Morphologic and immunohistochemical observation of explanted Proplast-Teflon temporomandibular joint interpositional implants

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would have to be followed in a nonmechanical situation. Such investigations are in progress.

stress 14.

References 15. 1. Brown WA: Internal derangement of the temporomandibular joint: Review of 214 patients following meniscectomy. Can J Surg 23:30, 1980 2. Markowitz NR, Patterson T, Caputa L: A two-stage procedure for temporomandibular joint disc replacement usingfree pericranial grafts. J Oral Maxillofac Surg 49:476. 1991 3. Eriksson L: Westesson PL: Long-term &aluation of meniscectomy of the temporomandibular joint. J Oral Maxillofac Surg 43:263, 1985 4. Gundlach KKH: Long-term results following surgical treatment of internal derangement of the temporomandibular joint. J Craniomaxillofac Surg 18:206, 1990 5. Ioannides C, Freihofer HPM: Replacement of the damaged interarticular disc of the TMJ. J Craniomaxfac Surg 16:273, 1988 6. Westesson PL, Eriksson L, Lindstrom C: Destructive lesions of the mandibular condyle following discectomy with temporary silicone implant. Oral Surg Oral Med Oral Path01 63:143, 1987 7. Wagner JD, Mosby EL: Assessment of Proplast-Teflon disc replacements. J Oral Maxillofac Surg 48:1140, 1990 8. McBride KL: Clinical behaviour of synthetic meniscus substitutes. Symposium on partial and total TMJ reconstruction, 68th Annual Meeting of the American Association of Oral and Maxillofacial Sturgeons, New Orleans, LA, 1986 (abstr) 9. Wade ML, Gatto D, Florine B: Assessment of Proplast implants in meniscoplasties as temporomandibular joint surgical procedures. 68th Annual Meeting of the American Association of Oral and Maxillofacial Surgeons, New Orleans, LA, 1986 (abstr) 10. Lagrottetia L, Scapino R, Granston AS, et al: Patient with lymphadenopathy following temporomandibular joint arthroplasty with Proplast. J Craniomandib Pratt 4: 172, 1986 11. Trumpy IG, Lyberg T: In vivo deterioration of Proplast-Teflon temporomandibular joint interpositional implants: A scanning electron microscopic and energy-dispersive X-ray analysis. J Oral Maxillofac Surg 51:624, 1993 12. Timmis DP, Aragon SB, van Sickels JE, Aufdemorte TB: Comparative study of alloplastic materials for temporomandibular joint disc replacement in rabbits. J Oral Maxillofac Surg 44:541, 1986 13. Trumpy IG, Lyberg T: Surgical treatment of internal derange-

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ment of the temporomandibular joint: Long-term evaluation of three techniques. J Oral Maxillofac Surg 53:740, 1995 Cordell JL, Falini B, Erber WN, et al: Immunoenzymatic labeling of monoclonal antibodies using immune complexes of alkaline phosphatase and monoclonal anti-alkaline phosphatase (APAAP complexes) .I Histochem Cytochem 32:219, 1984 Feinermann DM, Piecuch JF: Long-term retrospective analysis of twenty-three Proplasp-Teflo# temporomandibular joint interpositional implants. Int J Oral Maxillofac Surg 22:11, 1993 Henry CH, Wolford LM: Treatment outcomes for temporomandibular joint reconstruction after Proplast-Teflon implant failure. .I Oral Maxillofac Surg 51:352, 1993 Chuong R, Piper MA, Bolan TJ: Recurrent giant cell reaction to residual Proplast in the temporomandibular joint. Oral Surg Oral Med Oral Path01 76:16, 1993 Lasser A: The mononuclear phagocytic system: A review. Hum Path01 14:108, 1983 Mundy GR, Altman AJ, Gondek MD, et al: Direct resorption of bone by human monocytes. Science 196:1109, 1977 Kahn AJ, Stewart CC, Teitelbaum SL: Contact-mediated bone resorption by human monocytes in vitro. Science 196:988, 1978 Mundy GR, Varani J, Orr W, et al: Resorbing bone is chemotactic for monocytes. Nature 275:132, 1978 Malone JD, Teitelbaum SL, Griffin GL, et al: Recruitment of osteoclast precursors by purified bone matrix constituents. J Cell Biol 92:227, 1982 Erdohazi M, Newman RL: Aluminum hydroxide granuloma. Br Med J 3:621, 1971 Savage J: Aluminum hydroxide granuloma. Proc R Sot Med 66:984, 1973 Slater DN, Underwood JCE, Durrant TE, et al: Aluminum hydroxide granulomas: Light and electron microscopic studies and X-ray microanalysis. Br J Dermatol 107: 103, 1982 McFadden N, Lyberg T, Hensten-Pettersen A: Aluminum-induced granulomas in a tattoo. J Am Acad Dermatol 20:903, 1989 Epstein WL: Cutaneous granulomas. Int .J Dermatol 16:574, 1977 Bronstein SL: Retained alloplastic temporomandibular joint disk implants: A retrospective study. Oral Surg Oral Med Oral Pathol 64:135, 1987 DeChamplain RW, Gallagher CS, Marshall ET: Autopolymerizing Silastic for interpositional arthroplasty. J Oral Maxillofac Surg 46:522, 1988 Bosanquet AG, Ishimaru JI, Goss AN: The effect of Silastic replacement following discectomy in sheep temporomandibular joints. J Oral Maxillofac Surg 49: 1204, 1991

