It was decided, in order
to alleviate the pain, that ethyl chloride should be ... - New
York Times - Nov 3, 1907
As I had mentioned in the previous issue , I will be pubishing some
of the best papers of the last 5 years in these months to come.
Today's paper is from Dr.Vinayak Joshi. Till date the highest number
of hits are to his papers. Dental Follicle team salutes this Doctor
for this achievement.
Patient: Doctor, what does the X-ray of my head
Doctor: Absolutely nothing!
protein— Part II
C-reactive protein (CRP) values can be increased for
multiple reasons. A major increase in CRP values is seen
with infections (e.g. Bacterial, viral, fungal, or parastic
infection), hypersensitive complications of infections (e.g.
Rheumatic fever), acquired and inherited inflammatory
diseases (e.g. Rheumatoid arthritis, Ankylosing spondylitis),
tissue necrosis (e.g. Myocardial infection, Tumor
embolization), trauma ( e.g. burns, surgery), neoplasia (
e.g.carcinoma, sarcoma), and also moderate increase in
systemic lupus erthematousus, scleroderma, and graft vs.-
However the relation between CRP values and cardiovascular
diseases (CVD) is the major area of focus, reason being the
high prevalence of this disease in the developed and
developing countries alike.
If you consider the number of studies coming out of the
literature trying to link the high CRP levels and the
occurrence of cardiovascular events, the relations seems to
Possible hypothesis for occurrence of CVD:
CRP is regulated by interleukin -6 (IL6), interleukin 1,
tumor necrosis factor alpha, and other cytokines. CRP is
thought to stimulate tissue factor production and activate
complement when aggregated. Tissue factor may be the main
stimulus to initiating coagulation, which could be crucial
in CVD development. Also its shown that CRP binds to low
density lipoprotein, which in turn activates complement,
tissue factor production by macrophages leading to
Another hypothesis based on findings, that an infection,
possibly a bacterial or a viral (e.g. Helicobacter pylori,
Chlamydia pneumoniae, Herpes simplex virus and
cytomegalovirus) might contribute to atherosclerosis. Having
known that CRP levels are increased in bacterial and viral
infections this is quite possible.
A third theory suggests that CRP is a pro coagulant,
increases opsonization and artherogenesis. CRP not only
correlates with the increase in the other inflammatory
markers but also is know to bind selectively to low and very
low density lipoprotein (LDL and VLDL), found in the
atheromatous plaque. CRP is also known to be deposited in
these plaques, and along with its range of pro-inflammatory
properties it could potentially contribute to the
pathogenesis, progression and complications of atheroma.
Data suggest that CRP is involved in foam cell formation by
mediating the LDL uptake by the macrophages, and also its
known presence in the plaques with pro inflammatory
properties, may play a role in destabilizing the plaque.
During myocardial infraction (MI) the tissue necrosis
occurring is a stimulus for CRP response. The CRP is
deposited in and around infract not only reflects the extent
of myocardial necrosis but also contributes significantly to
the severity of ischaemic myocardial injury.
The higher CRP levels are been strongly associated with
increased body mass index and metabolic syndrome. Adipocytes
are the source of substantial portion of baseline IL6
production. Weight loss leads to reduction in baseline CRP
concentration. CRP production predicts the development of
type 2 diabetes independently of traditional risk factors.
Low-insulin response diets may decrease plasma CRP by
influencing adipocyte function. The elevated CRP levels may
provide an additional marker for risk of progression to type
1 diabetes. Oral contraceptive use and systemic hormone
replacement therapy are associated with significantly raised
baseline CRP levels. Other associations with elevated
baseline CRP values include periodontal disease, smoking,
consumption of coffee, and stress.
With this little knowledge of CRP it would be certainly
interesting to see the relation between CRP and periodontal
disease, and that is what you would read in the third and
~As Understood by me~
References for Part I and II:
3) Saran de Ferranti, Nadir Rifai, C-reactive protein and
cardiovascular disease: a review of risk prediction and
interventions. Clinical Chimica Acta 2000; 317: 1-15
4) G.M. Hirschfield and M.B. Pepys, C-reactive protein and
cardiovascular disease: new insights from an old molecule. Q
J Med 2003; 96: 793 – 807.