Re: NICO Historical Review

From: Joel M. Eichen (joeleichen_at_yahoo.com)
Date: 03/18/05 

Date: Fri, 18 Mar 2005 07:51:16 -0500

On Fri, 18 Mar 2005 05:33:45 GMT, "LadyLollipop"
<LadyLollipop@insightbb.com> wrote:

>
>"John Chewter" <john@LESS_SPAMchewter.f9.co.uk> wrote in message
>news:d1cnqs$cj6$1@hercules.btinternet.com...
>> Jan - do tell us that you understood all these papers? Some of the words
>> are longer than 'Marmalade, Can you understand trans-marmaladic words?
>
>John, do back up you claims and you lies, rather than stalk me, then do post
>something besides criticiisms od everything I post.

John!

Yeah, Jan wants to know about YOU claims and YOU lies .........

(This is not standard English but its heard of the street.)

YOU friend,

Joel

>
>You have number of of questions you have never answered, is that your
>problem?
>
>Shall I ask them again, and post you insults, rather than answers.
>
>Do grow up, John.
>
>As a claimed amalgamist, I asked you why you didn't post any articles
>showing us why you believe amalgams are toxic, here is your reply:
>
>> LL Have you ever posted any studies of this toxicity????
>
>
>JC Certainly not. I am an imaging specialist.
>
>So I kindly suggest, you shut up.
>
>LL
>
>> John Chewter
>> http://www.keyneimage.co.uk
>> "LadyLollipop" <LadyLollipop@insightbb.com> wrote in message
>> news:TW8_d.76748$Ze3.41700@attbi_s51...
>>> http://maxillofacialcenter.com/NICOhistory.html
>>>
>>> The History of Maxillofacial Osteonecrosis (NICO)
>>>
>>> ©The Maxillofacial Center for Diagnostics & Research
>>>
>>> Other Links
>>>
>>> NICO Clinical Page
>>> NICO Home Page
>>> Home Page
>>>
>>>
>>>
>>>
>>> Topics
>>> Historical Overview
>>> 1800-1930
>>> 1930-1970
>>> 1970-1990
>>> 1990-2000
>>> References
>>> Tables
>>> Painful osteonecrosis/osteomyelitis, or "phossy jaw," of upper and
>>> lower jaws sloughed out when dentist tried to
>>> extract several teeth because of "toothache." Source: American
>>> Journal of Dental Science, 1859.
>>>
>>>
>>> The Maxillofacial Center, 165 Scott Avenue, Suite 100, Morgantown, WV
>>> 26508 USA
>>> Phone: 304-292-4429 Fax: 304-291-5149 Email: MFC@aol.com
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> History of Maxillofacial Osteonecrosis (NICO)
>>>
>>> First described in 1794 in a case of septic necrosis of the femoral head,
>>> this enigmatic disease is as old as the dinosaurs but has been poorly
>>> understood and has such subtle radiographic changes that until recently
>>> it was seldom diagnosed prior to end-stage damage.[11-13] Contemporary
>>> research has so enhanced our understanding of its basic pathophysiology
>>> that it now bears little resemblance to the entity once known as "aseptic
>>> osteomyelitis."
