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Hyperplastic soft-tissue formation in the temporomandibular joint associated with internal derangement
Hyperplastic soft-tissue formation in the temporomandibular joint associated with internal derangement A radiographic
and histologic
study
Annika Isberg, D.D.S., Ph.D.,* Giiran Isacsson, D.D.S.. Ph.D.,** Ann-Sofi Johansson, D.D.S..*** and Ola Larson, D.D.S., M.D., D.iU.S.,*** Stockholm, Sweden KAROLINSKA
INSTITUTET
AND
KAROLINSKA
HOSPITAL
Hyperplastic connective tissue formation in the posterior part of the temporomandibular joint glenoid fossa has previously been described in autopsy specimens. The frequency of such hyperplastic tissue formation in patients with long-standing temporomandibular joint pain was studied in 103 joints from 80 patients by means of double-contrast arthrotomography. Five joints in four patients (5%) demonstrated hyperplastic tissue formation; in four cases this was associated with permanently displaced and deformed disks. All five joints were refractory to nonsurgical treatment. Surgically extirpated hyperplastic tissue and disk attachments contained nerve fibers and thickened adventitia of vessels, resulting in narrowed or obliterated lumina, extravasated erythrocytes, and fibrinlike deposits. The synovial membrane showed fibrinoid necrosis or was lost. The pain reaction in temporomandibular joints with hyperplastic soft-tissue formation may be released by compression or tension of nerves, breaking down products from blood or tissue ischemia. Contrast filling of both joint spaces, combined with tomography, was required for detection of the hyperplastic tissue formation. (ORAL SURC. ORAL MED. ORAL PATHOL. 61:32-38.
1986)
I n an autopsy investigation of temporomandibular joint specimens, Isberg and Isacsson’
(TMJ)
reported on the presence of hyperplastic connective tissue in the posterior part of the glenoid fossa that could be associated with fibrous ankylosis. The condition was related to anterior disk displacement or trauma. The hyperplastic tissue was found to contain extravasated blood, enlarged cavernous structures lacking endothelial lining, and extensive pathologic changes in the arteries and veins. The present investigation was undertaken to study the frequency of hyperplastic connective tissue formation in patients with long-standing TMJ pain and to
This study was supported by grants from the Ragnar and Torsten Siiderbergs Foundations, Stockholm, Sweden, and the Swedish Medical Research Council, Project No. 06877. *Department of Oral Radiology, School of Dentistry, Karolinska Institutet. **Department of Oral Radiology and Department of Stomatognathic Physiology, School of Dentistry, Karolinska Institutet. ***Department of Plastic Surgery, Karolinska Hospital.
32
relate arthrographic findings to morphologic and histologic features. MATERIAL Patients
AND METttODS
Eighty consecutive patients who had been referred to the Department of Oral Radiology with severe pain from one or both TMJs (103 joints in all) were subjected to radiographic examination of the hard as well as the soft tissues of the joint. All patients had suffered severepain for at least 1 year. Five joints in four women, 40, 41, 46, and 67 years of age, demonstrated soft-tissue hyperplasia as described by Isberg and Isacsson.’ These joints were selected for further investigation. The severe joint pain in the patients with hyperplastic soft tissue in the TMJ had lasted for 2 to 5 years (mean, 3.5 years). Pain was constant in four joints and consistent in association with mandibular movements in one joint. Two patients had been unable to work for more than 1 year becauseof the TMJ pain. The remaining two
Hyperplastic
Volume6 I Number 1
soft tissue
33
Fig. 1. Double-contrast arthrotomogram and schematic drawing of TMJ without arthropathosis. Disk is shown in black.
Fig. 2. Double-contrast arthrotomogram and schematic drawing of TMJ with hyperplastic connective tissue (arrow) adherent to condyle. Disk (marked in black) is in a normal superior position.
patients reported that the joint pain caused difficulties with concentration at work or during other activities. All patients said that their lives were severely affected by the chronic pain condition. Four joints in three patients demonstrated significant clinical signs and a case history of disk displacement without reduction,2-4 while one patient had disk displacement with reduction, which clinically became normal over a period prior to radiographic examination. Control material
The control material included four TMJ autopsy specimens from three men and one woman with an age range from 77 to 81 years. The selection was based on the following criteria: (1) no clinical signs of arthropathosis, such as crepitations, clicking, or limited condylar translation, (2) no radiographic signs of hard-tissue changes as controlled by corrected serial tomography in lateral and frontal projections, and (3) normal disk position and config-
uration as checked by double-contrast arthrotomography, including injections of iodinated, nonionic contrast medium (Omnipaque, 350 mg iodine per milliliter, Nyegaard & Co A/S, Oslo, Norway) and air into both joint compartments (Fig. 1). The normal disk position and configuration were verified at dissection. The disks were then sagittally sectioned into lateral, central, and medial thirds, still attached to the posterior part of the condyle.5 After position control, the disks with attachments were removed, pinned on to a plastic plate, and immersed in 5% neutral buffered formaldehyde solution. Radiology
In the patients, changes in the bony joint components and condylar translation ability on maximum opening were registered on radiographs taken in the submentovertical projection and in individualized lateral oblique transcranial projection at intercuspida1 position, rest position, and maximum opening. Furthermore, radiologic studies included posteroan-
