Re: NICO Historical Review

From: LadyLollipop (LadyLollipop_at_insightbb.com)
Date: 03/18/05 

Date: Fri, 18 Mar 2005 16:55:42 GMT

"John Chewter" <john@LESS_SPAMchewter.f9.co.uk> wrote in message
news:d1ermg$dtl$1@sparta.btinternet.com...
> My claim is that you do not understand the long medical terms that you
> quote.

That's just ONE of yur claims.

There are a list of others, when sked to prove them, you couldn't, all you
did was insult.

> This is backed up by your comments showing non-comprehension.
>
> Case Proven

Hadly, that's opinion.

> John Chewter
><snip adsvertising>
>
> "Joel M. Eichen" <joeleichen@yahoo.com> wrote in message
> news:sjjl315setievto2evl5iqvft454mkno53@4ax.com...
>> 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!

<snip Joel's blatherings>
>>
>>
>>
>>
>>>
>>>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
>>>> <snip advertising>
>>>> "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
>>>>> diseases of bones and joints. Northbrook, Illinois, Northbrook
>>>>> Publishing, 1990, vol 2, p 868.
>>>>>
>>>>> 3. Ono K, ed. Symposium: recent advances in avascular necrosis. Clin
>>>>> Orthop 1992; 277:2.
>>>>>
>>>>> 4. Schoutens A, Arlet J, Gardeniers JWM, Hughes SPF. Bone circulation
>>>>> and vascularization in normal and pathological conditions. New York,
>>>>> Plenum Press, 1993.
>>>>>
>>>>> 5. Steinberg ME, Steinberg DR. Osteonecrosis. In: Kelly WN, Harris ED
>>>>> Jr, Ruddy S, Sledge CB. Textbook of rheumatology (4th ed).
>>>>> Philadelphia,
>>>>> W.B. Saunders; 1993, p 1628.
>>>>>
>>>>> 6. Mazieres B. Osteonecrosis. In: Klippel JH, Dieppe PA (eds).
>>>>> Rheumatology. St. Louis, Mosby; 1994, 41.1.
>>>>>
>>>>> 7. Bullough, PG. Orthopaedic pathology (3rd ed). Baltimore,
>>>>> Mosby-Wolfe,
>>>>> 1997.
>>>>>
>>>>> 8. Jones JP Jr. Osteonecrosis. In: Koopman WJ (ed). Arthritis and
>>>>> allied
>>>>> conditions; a textbook of Rheumatology (13th ed). Baltimore, Williams
>>>>> &
>>>>> Wilkins, 1997,1923
>>>>>
>>>>> 9. Urbaniak JR, Jones, JP Jr (eds). Osteonecrosis -- etiology,
>>>>> diagnosis, and treatment. American Academy of Orthopaedic Surgeons;
>>>>> Chicago, Illinois, 1997.
>>>>>
>>>>> 10. Phemister, DB. Repair of bone in the presence of aseptic necrosis
>>>>> resulting from fractures, transplantations, and vascular obstruction.
>>>>> J
>>>>> Bone Joint Surg 1930; 12:769.
>>>>>
>>>>> 11. Russell J. A practical essay on a certain disease of bones termed
>>>>> necrosis. Edinburgh, Neill and Co, 1794.
>>>>>
>>>>> 12. Martin LD, Rothschild BM. Paleopathology and diving monasaurs.
>>>>> Amer
>>>>> Scientist 1989; 77:460.
>>>>>
>>>>> 13. Norgard MJ, Carpenter JT, Conrad ME. Bone marrow necrosis and
>>>>> degeneration. Arch Intern Med 1979; 139:905.
>>>>>
>>>>> 14. Arlet J, Mazieres B (eds). Bone circulation and bone necrosis.
>>>>> Heidelberg, Springer-Verlag, 1990.
>>>>>
>>>>> 15. Ficat RP. Idiopathic bone necrosis of the femoral head: early
>>>>> diagnosis and treatment. J Bone Joint Surg 1985; 67B:3.
>>>>>
>>>>> 16. Arnoldi CC. Intraosseous engorgement-pain syndromes. The
>>>>> pathomechanism of pain. In: Arlet J, Mazieres B (eds). Bone
>>>>> circulation
>>>>> and bone necrosis. Proceedings of the IVth International Symposium on
>>>>> Bone Circulation, Toulouse (France), 17th-19th September, 1987. New
>>>>> York,
>>>>> Springer-Verlag, 1990.
>>>>>
>>>>> 17. Jones JP Jr. Intravascular coagulation and osteonecrosis. Clin
>>>>> Orthop 1992; 277:41.
>>>>>
>>>>> 18. Van Veldhuizen PJ, Neff J, Murphey MD, et al. Decreased