>>>
>>> Heightened awareness and improved imaging techniques have confirmed this
>>> once rare disorder to be one of the most common of bone disorders. In
>>> certain diseases, such as lupus erythematosus, almost a third of patients
>>> may be affected.[9] IO is able to affect any bone of the human skeleton
>>> and is represented by a large number of orthopedic diseases now seen as
>>> simple anatomic- and age-related variations of intramedullary ischemia
>>> and infarction.[1-5,9,14,15]
>>>
>>> The old, overly-simplified histopathologic definition of IO as massive
>>> loss of osteocytes without pus is now substantially expanded to include
>>> specific and often subtle signs of ischemic marrow damage which may not
>>> even include obviously dead tissues.[2-9,14-16] Histopathologically less
>>> severe or nascent involvement has begun to be consolidated under a common
>>> diagnostic term, bone marrow edema (Table 1), and the disease is now
>>> known primarily as a vascular disorder readily influenced by a variety of
>>> risk factors or trigger events ("hits") which promote
>>> thrombosis.[7,9,17-21] Persons with multifocal IO are more likely to
>>> suffer from systemic risk factors than those with single site involvement
>>> and the great majority of patients have inherited or acquired a systemic
>>> tendency toward fibrin generation (Table 2) which predisposes them to
>>> microinfarction and ischemic marrow damage.[8,9,15-22]
>>>
>>> Usually associated with pain, IO can nevertheless show a surprising
>>> capacity to remain painless until great destruction has occurred, even to
>>> the point of joint collapse for hip lesions -- there is little
>>> correlation between the degree of bone involvement and the intensity of
>>> associated pain.[5,9] The pain can take on a neuralgic character but its
>>> etiology is primarily a function of intraosseous fluid dynamics and
>>> inflammatory mediators rather than damaged nerves, as discussed
>>> later.[4,5,9,11,14-16]
>>>
>>> Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> The Pre-Antibiotic Era: 1850-1930.
>>>
>>> IO of the maxillofacial region is not new to dentistry. During the
>>> pre-antibiotic era "phossy jaw" and other forms of "chemical
>>> osteomyelitis" resulted from environmental pollutants, such as lead and
>>> the phosphorus used in safety matches, as well as from popular
>>> medications containing mercury, arsenic or bismuth.[23-29] This disease
>>> was well established by 1867, did not often occur in individuals with
>>> good gingival health, and appeared to "attack" the mandible first.[25]
>>> It was associated with localized or generalized deep ache or pain, often
>>> of multiple jawbone sites. The teeth often appeared sound and
>>> suppuration was not present. Even so, the dentist often began extracting
>>> one tooth after another in the region of pain, often with temporary
>>> relief but usually to no real effect.[24] Occasionally, large fragments
>>> of necrotic bone would come out with the tooth, sometimes involving much
>>> of an entire quadrant, as depicted in the figure at the top of this page.
>>> Apparently, Lorinser of Vienna in 1845 was the first to call attention to
>>> the problem.[25]
>>>
>>> Less severe cases of maxillofacial osteonecrosis were discussed in the
>>> classic 1898 oral pathology text by Barrett,[28] wherein he described
>>> "caries" and "necrosis" of bone with cellular "devitalization" and
>>> "inhibition of nutrient currents," characterized by a slowly progressive
>>> "breaking down" of the "territory" of marrow tissues receiving those
>>> nutrients and resulting in little or no production of granulation tissue.
>>> He had no suggested etiology for his cases. Thirty years earlier and
>>> more than a century ahead of his time, Noel[27] separated bone caries
>>> into two distinct categories: "bone death" and the less intense "reduced
>>> vitality." Even earlier, the 1848 text by Thomas Bond[23], which appears
>>> to be the first true oral pathology text, was the first book to discuss
>>> bone necrosis as such, emphasizing that this disease did not require
>>> abscessed teeth or gums, could result in the complete death of bone.
>>> Bond mentioned that "necrosis may be caused by any means which destroys
>>> the nutrition of the bone or any part of it"-- usually from
>>> "constitutional vitiations, or defects of nutrition consequent upon
>>> general pravity." His recommended treatment: "when necrosis has taken
>>> place, the bone must be removed."
>>>
>>> G. V. Black,[29] the father of modern dentistry, described in 1915 an
>>> osteomyelitis look-alike disease which he called "chronic osteitis." He
>>> described slow bone death "cell by cell" with the creation of alveolar
>>> intramedullary "cavities" up to 5 cm. in size and wondered about its
>>> unique ability to produce extensive bone destruction without pus, without
>>> redness and swelling of the overlying tissues, without an increase in the
>>> patient's body temperature, and often without pain. His suggestion to
>>> curette diseased bone reiterated the treatment proposed by Ferguson[24]
>>> in 1868 and by Bond[23] in 1848. Around the same time period
>>> osteonecrosis of the hip in children was being recognized by the author's
>>> whose names would eventually be affixed to that disease, i.e. the
>>> Legg-Calvé-Perthes disease.[31-33]
>>>
>>> Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> The Forgotten Decades: 1930-1970.