34 Zsberg et al.
Fig. 3. A, Medial part of biconvex disk (0). Hyperplastic tissue (H) posterior to disk continues as overgrowth (framed) on inferior disk surface. Dotted line indicates borderline between disk and connective tissue overgrowth. (Hematoxylin and eosin stain. Magnification, X 10.) B, Higher magnification of framed area in A, showing disk tissue (D) covered by connective tissue (Cl harboring vessels(V,. (Hematoxylin and eosin stain, Magnification, X80.)
terior projections and corrected serial lateral tomograms. Changes in the soft-tissue components were radiographically interpreted at arthrography. The arthrographic examination included double-contrast arthrotomography,6 permitting visualization of the disk position/configuration and the length and condition of the posterior disk attachment, adhesions, and hyperplastic tissue formation. Perforations were seen at fluoroscopy if the contrast medium injected into the lower joint compartment also made the upper joint compartment opaque. The disk position was classified as normal superior or anteriorly displaced, with or without reduction. The disk configuration was classified as biconcave, biconcave with thickened posterior disk band, biplanar, or biconvex.
reduced the pain only slightly. Three of the patients had previously been given several intra-articular corticosteroid injections (Depo-Medrone, the Upjon Company, Kalamazoo, Mich.) without persistent relief of pain. Physiotherapy was given to three patients, with limited effect on the aching muscles. All five joints were refractory to nonsurgical treatment. Surgical intervention was therefore carried out; this included removal of hyperplastic tissue combined with diskectomy in four joints. Shortening of the disk attachment to achieve surgical repositioning of the disk was performed in one joint. Immediately after extirpation, the disk specimens were pinned onto a plastic plate and immersed in 5% neutral buffered formaldehyde solution.
Treatment
After routine histotechnical procedures, the specimens obtained surgically and by dissection were embedded in paraffin. Five-micrometer sections were taken from the sagittal plane throughout the specimen and stained with hematoxylin and eosin and van Gieson’s stain for tissue identification. Sagittal sections, 15 pm thick, were also taken and
The patients were treated nonsurgically by means of splints in three casesand by careful adjustment of a full denture in one case. The splints and the occlusal surfaces of the denture were made flat and free from interferences. The splints were used 24 hours a day and adjusted weekly. The splint therapy
Tissue
preparation
Volume Number
Hyperplastic
61 I
soft tissue
35
Fig. 4. Dense posterior disk band (0) of control specimen. Posterior disk attachment (A) to right is composedof loose connective tissue. Dotted line indicates border between disk and attachment. (Hematoxylin and eosin stain. Magnification, X10.)
used for the identification modified silver impregnation
of nerve fibers via a
technique.7*8
RESULTS
In four joints the hyperplastic soft tissue was associatedwith disk displacement without reduction. In the fifth joint the position of the disk was normal; that is, the posterior disk band was located above the top of the condyle. This joint, however, had previously demonstrated disk displacement with reduction caused by a blow to the chin. At surgery, erosion of the cartilage was detected in two joints. Radiology
None of the joints in the patients demonstrated any hard-tissue changes. No perforations were detected on contrast injection during fluoroscopic control. In the patients the four displaced disks showed altered disk configuration, three were biconvex, and one was biplanar. The fifth, normally positioned disk was biconcave without any thickening of the posterior disk band. Three of the displaced disks showed grossly elongated posterior disk attachments. Adhesions between the condyle and the posterior disk attachment were present in three joints with disk displacement. Contrast filling of both joint spaces combined with tomography was required to detect the hyperplastic tissue formation. In all cases this tissue was located in the posterior part of the glenoid fossa (Fig. 2). A control joint without hyperplasia is illustrated in Fig. 1.
Fig. 5. Posterior disk attachment of control specimen showing loose connective tissue harboring small arteries (A) and endothelium-lined cavernous structures (Cl. (Hematoxylin and eosin stain. Magnification, X 100.)
Macroscopic
and histologic
examination
Disk. At inspection of the dissected controls, the smooth white stiff tissue of the disk with its welldefined anterior and posterior bands was easily distinguished from its pale red loose attachments. The visual tissue identification was histologically verified. At inspection, the surgically extirpated specimensshowed deformation, verifying the arthrographic findings. In four cases the posterior part of the surgically extirpated specimens was incorrectly visually determined as the disk but was histologically identified as the posterior disk attachment, exhibit-
36
Isberg et al.
