Necrosis and Hypercoagulation

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Infections thrive in low oxygen environments. Many of us suffer from

hypercoagulation, and I am talking about the form that is not

genetic but rather brought on by chronic infection. Hypercoagulation

sets up the perfect environment for these infections. Which comes

first the infection or the hypervoagulation, not sure, probably the

infection. But it becomes a viscious cycle, and the bacteria love it.

Here is some research that discusses the role of hypercoagulation on

bone cavitations. Maybe someone has already brought this up, in that

case sorry.

http://www.maxillofacialcenter.com/NICOcoag.html#Overview

Ischemic osteonecrosis is not so much a disease in its own right as

it is the natural consequence of a wide variety of systemic and

local factors capable of compromising marrow blood flow. Recent

investigation has found that the more than 80% of persons with

osteonecrosis of the hips, knees or jaws have a previously

undiagnosed clotting disorders or " hypercoagulable state " (Table 1).

These coagulopathies typically are not picked up on routine clotting

tests but appear to provide a logical pathophysiological mechanism

for marrow infarctions and clots, with subsequent inflammatory

increase in intramedullary pressures and stagnation of blood. Clots

in capillaries and veins of the marrow are found in approximately 1

of every 7 biopsy samples of jawbone osteonecrosis and in only 1 of

every 242 biopsy samples from routine bone infection of dental

origin, i.e. periapical granulomas and inflamed periapical cysts.

Hypercoagulability is the increased risk of thrombosis or blood clot

formation in blood vessels. The disorder comes in two forms,

thrombophilia (increased tendency to form thrombi) and

hypofibrinolysis (reduced ability to lyse thrombi once they form),

both of which imply poor control of one or more aspects of the

incredibly complicated coagulation homeostasis system. At least 6%

of Western populations have an hypercoagulability state, usually as

an autosomal dominant inherited defect or mutation.

Hypercoagulability can also be caused by an ongoing environmental

stimulus to thrombosis, such as a focal infection, medications

(estrogen & corticosteroids), or autoimmune diseases ( lupus

erythematosus). Moreover, the inherited disorders can be amplified

by environmental factors. Table 2 lists the specific

hypercoagulation disorders found thus far in patients with

osteonecrosis of the hips, knees and jaws.

Hypercoagulability should be suspected in persons with one or more

of the following clinical features: thrombosis at a young age,

family history of thrombosis, recurrent thrombosis, thrombosis in an

unusual site, thrombosis for which no underlying mechanism can be

identified, thrombosis in pregnancy, frequent spontaneous abortions,

hip pain or replacement at an early age, stroke or myocardial

infarction at an early age, osteonecrosis, Behçet's disease, chronic

fatigue syndrome, headache, fibromyalgia, idiopathic chronic facial

pain, idiopathic death of tooth pulps. Before the 1990s, the chances

of identifying the underlying coagulation defect was extremely

small, but ongoing research since then has established tests for

more than 15 different disorders, most of them previously unknown to

medicine (no test, no disease).

Treatment with the anticoagulants Coumadin, heparin and warfarin

(targeted INR of 2.0-2.5), and with the anabolic-androgenic steroid

Winstrol (6 mg daily) has normalized thrombophilia and

hypofibrinolysis in osteonecrosis patients, with reversal or

retardation of the osteonecrosis, although some patients with

normalized fibrinolysis experienced no change in symptoms or in

imaging features