Re: NICO Historical Review
From: LadyLollipop (LadyLollipop_at_insightbb.com)
Date: 03/18/05
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Date: Fri, 18 Mar 2005 05:33:45 GMT
"John Chewter" <john@LESS_SPAMchewter.f9.co.uk> wrote in message
news:d1cnqs$cj6$1@hercules.btinternet.com...
> Jan - do tell us that you understood all these papers? Some of the words
> are longer than 'Marmalade, Can you understand trans-marmaladic words?
John, do back up you claims and you lies, rather than stalk me, then do post
something besides criticiisms od everything I post.
You have number of of questions you have never answered, is that your
problem?
Shall I ask them again, and post you insults, rather than answers.
Do grow up, John.
As a claimed amalgamist, I asked you why you didn't post any articles
showing us why you believe amalgams are toxic, here is your reply:
> LL Have you ever posted any studies of this toxicity????
JC Certainly not. I am an imaging specialist.
So I kindly suggest, you shut up.
LL
> John Chewter
> http://www.keyneimage.co.uk
> "LadyLollipop" <LadyLollipop@insightbb.com> wrote in message
> news:TW8_d.76748$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
>>
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>>
>> 2. Milgram JW. Radiologic and histologic pathology of nontumorous
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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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>>
>> 60. Lerner UH. Regulation of bone metabolism by the kallikrein-kinin
>> system, the coagulation cascade, and the acute-phase reactants. Oral Surg
>> Oral Med Oral Pathol 1994; 78:481.
>>
>> 61. Stashenko P, Want C-Y, Tani-Ishii N, Yu SM. Pathogenesis of induced
>> rat periapical lesions. Oral Surg Oral Med Oral Pathol 1994; 78:494.
>>
>> 62. Torabinejad M. Mediators of acute and chronic periradicular lesions.
>> Oral Surg Oral Med Oral Pathol 1994; 78:511.
>>
>> 63. Shenkman B, Runinstein E, Tamarin I, et al. Staphylococcus aureus
>> adherence to thrombin-treated endothelial cells is mediated by fibrinogen
>> but not by platelets. J Lab Clin Med 2000; 135:43.
>>
>> 64. Neville B, Damm D, Allen C, Bouquot JE. Oral & maxillofacial
>> pathology. Philadelphia: W. B. Saunders, 1995, p 631.
>>
>> 65. Glueck CJ, McMahon RE, Bouquot JE, et al. Thrombophilia,
>> hypofibrinolysis and osteonecrosis of the jaws. Oral Surg Oral Med Oral
>> Pathol 1996; 81:557.
>>
>> 66. Gruppo R, Glueck CJ, McMahon RE, et al. The pathophysiology of
>> osteonecrosis of the jaw: anticardiolipin antibodies, thrombophilia, and
>> hypofibrinolysis. J Lab Clin Med 1996; 127: 481.
>>
>> 67. Glueck CJ, McMahon RE, Bouquot JE, Tripplet D, et al. Heterozygosity
>> for the Leiden mutation V gene, a common pathoetiology for osteonecrosis
>> of the jaw with thrombophilia augmented by exogenous estrogens. J Lab
>> Clin Med 1997; 130:540.
>>
>> 68. Glueck CJ, Freiberg R, Glueck HI, et al. Idiopathic osteonecrosis,
>> hypofibrinolysis, high plasminogen activator inhibitor, high lipoprotein
>> (a), and therapy with stanozolol. Am J Hematol 1995; 48:213.
>>
>> 69. Glueck CJ, McMahon RE, Bouquot JE, Tracy T, et al.. Preliminary
>> pilot study of the treatment of thrombophilia and hypofibrinolysis and
>> the amelioration of the pain of osteonecrosis of the jaws. Oral Surg Oral
>> Med Oral Pathol Oral Radiol Endod 1998; 85:64.
>>
>> 70. Hammerschmidt DE. Thrombophilic osteonecrosis: another chapter. J
>> Lab Clin Med 1997; 130:451.