6. Posterior disk band (fIj and attached posterior disk attachment/hyperplastic connective tissue (H) of surgical specimen with denser connective tissue than controls. Dotted line indicates borderline between disk and posterior disk attachment/hyperplastic tissue. (Hematoxylin and eosin stain. Magnification, X10.) Fig.
Fig. 7. Hyperplastic connective tissue from surgical specimen, exhibiting vessels with thickened adventitia causing narrowed (Nj or oblititerated (01 lumen. Extravasated erythrocytes (Ej appear in connective tissue. (Hematoxylin and eosin stain. Magnification, X 100.)
Fig. 8. Vessels surrounded by connective tissue with myxomatous degeneration (A4j. Fibrinlike deposits (Fj and extravasated erythrocytes (arrows) appear in hyperplastic connective tissue of surgical specimen. (Hematoxylin and eosin stain. Magnification, X 150.)
ing adaptive changes by means of connective tissue
overgrowth of vascularized loose but organized collagenous tissue (Fig. 3). The disk in both control and patient specimens contained no nerves or vessels.
hyalinization. The disk tissue from both controls and patients was composed of a very dense cell-poor structure, rich in ground substance and containing thick collagenous bundles. The cells of the disk were mainly small and similar to fibroblasts, but rounded cells with a transparent halo, interpreted as chondrocytes, were also present. The inferior surface of the posteromedial part of the surgically extirpated nondisplaced disk had an
Disk attachment and hyperplastic
connective tis-
sue. The posterior disk attachment of the surgically extirpated tissue showed considerable changes compared to the controls. The attachments of the controls were composed of a loose connective tissue harboring nerve bundles and large endothelium-lined cavernous structures, small veins, arteries, and capil-
Volume Number
Hyperplastic
6I I
9. Myelinated and nonmyelinated nerve bundles (large arrow) and small nerve fibers (small arrow) in hyperplastic tissue. (Silver impregnation stain. Magnification, X50.) Fig.
laries. No detectable pathologic changes were observed (Figs. 4 and 5). In contrast, four surgical specimens included a posterior disk attachment with large areas of dense connective tissue that was poor in cells and ground substance (hyalinization) with few, if any, blood vesselsand no nerves. The extirpated nonhyalinized posterior disk attachment and the hyperplastic connective tissue from patients appeared visually as a loose, intensely red, fleshy structure, which displayed similar histopathologic characteristics (Fig. 6). Capillaries, veins, and arteries in the surgical specimens exhibited thickened walls, and the lumina were narrowed and occasionally obliterated (Fig. 7). One specimen showed advanced myxomatous degeneration of the connective tissue circumscribing the vessels(Fig. 8). Four of the five surgical specimenscontained extravasated erythrocytes gathered together. Structureless eosinophilic deposits in the tissue, interpreted as fibrin, were found in all surgical specimens (Fig. 8). In one case there was a local pronounced accumulation of histiocytes. None of the specimens contained inflammatory aggregates. In no case did the controls show thickened blood vessel walls, extravasated erythrocytes, fibrinlike deposits, or histiocytic or inflammatory cell accumulation. The looseconnective tissue of the disk attachments in controls and surgical specimensand the hyperplastic tissue in patients were innervated by myelinated and nonmyelinated silver-positive nerve bundles with diameters ranging from 1 to 60 pm (Fig. 9), mainly associated with the blood vessels. The synovial membrane outlining the disk attachments of the controls appeared morphologically normal (Fig. 10). In contrast, the synovial membrane in
soft tissue
37
Fig. 10. Well-defined synovial membrane (Sj from control specimen. (Hematoxylin and eosin stain. Magnification, X 100.)
Fig. 11. Fibrinoid necrosis of synovial membrane (Sj. Synovial connective tissue (C) is compact and partly structureless. (Hematoxylin and eosin stain. Magnification, X 100.)
three of the surgical specimens was edematous and displayed fibrinoid necrosis (Fig. 11); in the remaining two cases the structure was not even observable. Foreign-body material showing no birefringence or giant cell formation was found in three of the surgical specimens.The controls did not harbor any foreign-body material. DISCUSSION
Hyperplastic connective tissue formation in the posterior part of the TMJ fossawas found to be present in 5% of a group of patients with severeTMJ pain. In the present investigation, the connective tissue hyperplasia in TMJs was related to disk displacement or trauma, in agreement with the findings in autopsy specimens.’ Our investigation indicated that the pain associated with the presence of hyperplastic joint
38
Isberg et al.