>>>>> fibrinolytic
>>>>> potential in patients with idiopathic avascular necrosis and transient
>>>>> osteoporosis of the hip. Am J Hematol 1993; 44:243.
>>>>>
>>>>> 19. Glueck CJ, Freiberg R, Glueck HI, et al. Hypofibrinolysis; a
>>>>> common,
>>>>> major cause of osteonecrosis. Am J Hematol 1994; 45:156.
>>>>>
>>>>> 20. Glueck CJ, Crawford A, Roy D, Freiberg R, et al. Association of
>>>>> antithrombotic factor deficiencies and hypofibrinolysis with
>>>>> Legg-Perthes
>>>>> Disease. J Bone Joint Surg 1996; 78A:3.
>>>>>
>>>>> 21. Glueck CJ, Freiberg R, Gruppo R, Crawford A, et al. Thrombophilia
>>>>> and hypofibrinolysis: reversible pathogenetic etiologies of
>>>>> osteonecrosis. In: Urbaniak Jr, Jones, JP Jr (eds). Osteonecrosis:
>>>>> etiology, diagnosis, and treatment. Chicago, Illinois, American
>>>>> Academy
>>>>> of Orthopaedic Surgeons, 1997 p 105.
>>>>>
>>>>> 22. Mont MA, Jones LC, La Porte DM, et al. Symptomatic multifocal
>>>>> osteonecrosis: a multicenter study. Clin Orthop 1999; 369:312.
>>>>>
>>>>> 23. Bond TE Jr. A practical treatise on dental medicine.
>>>>> Philadelphia:
>>>>> Lindsay & Blakiston, 1848.
>>>>>
>>>>> 24. Am J Dent Sc 1859 [phossy jaw photo]
>>>>>
>>>>> 25. Anonymous. Necrosis of the lower jaw in makers of Lucifer
>>>>> matches.
>>>>> Am J Dent Science 1867; 1 (series 3):96-97.
>>>>>
>>>>> 26. Ferguson W. New treatment of necrosis. Am J Dent Science 1868; 1
>>>>> (series 3):189.
>>>>>
>>>>> 27. Noel HR. A lecture on caries and necrosis of bone. Am J Dent
>>>>> Science
>>>>> 1868; 1 (series 3):425, 482.
>>>>>
>>>>> 28. Barrett WC. Oral pathology and practice. Philadelphia, S.S. White
>>>>> Dental Mfg Co, 1898.
>>>>>
>>>>> 29. Black GV. A work on special dental pathology (2nd ed). Chicago,
>>>>> Medico_Dental Publ Co, 1915.
>>>>>
>>>>> 30. [old: discolored nerve]
>>>>>
>>>>> 31. Calve J Sur une forme particuliere de pseudo-coxalgie greffee sur
>>>>> des formations caracteristiques de l'extremite superieure du femur.
>>>>> Rev
>>>>> Chir 1910; 42:54-84.
>>>>>
>>>>> 32. Legg AT. An obscure affection of the hip joint. Boston Med Surg J
>>>>> 1910; 162:202-204.
>>>>>
>>>>> 33. Perthes G. Uber Osteochondritis Deformans Juvenalis. Arch Klin
>>>>> Chir
>>>>> 1913; 101:779-807.
>>>>>
>>>>> 34. Wilensky AO. Osteomyelitis of the jaw. Arch Surg 1932; 25:215.
>>>>>
>>>>> 35. Hankey GT. Osteomyelitis (necrosis) of the jaws: it pathology and
>>>>> treatment. Brit Dent J 1938; 63:552.
>>>>>
>>>>> 36. Brosch F. Die histopathologische Grundlage der Symptome bei
>>>>> Keifer-osteomyelitis. Deutsch Zahnartz Zeit 1958; 13:426.
>>>>>
>>>>> 37. Thoma KH. Clinical pathology of the jaws, with a histologic and
>>>>> roentgen study of practical cases. Baltimore, Charles C. Thomas, 1934,
>>>>> p
>>>>> 94.
>>>>>
>>>>> 38. Thoma KH. Oral surgery ( vol 1). St. Louis, C V Mosby; 1948, p
>>>>> 773.
>>>>>
>>>>> 39. Box RM. Post-extraction oral sepsis. Ontario Dent J 1955:
>>>>> Oct/Nov:1.
>>>>>
>>>>> 40. Ratner EJ, Person P, Kleinman DJ, et al. Jawbone cavities and
>>>>> trigeminal and atypical facial neuralgias. Oral Surg Oral Med Oral
>>>>> Pathol
>>>>> 1979; 48:3.
>>>>>
>>>>> 41. Roberts AM, Person P. Etiology and treatment of idiopathic
>>>>> trigeminal and atypical facial neuralgias. Oral Surg Oral Med Oral
>>>>> Pathol
>>>>> 1979; 48:298.
>>>>>
>>>>> 42. Shaber EP, Krol AJ. Trigeminal neuralgia __ a new treatment
>>>>> concept.
>>>>> Oral Surg Oral Med Oral Pathol 1980; 49:286.
>>>>>
>>>>> 43. Mathis BJ, Oatis GW, Grisius RJ. Jaw bone cavities associated
>>>>> with