>>>
>>> For most of the twentieth century this disease was largely forgotten by
>>> the dental profession, although a few investigators made significant
>>> contributions to the advancement of our understanding. Wilensky[24] and
>>> Hankey[25] suggested that persistent regional necrosis in osteomyelitis
>>> of the jaws was secondary to vascular insufficiency, while Brosch[26]
>>> described the potential for hollow medullary spaces to enlarge and
>>> coalesce one with another. Thoma[37,38] was likely the first to
>>> specifically correlate this "residual infection" or "osteitis" with old
>>> extraction sites, many of which demonstrated focal "necrotic exudates,"
>>> fibrosis and "osteoclastic resorption" of surrounding bone. His
>>> observations were affirmed in 1955 by Box,[34] who reported a very large
>>> series of limited intraosseous cavitations or "vacuolations" in old
>>> extraction sites with no production of pus or bony sequestra. Box was
>>> especially intrigued by the radiographic subtlety of the disease, by its
>>> multifocal nature, its localized tenderness without inflammatory signs,
>>> and the neuralgia-like nature of accompanying pain.
>>>
>>> Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> The Over-Emphasis of Pain: 1970-1990.
>>>
>>> The 1970s and 1980s saw a strong emphasis placed on the neuralgia-like
>>> pains often accompanying osteonecrosis of the maxillofacial region, an
>>> influence embodied in the currently popular diagnostic name NICO
>>> (neuralgia-inducing cavitational osteonecrosis).[40-48] Significant or
>>> complete pain reduction was achieved in chronic "idiopathic" facial pain
>>> by the simple expedient of decortication and curettage of damaged
>>> alveolar bone (Table 3), supporting the contention by neural researchers
>>> that persistent odontogenic and osseous disease can be important
>>> contributing factors for such neuralgias.44-49 None of these
>>> investigations included a control group, nor has any facial neuralgia
>>> follow-up study. Ethical considerations and the ever-present potential
>>> for silent or subclinical disease will likely prevent valid control
>>> groups from being identified, but a 1995 NICO follow-up investigation
>>> confirming earlier surgical successes went so far as to guarantee patient
>>> anonymity, to use a well-established pain evaluation instrument instead
>>> of surgeon records to determine outcomes, and to use a third party to
>>> collect and analyze data in order to reduce potential biases.[50]
>>>
>>> Unfortunately, the major emphasis on the association with neuralgic pain
>>> initiated significant controversy among professionals treating
>>> "idiopathic" facial pain and kept involved researchers from focusing on
>>> other features of the disease process, such as more appropriate diagnoses
>>> and diagnostic techniques, and better understanding of the
>>> pathophysiology and pathoetiology of the disease. Early lesions were
>>> diagnosed by a number of independent pathologists as chronic
>>> osteomyelitis, and microorganisms cultured from many NICO lesions,
>>> combined with occasional facial pain relief with antibiotic therapy,
>>> assured that these cases would be diagnosed and treated as chronic
>>> osteomyelitis. And yet, a significant number of patients did not respond
>>> in a fashion appropriate to that diagnosis. This led some investigators
>>> to seek alternative interpretations for the biological behavior and
>>> histopathology. A critical shift in perspective (return to the original
>>> concepts?) occurred in 1989 when this odd alveolar disease began to be
>>> viewed primarily as a problem of compromised medullary blood flow driven
>>> by progressive thrombosis, rather than as a unique infection unknown to
>>> other bones.[56,57]
>>>
>>> This new perspective as a maxillofacial manifestation of IO provided, for
>>> the first time, a logical explanation for the curiously multifocal nature
>>> of the disease; its frequent intermingling of ischemically damaged and
>>> normal marrow (also influenced by the perfusion irregularities of fatty
>>> marrow[58]), its frequent lack of inflammatory cells, its remarkably
>>> chronic and recurring character, its deep bone pain and varied pain
>>> syndromes, its relatively high failure rate with local interventions, and
>>> its primary localization at the ends of the arterial inflow (retromolar
>>> and subcrestal alveolar regions) where weak, irregular blood flow favors
>>> the formation of intravascular thrombi.[5,7,9,14,15,59]
>>>
>>> This is not to say that intraosseous microorganisms do not represent a
>>> significant risk factor or triggering mechanism for thrombosis in these
>>> stagnant zones of cancellous bone. Affected bone is ideal fodder for
>>> periodontal and periapical bacteria chronically stimulating inflammatory
>>> and immune responses.[60-62] Impaired medullary circulation prevents
>>> proper healing in these instances and the chronic infection, in turn,
>>> enhances local and systemic clotting. This further exacerbates the
>>> medullary ischemia and initiates a slow, ever-increasing spiral of
>>> thrombosis and microinfarction with progressively elevating
>>> intramedullary pressures, additional thrombosis, and frequent propagation
>>> of spontaneous pain. Prothrombotic factors, especially fibrinogen, also
>>> allow increased adherence of bacteria to thrombin-activated endothelial
>>> cells.[63]
>>>
>>> Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> Decade of Major Advances: 1990-2000.