tissue was refractory to nonsurgical treatment. In the majority of casespain associated with disk displacement is cured by nonsurgical treatment.9,‘o Only a minority of the patients with TMJ disk displacement are refractory to nonsurgical treatment and must be subjected to surgical intervention. Even though extensive tissue alterations were present within the soft tissues of the joint, none of the corresponding conventional radiographs or tomograms depicted any hard-tissue changes. It should be stressedthat radiographically observable hard-tissue alterations are comparatively late signs of joint disease. The TMJ pain reaction in association with hyperplastic connective tissue could be explained by the presenceof nerve fibers in hyperplastic tissue/posterior disk attachment, which becomescompressedon mouth closure and also herniated on condylar translation. The silver-impregnation technique used in this investigation has been shown in the iris to stain trigeminal sensory nerves exclusively,s leaving substance-p-like fibers and autonomic nerve fibers unstained. It is postulated that substance P nerve fibers are involved in pain transmission,“, ‘* and they have been shown to be present in the TMJ soft tissues.13In addition to compressed nerves, painreleasing breakdown products from extravasated blood may trigger the pain.’ The advanced alterations of the vessels found in both the hyperplastic tissue and posterior attachments are in agreement with observations by Hall and associates,‘4 who studied extirpated posterior disk attachments. Thickened arterial and venous walls, as well as narrow lumina of the vessels, suggest decreased blood flow with secondary ischemia and altered pH, which is another plausible source of pain. The formation of the connective tissue hyperplasia in the TMJ probably originates from a blood clot occurring at the initial disk displacement as a result of laceration of the capsule and disk attachments. The blood clot then becomes organized with ingrowth of fibroblasts and vessels.In mouth closure, the condyle will compress the organizing tissue, causing small amounts of bleeding and organization of new blood clots. Thus, a slow, continuous growth of the tissue may occur. This explanation is supported by the findings of extravasated erythrocytes and fibrin in the tissue, which indicates an ongoing tissue damage, since erythrocytes and fibrin are visible in the tissue for a limited time after injury. All classic signs of inflammation except the presenceof inflammatory cells15were present in the hyperplastic connective tissue and also in the posterior disk attachment.
Oral January,
Surp. I9Xh
The foreign-body material found in some of our surgical specimens must have originated from the injection of corticosteroids or contrast medium. Since no foreign-body reaction was present, this observation has no relevance in explaining the pathologic alteration of the tissue. According to clinical signs and symptoms from TMJs, the presenceof hyperplastic connective tissue could not be discovered. In the diagnosis of hyperplastic soft-tissue formation, arthrotomography with injection of contrast medium into both joint spacesis required. REFERENCES
1. lsberg A, lsacsson G: Tissue reactions
2. 3.
4.
5.
6.
I.
x.
9.
IO
II
12 13
14
15
associated with internal derangement and trauma of the temporomandibular joint: a radiographic, cryomorphological and histological study. Submitted to Acta Odontol Stand, 1985. Farrar WB, McCarty WL Jr: The TMJ dilemma. J Ala Dent Assoc 63: 19-26, 1979. Farrar WB. McCarty WL: Inferior joint space arthrography and characteristics of condylar path in internal derangements of the TMJ. J Prosthet Dent 41: 548-555, 1979. Eriksson L: Diagnosis and surgical treatment of internal derangement of the temporomandibular joint. Swed Dent J Suppl 25: 8-47, 1985. Rohlin M, Westesson P-L, Eriksson L: The correlation of temporomandibular joint sound with joint morphology in hfty-five autopsy specimens. J Oral Maxillofac Surg 43: 194-200, 1985. Westesson P-L: Double-contrast arthrotomography of the temporomandibular joint: introduction of an arthrographic technique for visualization of the disc and articular surfaces. .I Oral Maxillofac Surg 41: 163-172. 1983. Linder JE: A simple and reliable method for the silver impregnation of nerves in paraffin sections of soft and mineralized tissues. J Anat 127: 543-55 I ,, 1978. Ayer Lelievre C. Granholm A-C, Seiger A: Silver impregnation of the intrinsic sensory innervation of rat iris in toto. J Anat 138: 309-22 I, 1984. McCarty WL Jr, Farrar WB: Surgery for internal derangements of the temporomandibular joint. J Prosthet Dent 4t: 191-196, 1979. McNeil1 C: Nonsurgical management. In Helms, CA, Katzberg, RW, Dolwick MF (editors): Internal derangements of the temporomandibular joint. San Francisco 1983, Radiology Research and Education Foundation, p. 193. Henry JL: Relation of substance P to pain transmission: in Substance P in the nervous system (Ciba Foundation Symposium 91). London, 1982, Pitman Medical, pp. 206-224. lversen LL: Substance P. Br Med Bull 38: 227-282, 1982. Johansson A-S, lsacsson G, lsberg A, Granholm A-C: Distribution of substance P-like immunoreactive nerve tibres in the temporomandibular joint soft tissues in monkey. Stand J Dent Res (in press, 1986). Hall MB, Brown RW, Baughman RA: Histologic appearance of the bilaminar zone in the internal derangement of the temporomandibular joint. ORAL SURG ORAL MED ORAL PATHOL 58: 375-38 1, 1984. Robbins SL: Pathologic basis of disease, Philadelphia, 1974. W.B. Saunders Company, pp. 55-105.
