations of
sickle cell disease are the result of changes in
bone and
bone marrow caused by the chronic tissue hypoxia that is exacerbated by episodic occlusion of the microcirculation by the abnormal
sickle cells. The main processes that lead to
bone and joint destruction in
sickle cell disease are infarction of
bone and
bone marrow, compensatory
bone marrow hyperplasia, secondary
osteomyelitis, and secondary growth defects.
When the rigid erythrocytes jam in the arterial and venous sinusoids of skeletal tissue, the resultant effect is intravascular thrombosis, which leads to infarction of
bone and
bone marrow. Repeated episodes of these crises eventually lead to irreversible
bone infarcts and
osteonecrosis, especially in weight-bearing areas. These areas of osteonecrosis (avascular necrosis/aseptic necrosis) become radiographically visible as sclerosis of
bone with secondary reparative reaction and eventually result in degenerative
bone and joint destruction.
nfarction of
bone and
bone marrow in patients with
sickle cell disease can lead to the following changes: osteolysis (in acute infarction), osteonecrosis (avascular necrosis/aseptic necrosis), articular disintegration, myelosclerosis, periosteal reaction (unusual in the adult),
H vertebrae (steplike endplate depression also known as the Reynold sign or codfish vertebrae),dystrophic medullary calcification.and
bone-within-
bone appearance
The shortened survival time of the erythrocytes in
sickle cell (10-20 days) leads to a compensatory
marrow hyperplasia throughout the skeleton. The
bone marrow hyperplasia has the resultant effect of weakening the skeletal tissue by widening the medullary cavities, replacing trabecular
bone and thinning cortices.Deossification due to
marrow hyperplasia can bring about the following changes in
bone: decreased density of skull, decreased thickness of outer table of skull due to widening of diploe, hair on-end striations of the calvari and osteoporosis sometimes leading to biconcave vertebrae, coarsening of trabeculae in long and flat bones, and pathologic fractures.
