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Tables 88: NICO Tables

Table 88a: Radiographic staging for ischemic osteonecrosis (applies predominantly to hip lesions and ends of long bones); patients at all stages may or may not have pain.

Stage

Findings

Techniques to Use

0 All techniques normal or nondiagnostic; necrosis on biopsy Biopsy and histology

1 X-rays & CT scan normal; positive results from at least one of tests to right Radionuclide scan
MRI
Functional bone investigation
Biopsy and histology

2 X-ray abnormalities (osteopenia; cysts; sclerosis) without collapse of cortex

3 Subcortical radiolucencies; "crescent sign" in hip Radiographs
CT scan initially

4 Flattening or collapse of cortex

5 As for Stage 4, with narrowing of the joint space Radiographs only

6 As for Stage 5, with destruction and degeneration of the joint/bone

Table 88b: Coagulation disorders found in NICO patients who failed to improve with decortication and surgical debridement.

Coagulation Disorder

in NICO

High levels of plasminogen activator inhibitor (the major inhibitor of fibrinolysis) 18%

Low levels of stimulated tissue plasminogen activator (the major stimulator of fibrinolysis) 22%

Low levels of Protein C or Protein S (thrombophilia) 8%

Resistance to activated Protein C (thrombophilia) 18%

High levels of lipoprotein A (a strongly atherogenic and hypofibrinolysis lipoprotein) 36%

Elevated levels of anticardiolipin antibodies (associated with thrombophilia and damaged endothelial cells) 33%

Factor V Leiden gene, heterozygotic by PCR DNA analysis (causes resistance to protein C) 23%

Methylene tetrahydrofolate reductase (MTHFR) mutation, heterozygotic or homozygotic by PCR DNA analysis (causes homocystinemia and thrombophilia) 65%

Total: 78%

* includes patients with multiple coagulopathies

Table 88c: Coagulation disorders found in patients with ischemic osteonecrosis of the hips, knees and jaws, compared to the proportions found in patients with deep vein thrombosis of soft tissues and with the normal population. Thrombophilia = increased tendency to develop thrombi; hypofibrinolysis = reduced ability to lyse thrombi.

Coagulation Defect	Normal Population	Deep Vein Thrombosis	Osteonecrosis
Thrombophilia, hereditary types*	2-5%	5-9%	50-70%
Thrombophilia, acquired types	3-7%	20-50%	33%
Hypofibrinolysis, hereditary types *	<1%	5-15%	18-22%
Hypofibrinolysis, acquired types	<1%	20-25%	50%
Total (includes multiple coagulopathies)	2-7%	20-50%	65-87%

* usually autosomal dominant

Table 88d: Location of 2,301 NICO lesions as reported on biopsy request forms from 1,333 patients with facial pain.Numbers represent the proportion (%) of all cases found at a specific site, first surgery only.

Alveolar location Maxilla (%) Mandible (%) Total (%)

Central incisor area 2.5 0.2 2.7

Lateral incisor area 3.6 0.2 3.8

Cuspid area 5.0 2.0 7.0

First bicuspid area 5.2 1.1 6.3

Second bicuspid area 4.8 3.4 8.2

First molar area 6.8 12.6 19.4

Second molar area 2.6 5.1 7.7

Third molar area * 20.0 24.9 44.9

Total: 51.5 48.5 100.0

* includes tuberosity and retromolar areas

Stage	Findings	Techniques to Use
0	All techniques normal or nondiagnostic; necrosis on biopsy	Biopsy and histology
1	X-rays & CT scan normal; positive results from at least one of tests to right	Radionuclide scan MRI Functional bone investigation Biopsy and histology
2	X-ray abnormalities (osteopenia; cysts; sclerosis) without collapse of cortex
3	Subcortical radiolucencies; "crescent sign" in hip	Radiographs CT scan initially
4	Flattening or collapse of cortex	Radiographs CT scan initially
5	As for Stage 4, with narrowing of the joint space	Radiographs only
6	As for Stage 5, with destruction and degeneration of the joint/bone	Radiographs only

Coagulation Disorder	in NICO
High levels of plasminogen activator inhibitor (the major inhibitor of fibrinolysis)	18%
Low levels of stimulated tissue plasminogen activator (the major stimulator of fibrinolysis)	22%
Low levels of Protein C or Protein S (thrombophilia)	8%
Resistance to activated Protein C (thrombophilia)	18%
High levels of lipoprotein A (a strongly atherogenic and hypofibrinolysis lipoprotein)	36%
Elevated levels of anticardiolipin antibodies (associated with thrombophilia and damaged endothelial cells)	33%
Factor V Leiden gene, heterozygotic by PCR DNA analysis (causes resistance to protein C)	23%
Methylene tetrahydrofolate reductase (MTHFR) mutation, heterozygotic or homozygotic by PCR DNA analysis (causes homocystinemia and thrombophilia)	65%
Total:	78%

*Alveolar location*	Maxilla (%)	Mandible (%)	Total (%)
Central incisor area	2.5	0.2	2.7
Lateral incisor area	3.6	0.2	3.8
Cuspid area	5.0	2.0	7.0
First bicuspid area	5.2	1.1	6.3
Second bicuspid area	4.8	3.4	8.2
First molar area	6.8	12.6	19.4
Second molar area	2.6	5.1	7.7
Third molar area *	20.0	24.9	44.9
Total:	51.5	48.5	100.0

Tables 88: NICO Tables

Table 88a: Radiographic staging for ischemic osteonecrosis (applies predominantly to hip lesions and ends of long bones); patients at all stages may or may not have pain.

Table 88b: Coagulation disorders found in NICO patients who failed to improve with decortication and surgical debridement.

Table 88d: Location of 2,301 NICO lesions as reported on biopsy request forms from 1,333 patients with facial pain. Numbers represent the proportion (%) of all cases found at a specific site, first surgery only.

Table 88d: Location of 2,301 NICO lesions as reported on biopsy request forms from 1,333 patients with facial pain.Numbers represent the proportion (%) of all cases found at a specific site, first surgery only.