Reprint rryuesi.s to: Dr. Annika lsberg School of Dentistry Box 4064 S- I4 I 04 Huddinge.
Sweden
and histologic
study
Annika Isberg, D.D.S., Ph.D.,* Giiran Isacsson, D.D.S.. Ph.D.,** Ann-Sofi Johansson, D.D.S..*** and Ola Larson, D.D.S., M.D., D.iU.S.,*** Stockholm, Sweden KAROLINSKA
INSTITUTET
AND
KAROLINSKA
HOSPITAL
Hyperplastic connective tissue formation in the posterior part of the temporomandibular joint glenoid fossa has previously been described in autopsy specimens. The frequency of such hyperplastic tissue formation in patients with long-standing temporomandibular joint pain was studied in 103 joints from 80 patients by means of double-contrast arthrotomography. Five joints in four patients (5%) demonstrated hyperplastic tissue formation; in four cases this was associated with permanently displaced and deformed disks. All five joints were refractory to nonsurgical treatment. Surgically extirpated hyperplastic tissue and disk attachments contained nerve fibers and thickened adventitia of vessels, resulting in narrowed or obliterated lumina, extravasated erythrocytes, and fibrinlike deposits. The synovial membrane showed fibrinoid necrosis or was lost. The pain reaction in temporomandibular joints with hyperplastic soft-tissue formation may be released by compression or tension of nerves, breaking down products from blood or tissue ischemia. Contrast filling of both joint spaces, combined with tomography, was required for detection of the hyperplastic tissue formation. (ORAL SURC. ORAL MED. ORAL PATHOL. 61:32-38.
1986)
I n an autopsy investigation of temporomandibular joint specimens, Isberg and Isacsson’
(TMJ)
reported on the presence of hyperplastic connective tissue in the posterior part of the glenoid fossa that could be associated with fibrous ankylosis. The condition was related to anterior disk displacement or trauma. The hyperplastic tissue was found to contain extravasated blood, enlarged cavernous structures lacking endothelial lining, and extensive pathologic changes in the arteries and veins. The present investigation was undertaken to study the frequency of hyperplastic connective tissue formation in patients with long-standing TMJ pain and to
This study was supported by grants from the Ragnar and Torsten Siiderbergs Foundations, Stockholm, Sweden, and the Swedish Medical Research Council, Project No. 06877. *Department of Oral Radiology, School of Dentistry, Karolinska Institutet. **Department of Oral Radiology and Department of Stomatognathic Physiology, School of Dentistry, Karolinska Institutet. ***Department of Plastic Surgery, Karolinska Hospital.
32
relate arthrographic findings to morphologic and histologic features. MATERIAL Patients
AND METttODS
Eighty consecutive patients who had been referred to the Department of Oral Radiology with severe pain from one or both TMJs (103 joints in all) were subjected to radiographic examination of the hard as well as the soft tissues of the joint. All patients had suffered severepain for at least 1 year. Five joints in four women, 40, 41, 46, and 67 years of age, demonstrated soft-tissue hyperplasia as described by Isberg and Isacsson.’ These joints were selected for further investigation. The severe joint pain in the patients with hyperplastic soft tissue in the TMJ had lasted for 2 to 5 years (mean, 3.5 years). Pain was constant in four joints and consistent in association with mandibular movements in one joint. Two patients had been unable to work for more than 1 year becauseof the TMJ pain. The remaining two
Hyperplastic
Volume6 I Number 1
soft tissue
33
Fig. 1. Double-contrast arthrotomogram and schematic drawing of TMJ without arthropathosis. Disk is shown in black.
Fig. 2. Double-contrast arthrotomogram and schematic drawing of TMJ with hyperplastic connective tissue (arrow) adherent to condyle. Disk (marked in black) is in a normal superior position.
patients reported that the joint pain caused difficulties with concentration at work or during other activities. All patients said that their lives were severely affected by the chronic pain condition. Four joints in three patients demonstrated significant clinical signs and a case history of disk displacement without reduction,2-4 while one patient had disk displacement with reduction, which clinically became normal over a period prior to radiographic examination. Control material
The control material included four TMJ autopsy specimens from three men and one woman with an age range from 77 to 81 years. The selection was based on the following criteria: (1) no clinical signs of arthropathosis, such as crepitations, clicking, or limited condylar translation, (2) no radiographic signs of hard-tissue changes as controlled by corrected serial tomography in lateral and frontal projections, and (3) normal disk position and config-
uration as checked by double-contrast arthrotomography, including injections of iodinated, nonionic contrast medium (Omnipaque, 350 mg iodine per milliliter, Nyegaard & Co A/S, Oslo, Norway) and air into both joint compartments (Fig. 1). The normal disk position and configuration were verified at dissection. The disks were then sagittally sectioned into lateral, central, and medial thirds, still attached to the posterior part of the condyle.5 After position control, the disks with attachments were removed, pinned on to a plastic plate, and immersed in 5% neutral buffered formaldehyde solution. Radiology
In the patients, changes in the bony joint components and condylar translation ability on maximum opening were registered on radiographs taken in the submentovertical projection and in individualized lateral oblique transcranial projection at intercuspida1 position, rest position, and maximum opening. Furthermore, radiologic studies included posteroan-