>>>
>>> Once it became clear that this disease of the jaws resembled avascular
>>> necrosis of other bones, investigators used newly available laboratory
>>> tests, including allele-specific polymerase chain reaction, to identify
>>> in NICO patients heritable disorders predisposing to adverse thrombotic
>>> events. At least 72% proved to be afflicted with a variety of such
>>> disorders, as compared to 70-87% for patients with IO of the hip and
>>> knee.[9,19-21,64-67 This was seen as a major breakthrough, eventuating in
>>> the use of anticoagulants (without surgery or antibiotics) in persons
>>> with NICO and hip osteonecrosis.[68-71] Although not all affected
>>> individuals benefited, the significant pain relief experienced by a large
>>> proportion of treated patients confirms an association in those persons
>>> between the symptoms of IO and the hypercoagulable disorders.[69,71]
>>>
>>> Viewing NICO as the oral manifestation of a systemic disease also allowed
>>> application of the clinicopathologic qualities of long bone disease to
>>> maxillofacial cases, especially the use of diagnostic imaging techniques
>>> such as 99technetium-MDP (99mTc-MDP) scintigraphy and Single Proton
>>> Emission Computed Tomography (SPECT) scans, instead of the indium and
>>> gallium scans typically used for bone infections.[64,72-74] The small
>>> number of chronic inflammatory cells found in NICO lesions makes
>>> radioisotopes which attach to leukocytes much less useful than those
>>> which attach to new or exposed bone matrix. There is usually a small
>>> amount of ongoing healing in IO lesions and so they present as "hot
>>> spots" of increased radioisotope uptake, with "cold spots" of extremely
>>> reduced uptake in the occasional severely desiccated lesion. Newly
>>> developed 99mTc isotopes directed at fibrin "-chain peptide may prove
>>> useful for patients actively forming microclots.[75]
>>>
>>> A substantial proportion (25-35%) of scans will be falsely negative
>>> because the disease has long periods during which no bone is destroyed or
>>> regenerated, even as symptoms and marrow damage progress. This holds true
>>> regardless of the affected bone, but maxillofacial involvement suffers
>>> from an unexpected false-negative phenomenon: radiologists not attuned to
>>> jawbone ischemia often interpret a hot spot of alveolar bone as "normal,"
>>> presuming it to relate to ubiquitous dental and periodontal disease. We
>>> recommend, therefore, that the surgeon review all films interpreted as
>>> negative. Thin-sliced spiral CT scans and ultrasonic scans have also
>>> proven effective in localizing NICO, although they require very careful
>>> evaluation.[76] MRI scans are valuable for the rounded ends of bones but
>>> in our experience are of little benefit in alveolar cases.[77,78]
>>>
>>> In a similar fashion the more contemporary histopathologic features of
>>> ischemic osteonecrosis and bone marrow edema (its less severe
>>> counterpart) often overlooked by or unfamiliar to oral pathologists,
>>> could be applied to maxillofacial examples with the notable caveat that
>>> there are no features of cortical collapse in jaw lesions and odontogenic
>>> infections are often superimposed.[1-9,57] Additionally, microscopic
>>> evaluation of maxillofacial biopsy samples is made much more difficult by
>>> the small number and size of available curettage fragments, especially
>>> when an intramedullary cavitation exists, in contradistinction to the
>>> large specimens available for study after resection and core biopsies of
>>> long bone cases. Recent analyses have, significantly, reported that
>>> almost 3/4 of jawbone biopsy samples of ischemic osteonecrosis and NICO
>>> can be classified as the histologically more subtle variants called bone
>>> marrow edema or regional ischemic osteoporosis.[81,82] This has helped
>>> to explain why some oral pathologists, certainly not the majority, have
>>> difficulty distinguishing the classic features from "normal" bone and
>>> bone marrow.