Surg

uscusslon Morphologic and lmmunohistochemical Observation of Explanted Proplast-Teflon Temporomandibular Joint Interpositional Implants Doran E. Ryan, DOS, MS Donald C. Hofheins, DDS Medical College of Wisconsin, Milwaukee,

WI

The authors of this article are to be commended for their contribution to our understanding of the reaction that occurs around Proplast/Teflon (P/T) interpositional implants (IPI) in the human temporomandibular joint (TMJ). In scientific

investigation seeking to determine the presence or absence of an immune response to an alloplast the clinical relevance lies in answering whether or not a systemic manifestation of illness can occur. Toxicity, autoimmune disease, systemic illness secondary to an immune response, and induction of neoplastic transformation are readily accepted by the publicat-large as answers to any lack of wellness exhibited by patients exposed to implanted alloplastic materials. This is particularly true when the patient has undergone reconstructive surgery with an alloplast that fails its functional requirements and is known to cause a chronic inflammatory reaction and local tissue destruction. Scientific research such as that presented here reaches beyond the superficial appearance of a cause and effect relationship to evidence of con-

RYAN

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firmation or denial of the same. This evidence is ideally obtained from randomized, double-blind, prospective investigation. In the case of implantation of an alloplast this must begin in the setting of a reasonable animal model before proceeding to human-use investigation. For obvious reasons this design cannot be applied to implantation of an established bio-incompatible material in human subjects. Hence, we are left with analysis of data obtained from patients with established exposure to the alloplast in question. As the remaining population of unfortunate patients with P/T TMJ IPIs still in place diminishes, the value of the data that can be obtained from the study of associated tissue increases tremendously. It behooves the oral and maxillofacial surgery community, and particularly TMJ surgeons, to ensure maximum evaluation of the available material. Previous investigators have characterized the response to implanted P/T in the human TMJ.‘.’ The investigation by Trumpy et al attempts to clarify the nature of the tissue reaction to P/T in patients from whom the material was removed. A complex set of variables interact to determine the nature of the reaction elicited by an alloplast undergoing degradation in a functional setting. These include the chemical composition, size, shape, and solubility of the particles; the rate of particulation; and the body’s ability to clear the particles from the region. The interaction between these variables, the inflammatory response, the exact role of specific cytokines, and the relative participation of the humoral and cellular immune responses are not fully understood.4” Elements of the immune system not only include the contributions of the humoral response of I3 lymphocytes and the cellmediated response of T lymphocytes, but also the acute and chronic inflammatory responses, the actions of complement, and the pervasive role of macrophages in each of the above components. The separate elements of immunity are interdependent on one another in terms of initiation, potentiation, and modulation of their role in host immunity through direct interaction and by remote control via secretion of cytokines. For the sake of organization, immunity has been conceptualized as the classic T and B cell responses. In biological function the two are usually operating in tandem. In the cellmediated response, T lymphocytes differentiate and proliferate in response to contact with an antigen and subsequently attack and kill the invading pathogens. The T lymphocyte may encounter the antigen directly or by interaction with a rnacrophage that has phagocytized the pathogen and acts as an antigen-presenting cell. T cells, through secretion of lymphokines, are also important for their role in modulation of both inflammation and the response of B cells. Another component of the cell-mediated response is manifested in the role of natural killer cells. These are a distinct lymphocytic cell line functioning to lyse host cells that exhibit nonself membrane labeling. The B lymphocyte response is classically described as the process by which exposure of these cells results in the production of plasma cells that produce antigen-specific immune globulins that neutralize toxins or opsonize pathogens, facilitating their destruction by phagocytes. Immune globulins also function to activate complement and thereby are instrumental in mediation of inflammation. The authors used an immunohistochemical (IHC) battery designed to exhibit the role of specific elements of the immune response in local tissue exposed to the P/T implants. Comments as to the relative merits of specific IHC markers may best be deferred in light of potential differences in personal preference or availability related to geographic marketing constraints. The IHC markers used showed an absence of B cell participation. Immune globulin assay has been used