34 Zsberg et al.
Fig. 3. A, Medial part of biconvex disk (0). Hyperplastic tissue (H) posterior to disk continues as overgrowth (framed) on inferior disk surface. Dotted line indicates borderline between disk and connective tissue overgrowth. (Hematoxylin and eosin stain. Magnification, X 10.) B, Higher magnification of framed area in A, showing disk tissue (D) covered by connective tissue (Cl harboring vessels(V,. (Hematoxylin and eosin stain, Magnification, X80.)
terior projections and corrected serial lateral tomograms. Changes in the soft-tissue components were radiographically interpreted at arthrography. The arthrographic examination included double-contrast arthrotomography,6 permitting visualization of the disk position/configuration and the length and condition of the posterior disk attachment, adhesions, and hyperplastic tissue formation. Perforations were seen at fluoroscopy if the contrast medium injected into the lower joint compartment also made the upper joint compartment opaque. The disk position was classified as normal superior or anteriorly displaced, with or without reduction. The disk configuration was classified as biconcave, biconcave with thickened posterior disk band, biplanar, or biconvex.
reduced the pain only slightly. Three of the patients had previously been given several intra-articular corticosteroid injections (Depo-Medrone, the Upjon Company, Kalamazoo, Mich.) without persistent relief of pain. Physiotherapy was given to three patients, with limited effect on the aching muscles. All five joints were refractory to nonsurgical treatment. Surgical intervention was therefore carried out; this included removal of hyperplastic tissue combined with diskectomy in four joints. Shortening of the disk attachment to achieve surgical repositioning of the disk was performed in one joint. Immediately after extirpation, the disk specimens were pinned onto a plastic plate and immersed in 5% neutral buffered formaldehyde solution.
Treatment
After routine histotechnical procedures, the specimens obtained surgically and by dissection were embedded in paraffin. Five-micrometer sections were taken from the sagittal plane throughout the specimen and stained with hematoxylin and eosin and van Gieson’s stain for tissue identification. Sagittal sections, 15 pm thick, were also taken and
The patients were treated nonsurgically by means of splints in three casesand by careful adjustment of a full denture in one case. The splints and the occlusal surfaces of the denture were made flat and free from interferences. The splints were used 24 hours a day and adjusted weekly. The splint therapy
Tissue
preparation
Volume Number
Hyperplastic
61 I
soft tissue
35
Fig. 4. Dense posterior disk band (0) of control specimen. Posterior disk attachment (A) to right is composedof loose connective tissue. Dotted line indicates border between disk and attachment. (Hematoxylin and eosin stain. Magnification, X10.)
used for the identification modified silver impregnation
of nerve fibers via a
technique.7*8
RESULTS
In four joints the hyperplastic soft tissue was associatedwith disk displacement without reduction. In the fifth joint the position of the disk was normal; that is, the posterior disk band was located above the top of the condyle. This joint, however, had previously demonstrated disk displacement with reduction caused by a blow to the chin. At surgery, erosion of the cartilage was detected in two joints. Radiology
None of the joints in the patients demonstrated any hard-tissue changes. No perforations were detected on contrast injection during fluoroscopic control. In the patients the four displaced disks showed altered disk configuration, three were biconvex, and one was biplanar. The fifth, normally positioned disk was biconcave without any thickening of the posterior disk band. Three of the displaced disks showed grossly elongated posterior disk attachments. Adhesions between the condyle and the posterior disk attachment were present in three joints with disk displacement. Contrast filling of both joint spaces combined with tomography was required to detect the hyperplastic tissue formation. In all cases this tissue was located in the posterior part of the glenoid fossa (Fig. 2). A control joint without hyperplasia is illustrated in Fig. 1.
Fig. 5. Posterior disk attachment of control specimen showing loose connective tissue harboring small arteries (A) and endothelium-lined cavernous structures (Cl. (Hematoxylin and eosin stain. Magnification, X 100.)
Macroscopic
and histologic
examination
Disk. At inspection of the dissected controls, the smooth white stiff tissue of the disk with its welldefined anterior and posterior bands was easily distinguished from its pale red loose attachments. The visual tissue identification was histologically verified. At inspection, the surgically extirpated specimensshowed deformation, verifying the arthrographic findings. In four cases the posterior part of the surgically extirpated specimens was incorrectly visually determined as the disk but was histologically identified as the posterior disk attachment, exhibit-
36
Isberg et al.
6. Posterior disk band (fIj and attached posterior disk attachment/hyperplastic connective tissue (H) of surgical specimen with denser connective tissue than controls. Dotted line indicates borderline between disk and posterior disk attachment/hyperplastic tissue. (Hematoxylin and eosin stain. Magnification, X10.) Fig.