>>
>> 71. Glueck CJ. NICO and anticoagulation therapy. Oral Surg Oral Med Oral
>> Pathol Oral Radiol Endod 1998; 86:5.
>>
>> 72. Langlais RP, Langland OE, Nortje CJ. Diagnostic imaging of the jaws.
>> Baltimore: Williams & Wilkins; 1994:393.
>>
>> 73. Boudreau RJ, Griffiths HJ. Bone infarcts and osteonecrosis. In:
>> Collier BD Jr, Fogelman I, Rosenthal L. Skeletal nuclear medicine. St.
>> Louis: Mosby, 1996;293.
>>
>> 74. Bouquot JE, LaMarche MG. Ischemic osteonecrosis under fixed partial
>> denture pontics: radiographic and microscopic features in 38 patients
>> with chronic pain. J Pros Dent 1999; 81:148.
>>
>> 75. Thakur ML, Pallela VR, Consigny PM, et al. Imaging vascular
>> thrombosis with 99mTc-labeled fibrin "-chain peptide. J Nucl Med 2000;
>> 41:161.
>>
>> 76. Nicol K, Klingman J, Holt J, et al. Ultrasonic gum/jaw bone
>> detection instrument. Thesis. Socorro, New Mexico, New Mexico Institute
>> of Mining & Technology, 1996.
>>
>> 77. Larheim TA, Westesson P-L, Hicks D, Eriksson L, et al. Osteonecrosis
>> of the temporomandibular joint: correlation of magnetic resonance imaging
>> and histology. J Oral Maxillofac Surg 1999; 57:888.
>>
>> 78. Sano T, Westesson P-L, Larheim TA, Rubin SJ, et al. Osteoarthritis
>> and abnormal bone marrow of the mandibular condyle. Oral Surg Oral Med
>> Oral Pathol Oral Radiol Endod 1999; 87:243.
>>
>> 80. Bouquot J, McMahon R. Bone marrow edema syndrome: new disease or
>> early presentation of ischemic osteonecrosis? J Oral Pathol Med 1998;
>> 27:346.
>>
>> 81. Bouquot J, McMahon R. Bone marrow edema syndrome, independent
>> disease or early presentation of ischemic osteonecrosis? Proceedings,
>> Annual Meeting, American Academy of Oral & Maxillofacial Pathology;
>> Williamsburg, Virginia; April, 2000.
>>
>> 82. Adams WR, Spolnick KJ, Bouquot JE. Maxillofacial osteonecrosis in a
>> patient with multiple facial pains. J Oral Pathol Med 1999; 28:423-432.
>>
>> 83. McMahon RE, Griep J, Marfurt CP, et al. Local anesthetic effects in
>> the presence of chronic osteomyelitis/necrosis of the mandible:
>> implications for localizing the etiologic sites of referred trigeminal
>> pain. J Craniomand Pract 1995; 13:212-226.
>>
>> 84. Brown RS, Hinderstein B, Reynolds DC, et al. Using anesthetic
>> localization to diagnose oral and dental pain. J Amer Dent Assoc 1995;
>> 126: 633-641.
>>
>> 85. McMahon RE, Adams W, Spolnik K. Diagnostic anesthesia for referred
>> trigeminal pain, Part I. Compendium Cont Educ Dent 1992; 11:870-881.
>>
>> 86.McMahon RE, Adams W, Spolnik K. Diagnostic anesthesia for referred
>> trigeminal pain, Part II. Compendium Cont Educ Dent 1992; 11:980-997.
>>
>> 87. Haley BE, Pendergrass JC. http://www.altcorp.com. [Affinity Labeling
>> Technologies; University of Kentucky]
>>
>> 88. Koski CL. Humoral mechanisms in immune neuropathies. Neurol Clin
>> 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.
>>
>> 90. McMahon R, Bouquot J, Mahan P, Saxen M. Elevated anti-myelin
>> 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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