>>>
>>> The first microscopic review of a large series of biopsied cases of NICO
>>> was reported during the 1990s, as was the first necropsy example.[57,82]
>>> These papers strongly emphasized the multifocal nature of the disease,
>>> while others reinforced the strong association between chronic facial
>>> pain and inflammatory or ischemic marrow disease.[55,83] In this light,
>>> one of the most important advances was the refinement of the old
>>> anesthesia/hyperesthesia and microanesthesia diagnostic tests to more
>>> successfully localize areas of medullary disease in facial pain
>>> patients.[84-86]
>>>
>>> During the 1990s sophisticated assays were also applied, for the first
>>> time, to maxillofacial osteonecrosis. Haley and Pendergras[87] used a
>>> well-established neurotoxicity assay on a very large number of tissue
>>> samples, finding almost all to be extremely toxic -- often more toxic
>>> than hydrogen sulfide, the chemical normally used to establish maximum
>>> level of neurotoxicity. The exact nature of the toxin is not yet known,
>>> but the discovery of the neurotoxicity led some to question whether or
>>> not this process damaged the peripheral nerve myelin of the alveolar
>>> nerves. This idea was further stimulated by the finding in a small
>>> number of NICO biopsy samples of an unusual form of nonwallerian
>>> degeneration in the majority of visible nerves.[55] To this end the
>>> blood of another small sample of NICO patients was evaluated by a
>>> newly-established assay which, for the first time, allowed the
>>> determination of circulating antibodies against peripheral nerve
>>> myelin.[88] The sera of healthy humans normally show none of these
>>> antibodies, as was true for a few of the NICO patients, but other NICO
>>> patients had antibody levels as high as or higher than those found in the
>>> classic demyelination disease, the Guillain-Barré syndrome.[89,90] This
>>> suggests chronic exposure of the peripheral myelin to the immune system,
>>> either as a primary attack (autoimmune) or secondary to myelin exposed or
>>> partially destroyed by a local inflammatory/ischemic phenomenon.
>>>
>>> While some patients had no such antibodies, others demonstrated Elevated
>>> levels of circulating anti-peripheral nerve myelin (anti-PNM) antibodies
>>> have been found in NICO patients, suggesting .120-122 Chronic nerve
>>> damage is likely enhanced by the very high levels of neurotoxicity found
>>> by bioassay in virtually all tissue samples of maxillofacial
>>> osteonecrosis, although the responsible neurotoxins have not yet been
>>> identified.123
>>>
>>> Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>> References
>>>
>>> 1. Burwell RG, Harrison MHM (eds). Symposium: Perthes' disease. Clin
>>> Orthop 1986; 209:2-161,234.
>>>
>>> 2. Milgram JW. Radiologic and histologic pathology of nontumorous
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>>> Publishing, 1990, vol 2, p 868.
>>>
>>> 3. Ono K, ed. Symposium: recent advances in avascular necrosis. Clin
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>>>
>>> 4. Schoutens A, Arlet J, Gardeniers JWM, Hughes SPF. Bone circulation
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>>
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>>> trigeminal pain, Part II. Compendium Cont Educ Dent 1992; 11:980-997.
>>>
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>>> Technologies; University of Kentucky]
>>>
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>>> 1992, 10:629.
>>>
>>> 89. McMahon R, Bouquot J, Mahan P, Gremillion H. Elevated serum
>>> peripheral nerve anti-myelin antibody titers in atypical facial pain
>>> patients with NICO. J Orofacial Pain 1994; 8:104.