Fig. 7. Hyperplastic connective tissue from surgical specimen, exhibiting vessels with thickened adventitia causing narrowed (Nj or oblititerated (01 lumen. Extravasated erythrocytes (Ej appear in connective tissue. (Hematoxylin and eosin stain. Magnification, X 100.)
Fig. 8. Vessels surrounded by connective tissue with myxomatous degeneration (A4j. Fibrinlike deposits (Fj and extravasated erythrocytes (arrows) appear in hyperplastic connective tissue of surgical specimen. (Hematoxylin and eosin stain. Magnification, X 150.)
ing adaptive changes by means of connective tissue
overgrowth of vascularized loose but organized collagenous tissue (Fig. 3). The disk in both control and patient specimens contained no nerves or vessels.
hyalinization. The disk tissue from both controls and patients was composed of a very dense cell-poor structure, rich in ground substance and containing thick collagenous bundles. The cells of the disk were mainly small and similar to fibroblasts, but rounded cells with a transparent halo, interpreted as chondrocytes, were also present. The inferior surface of the posteromedial part of the surgically extirpated nondisplaced disk had an
Disk attachment and hyperplastic
connective tis-
sue. The posterior disk attachment of the surgically extirpated tissue showed considerable changes compared to the controls. The attachments of the controls were composed of a loose connective tissue harboring nerve bundles and large endothelium-lined cavernous structures, small veins, arteries, and capil-
Volume Number
Hyperplastic
6I I
9. Myelinated and nonmyelinated nerve bundles (large arrow) and small nerve fibers (small arrow) in hyperplastic tissue. (Silver impregnation stain. Magnification, X50.) Fig.
laries. No detectable pathologic changes were observed (Figs. 4 and 5). In contrast, four surgical specimens included a posterior disk attachment with large areas of dense connective tissue that was poor in cells and ground substance (hyalinization) with few, if any, blood vesselsand no nerves. The extirpated nonhyalinized posterior disk attachment and the hyperplastic connective tissue from patients appeared visually as a loose, intensely red, fleshy structure, which displayed similar histopathologic characteristics (Fig. 6). Capillaries, veins, and arteries in the surgical specimens exhibited thickened walls, and the lumina were narrowed and occasionally obliterated (Fig. 7). One specimen showed advanced myxomatous degeneration of the connective tissue circumscribing the vessels(Fig. 8). Four of the five surgical specimenscontained extravasated erythrocytes gathered together. Structureless eosinophilic deposits in the tissue, interpreted as fibrin, were found in all surgical specimens (Fig. 8). In one case there was a local pronounced accumulation of histiocytes. None of the specimens contained inflammatory aggregates. In no case did the controls show thickened blood vessel walls, extravasated erythrocytes, fibrinlike deposits, or histiocytic or inflammatory cell accumulation. The looseconnective tissue of the disk attachments in controls and surgical specimensand the hyperplastic tissue in patients were innervated by myelinated and nonmyelinated silver-positive nerve bundles with diameters ranging from 1 to 60 pm (Fig. 9), mainly associated with the blood vessels. The synovial membrane outlining the disk attachments of the controls appeared morphologically normal (Fig. 10). In contrast, the synovial membrane in
soft tissue
37
Fig. 10. Well-defined synovial membrane (Sj from control specimen. (Hematoxylin and eosin stain. Magnification, X 100.)
Fig. 11. Fibrinoid necrosis of synovial membrane (Sj. Synovial connective tissue (C) is compact and partly structureless. (Hematoxylin and eosin stain. Magnification, X 100.)
three of the surgical specimens was edematous and displayed fibrinoid necrosis (Fig. 11); in the remaining two cases the structure was not even observable. Foreign-body material showing no birefringence or giant cell formation was found in three of the surgical specimens.The controls did not harbor any foreign-body material. DISCUSSION
Hyperplastic connective tissue formation in the posterior part of the TMJ fossawas found to be present in 5% of a group of patients with severeTMJ pain. In the present investigation, the connective tissue hyperplasia in TMJs was related to disk displacement or trauma, in agreement with the findings in autopsy specimens.’ Our investigation indicated that the pain associated with the presence of hyperplastic joint
38
Isberg et al.