>>>>> facial pain syndromes: case reports. Milit Med 1981; 146:719.
>>>>>
>>>>> 44. Demerath RR, Sist T. Treatment of osteocavitation lesions in
>>>>> facial
>>>>> pain patients: preliminary results. J Dent Res 1982; 61:218.
>>>>>
>>>>> 45. Wang M, Xiwei J, Qingrong I, Sanyou Z. [A study of the relation
>>>>> between the various trigger zones of idiopathic trigeminal neuralgia
>>>>> and
>>>>> jaw bone cavities.] Acta Acad Med Sichuan 1982; 13:233.
>>>>>
>>>>> 46. Grechko VE, Puzin MN. [Odontogenic trigeminal neuralgia] Zh
>>>>> Nevropathol Psikhiatr 1984; 84:1655.
>>>>>
>>>>> 47. Roberts AM, Person P, Chandran NB, et al. Further observations on
>>>>> dental parameters of trigeminal and atypical facial neuralgias. Oral
>>>>> Surg
>>>>> Oral Med Oral Pathol 1984; 58:121.
>>>>>
>>>>> 48. Ratner EJ, Langer B, Evins ML. Alveolar cavitational
>>>>> osteopathosis -- manifestations of an infectious process and its
>>>>> implication in the causation of chronic pain. J Periodontol 1986;
>>>>> 57:593.
>>>>>
>>>>> 49. Harris W: Forward. In: Wartenberg R: Neuritis, sensory neuritis,
>>>>> neuralgia, a clinical study with review of the literature. New York,
>>>>> Oxford University Press, 1958, p vii.
>>>>>
>>>>> 50. Mumford JM. Role of the dentist in trigeminal neuralgia. Pain
>>>>> 1978;
>>>>> 5:83.
>>>>>
>>>>> 51. Sisk AL. Management of chronic orofacial pain: surgical treatment
>>>>> of
>>>>> chronic facial pain. Anesth Prog 1983; 30:180.
>>>>>
>>>>> 52. Fromm GH, Terrence CF, Maroon JCL: Trigeminal neuralgia; current
>>>>> concepts regarding etiology and pathogenesis. Arch Neurol 1984;
>>>>> 41:1204.
>>>>>
>>>>> 53. Sessle BJ. Neurobiology of orofacial pain. Dent Clin North Am
>>>>> 1987;
>>>>> 31:595.
>>>>>
>>>>> 54. Raskin NH. Headache, 2nd ed. New York, New York, Churchill
>>>>> Livingstone, 1988.
>>>>>
>>>>> 55. Bouquot JE, Christian J. Long-term effects of jawbone curettage
>>>>> on
>>>>> the pain of facial neuralgia; treatment results in neuralgia-inducing
>>>>> cavitational osteonecrosis. J Oral Maxillofac Surg 1995; 53:387.
>>>>>
>>>>> 56. Bouquot JE, Roberts AM, Person, P, Christian J. The
>>>>> histopathology
>>>>> of neuralgia-inducing cavitational osteonecrosis (NICO). J Dent Res
>>>>> 1989;
>>>>> 68:952.
>>>>>
>>>>> 57. Bouquot JE, Roberts AM, Person P, et al. NICO (neuralgia_inducing
>>>>> cavitational osteonecrosis): osteomyelitis in 224 jawbone samples from
>>>>> patients with facial neuralgias. Oral Surg Oral Med Oral Pathol 1992;
>>>>> 73:307.
>>>>>
>>>>> Byron MA. A clinicopathologic review of 2278 NICO cases
>>>>> (neuralgia-inducing cavitational osteonecrosis). Master's Thesis
>>>>> (Endodontics). Morgantown, WV: West Virginia University, 1994.
>>>>>
>>>>> Bouquot J, McMahon R. Ischemic osteonecrosis of the jaws in 2,023
>>>>> patients with facial pain. J Oral Pathol Med 1996; 25:271.
>>>>>
>>>>> Bouquot JE, McMahon RE. Ischemic alveolar osteonecrosis in 2,023
>>>>> patients with chronic facial pain. J Orofacial Pain 1997; 11:180.
>>>>>
>>>>> Odell EW, Morgan PR. Biopsy pathology of the oral tissues. London:
>>>>> Chapman & Hall, 1998: 268-270.
>>>>>
>>>>> 58. Kiaer T. Bone perfusion and oxygenation. Animal experiments and
>>>>> clinical observations. Acta Orthop Scand 1994; 65 (Suppl 257):1.
>>>>>
>>>>> 59. Hiroshi I, Matsuno T, Kaneda K. Prognosis of early stage
>>>>> avascular
>>>>> necrosis of the femoral head. Clin Orthop 1999; 358:149.
>>>>>
>>>>> 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 %
>>>>>
>>>>>
>>>>>
>>>>
>>>>
>>>
>>
>
>