>>>
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>>> antibodies in patients with maxillofacial osteonecrosis (NICO). J Oral
>>> Pathol Med 1998; 27:345-346.
>>>
>>> Top Of This Page
>>>
>>>
>>> ------------------------------------------------------------------------------
>>>
>>> Table 1: Alternative diagnostic names used for bone marrow
>>> edema and ischemic osteonecrosis.1-9,14-16
>>>
>>> Bone Marrow Edema
>>> Ischemic Osteonecrosis
>>>
>>> Arlet Type I osteonecrosis
>>> Bone compartment disease
>>> Bone marrow edema syndrome
>>> Chronic traumatic edema
>>> Medullary engorgement-pain syndrome
>>> Migratory osteolysis
>>> Migratory osteoporosis
>>> NICO *
>>> Post-traumatic painful osteoporosis
>>> Post-traumatic reflex dystrophy
>>> Primary algodystrophy
>>> Regional ischemic osteoporosis
>>> Regional osteoporosis
>>> Roentgenologic transient osteoporosis
>>> Sudeck's disease (RSD) **
>>> Transient bone marrow edema syndrome
>>> Transient demineralization
>>> Transient ischemic osteoporosis
>>> Transient marrow edema
>>> Transient osteoporosis
>>> Transitory demineralization in pregnancy
>>> Aseptic necrosis
>>> Aseptic osteomyelitis
>>> Aseptic osteonecrosis
>>> Avascular necrosis
>>> Bone infarction
>>> Coronary disease of bone
>>> Ischemic necrosis
>>> NICO *
>>> Osteochondrosis desiccans
>>> Perthe's disease
>>>
>>>
>>> * NICO: neuralgia-inducing cavitational osteonecrosis
>>> ** RSD: reflex sympathetic dystrophy
>>>
>>> Return to Text Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>>
>>>
>>> Table 2: Coagulation disorders found in patients with ischemic
>>> osteonecrosis of the hips, knees and jaws. These are compared to the
>>> proportions found in patients with deep vein thrombosis of soft tissues
>>> and with the normal population. Resulting proportions do not total 100%
>>> because some patients had multiple disorders. Modified from Bouquot JE,
>>> LaMarche MG. J Pros Dent 1999; 81:148-158.
>>>
>>> Normal Population
>>> Deep Vein Thrombosis
>>> Osteonecrosis
>>>
>>> Thrombophilia
>>>
>>> Hereditary types*
>>> 2-5%
>>> 5-9%
>>> 50-70%
>>>
>>> Acquired types
>>> 3-7%
>>> 20-50%
>>> 33%
>>>
>>> Hypofibrinolysis:
>>>
>>> Hereditary types *
>>> <1%
>>> 5-15%
>>> 18-22%
>>>
>>> Acquired types
>>> <1%
>>> 20-25%
>>> 50%
>>>
>>> Total (includes multiple coagulopathies):
>>> 5-9%
>>> 20-50%
>>> 65-87%
>>>
>>>
>>> * usually autosomal dominant
>>>
>>> Return to Text Top Of This Page
>>>
>>>
>>> --------------------------------------------------------------------------------
>>>
>>>
>>>
>>>
>>>
>>> Table 2: Results of surgical curettage of jawbone NICO (Neuralgia-Induced
>>> Cavitational Osteonecrosis) lesions, an average of 4.5 years after last
>>> surgery, in 103 patients with "idiopathic" chronic facial pain for an
>>> average of 6 years (range: 2-18 years) prior to NICO surgery.
>>>
>>> Reference: Bouquot JE, Christian J. Long-term effects of jawbone
>>> curettage on the pain of facial neuralgia. J Oral Maxillofac Surg 1995;
>>> 53:387-397.
>>>
>>> Follow-up Rating Reduction % Pain Present Status of Pain % of Total
>>> Cases
>>> 0 0-10 % No improvement 8.8% *
>>> 1 11-33 Minimal improvement 2.9
>>> 2 34-75 Moderate improvement 15.5
>>> 3 76-99 Considerable improvement ** 13.6
>>> 4 100 No pain 59.2
>>> Total:
>>> 100.0 %
>>>
>>>
>>>
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