tissue was refractory to nonsurgical treatment. In the majority of casespain associated with disk displacement is cured by nonsurgical treatment.9,‘o Only a minority of the patients with TMJ disk displacement are refractory to nonsurgical treatment and must be subjected to surgical intervention. Even though extensive tissue alterations were present within the soft tissues of the joint, none of the corresponding conventional radiographs or tomograms depicted any hard-tissue changes. It should be stressedthat radiographically observable hard-tissue alterations are comparatively late signs of joint disease. The TMJ pain reaction in association with hyperplastic connective tissue could be explained by the presenceof nerve fibers in hyperplastic tissue/posterior disk attachment, which becomescompressedon mouth closure and also herniated on condylar translation. The silver-impregnation technique used in this investigation has been shown in the iris to stain trigeminal sensory nerves exclusively,s leaving substance-p-like fibers and autonomic nerve fibers unstained. It is postulated that substance P nerve fibers are involved in pain transmission,“, ‘* and they have been shown to be present in the TMJ soft tissues.13In addition to compressed nerves, painreleasing breakdown products from extravasated blood may trigger the pain.’ The advanced alterations of the vessels found in both the hyperplastic tissue and posterior attachments are in agreement with observations by Hall and associates,‘4 who studied extirpated posterior disk attachments. Thickened arterial and venous walls, as well as narrow lumina of the vessels, suggest decreased blood flow with secondary ischemia and altered pH, which is another plausible source of pain. The formation of the connective tissue hyperplasia in the TMJ probably originates from a blood clot occurring at the initial disk displacement as a result of laceration of the capsule and disk attachments. The blood clot then becomes organized with ingrowth of fibroblasts and vessels.In mouth closure, the condyle will compress the organizing tissue, causing small amounts of bleeding and organization of new blood clots. Thus, a slow, continuous growth of the tissue may occur. This explanation is supported by the findings of extravasated erythrocytes and fibrin in the tissue, which indicates an ongoing tissue damage, since erythrocytes and fibrin are visible in the tissue for a limited time after injury. All classic signs of inflammation except the presenceof inflammatory cells15were present in the hyperplastic connective tissue and also in the posterior disk attachment.
Oral January,
Surp. I9Xh
The foreign-body material found in some of our surgical specimens must have originated from the injection of corticosteroids or contrast medium. Since no foreign-body reaction was present, this observation has no relevance in explaining the pathologic alteration of the tissue. According to clinical signs and symptoms from TMJs, the presenceof hyperplastic connective tissue could not be discovered. In the diagnosis of hyperplastic soft-tissue formation, arthrotomography with injection of contrast medium into both joint spacesis required. REFERENCES
1. lsberg A, lsacsson G: Tissue reactions
2. 3.
4.
5.
6.
I.
x.
9.
IO
II
12 13
14
15
associated with internal derangement and trauma of the temporomandibular joint: a radiographic, cryomorphological and histological study. Submitted to Acta Odontol Stand, 1985. Farrar WB, McCarty WL Jr: The TMJ dilemma. J Ala Dent Assoc 63: 19-26, 1979. Farrar WB. McCarty WL: Inferior joint space arthrography and characteristics of condylar path in internal derangements of the TMJ. J Prosthet Dent 41: 548-555, 1979. Eriksson L: Diagnosis and surgical treatment of internal derangement of the temporomandibular joint. Swed Dent J Suppl 25: 8-47, 1985. Rohlin M, Westesson P-L, Eriksson L: The correlation of temporomandibular joint sound with joint morphology in hfty-five autopsy specimens. J Oral Maxillofac Surg 43: 194-200, 1985. Westesson P-L: Double-contrast arthrotomography of the temporomandibular joint: introduction of an arthrographic technique for visualization of the disc and articular surfaces. .I Oral Maxillofac Surg 41: 163-172. 1983. Linder JE: A simple and reliable method for the silver impregnation of nerves in paraffin sections of soft and mineralized tissues. J Anat 127: 543-55 I ,, 1978. Ayer Lelievre C. Granholm A-C, Seiger A: Silver impregnation of the intrinsic sensory innervation of rat iris in toto. J Anat 138: 309-22 I, 1984. McCarty WL Jr, Farrar WB: Surgery for internal derangements of the temporomandibular joint. J Prosthet Dent 4t: 191-196, 1979. McNeil1 C: Nonsurgical management. In Helms, CA, Katzberg, RW, Dolwick MF (editors): Internal derangements of the temporomandibular joint. San Francisco 1983, Radiology Research and Education Foundation, p. 193. Henry JL: Relation of substance P to pain transmission: in Substance P in the nervous system (Ciba Foundation Symposium 91). London, 1982, Pitman Medical, pp. 206-224. lversen LL: Substance P. Br Med Bull 38: 227-282, 1982. Johansson A-S, lsacsson G, lsberg A, Granholm A-C: Distribution of substance P-like immunoreactive nerve tibres in the temporomandibular joint soft tissues in monkey. Stand J Dent Res (in press, 1986). Hall MB, Brown RW, Baughman RA: Histologic appearance of the bilaminar zone in the internal derangement of the temporomandibular joint. ORAL SURG ORAL MED ORAL PATHOL 58: 375-38 1, 1984. Robbins SL: Pathologic basis of disease, Philadelphia, 1974. W.B. Saunders Company, pp. 55-105.
Reprint rryuesi.s to: Dr. Annika lsberg School of Dentistry Box 4064 S- I4 I 04 Huddinge.
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