69 in our laboratory as a simple mechanism for demonstrating the presence or absence of the production of antibodies by B lymphocytes. Similarly, our results to date have exhibited no participation by B cells. In their conclusions the authors state that no indication of immunologic pathogenesis was shown. This is not entirely consistent with their noted observations or the data presented. While it is true that no evidence of a humoral immune response was shown, the presence of a mild increase in T lymphocytes in the tissue was noted. The authors state that the lymphoid reaction was principally T cell activation. However, the markers used in the study did not have the capability to show T cell activation. Demonstration of the presence or absence of interleukin-2 (IL-2) would provide evidence for or against activation of these T lymphocytes. If the lymphocytes were activated, this would indeed describe an element of the immune response. Identification of specific T helper and suppressor subset populations using CD-4 and CD-S markers would also help to clarify the role of the T lymphocytes in the peri-implant tissue.’ Future investigations should also include immunofluorescence for C3 to show activation of the complement system. The presence of macrophages and multinucleated giant cells in the peri-implant tissue is also consistent with an inflammatory response. Macrophages play an active role in both cellular and humoral immunity, as well as a role in acute and chronic inflammation. The argument may be a semantic one: where does inflammation end and the immune response begin! In reality they are so inter-related that attempts to define boundaries may not be clinically relevant. The authors also state that light microscopy showed fibrosis and massive foreign body giant cell aggregation. They subsequently state that no granulomas were seen. This is somewhat confusing in that the former microscopic description defines a chronic foreign body giant cell granuloma (CFBGCG). The literature pertinent to P/T in the TMJ consistently refers to the well-known local tissue reaction as a CFBGCG formation. It would seem reasonable to accept the term granuloma for use in description of the cellular aggregation found around the P/T IPI with the understanding that it represents an entity distinct from the other classic granuloma subtypes. The authors have described the EDAX/SEM analysis of the same specimens in a previous report. They showed the presence of aluminum in peri-implant soft tissue but no evidence of a specific response to the metal. Comparison of the local reaction between groups with Proplast I and Proplast II implants would control for the presence of aluminum. Future research may show the role of degradation products of P/T implants in initiating macrophage production of cytokines such as IL-l, IL-6, TNF-alpha, and PGE-2, which are known to mediate local resorption of bone and affect connective tissue.7.8 Distinguishing the inflammatory reaction that occurs in response to the particulate breakdown products of the implant from the host responses to the nonfragmented material requires in vivo testing in a nonmechanical stress-bearing situation. The authors state that research showing the effects of P/T implanted in situations without functional loading are pending. In fact, the literature contains reports of such investigations with Proplast and similar polytetrafluoroethylene materials. These demonstrated a local inflammatory response consisting initially of a local accumulation of leukocytes followed by an invasion by monocytes and giant cells. A progressive fibrosis in and around the implanted material followed, with concomitant decrease in inflammatory cell presence.‘.‘”

70 When laboratory analysis provides conclusive evidence for or against a distinct immunologic mechanism at work in the host response to P/T, the clinical significance of this will have to be demonstrated.‘” Even when a model shows the absence of an immune response to an alloplast, the question of the existence or development of a distinct geneticallysusceptible population remains. As in the case of other alloplastic materials, future research needs to investigate the potential for genetic susceptibility to an immunologic reaction to PlT.14

References 1. Ryan DE: Discussion of “Severe cutaneous foreign body giant cell reaction after TMJ reconstruction with Proplast-Teflon.” J Oral Maxillofac Surg 53:722, 1995 2. Valentine JD, Reiman BE, Beuttenmuller EA, et al: Light and electron microscopic evaluation of Proplast II TMJ disc implants. 3 Oral Maxillofac Surg 47:689, 1989 3. Feinerman DM, Piecuch JF: Long-term retrospective analysis of twenty-three Proplast-Teflon temporomandibular joint interpositional implants. Int J Oral Maxillofac Surg 22: 11, 1993 4. Jasty M, Smith E: Wear particles of total joint replacements and their role in periprosthetic osteolysis. Curr Opin Rheumatol 4:204, 1992

DISCUSSION 5. Margevicius KJ, Bauer TW, McMahon JT, et al: Isolation and characterization of debris in membranes around total joint prostheses. J Bone Joint Surg [Am] 76:1664, 1994 6. Rogers SD, Pearcy MJ, Hay SJ, et al: A method for production and characterization of metal prosthesis wear particles. J Orthopaed Res 11:856, 1993 7. Al Saffar N, Revel1 PA: Interleukin-1 production by activated macrophages surrounding loosened orthopaedic implants: A potential role in osteolysis. Br J Rheumatol 33:309, 1994 8. Herman JH, Sowder WG, Hess EV: Nonsteroidal antiinflammatory drug modulation of prosthesis pseudomembrane induced bone resorption. J Rheumatol 21:338, 1994 9. Calnan J: The use of inert plastic material in reconstructive surgery. Br J Plast Surg 16:1, 1963 10. Halstead A, Jones CW, Rawlings RD: A study of the reaction of human tissue to proplast. J Biomed Mat Res 13:121, 1979 11. Arem AJ, Rasmussen D, Madden JW: Soft tissue response to proplast: Quantitation of scar ingrowth. Plast Reconstruct Surg 61:214, 1978 12. Westfal RL, Homsy CA, Kent JN: A comparison of porous composite PTwgraphite and PTFE/alummum oxide- facial implants in primates. J Oral Maxillofac Sure 40:771. 1982 13. Namey TC, Henry CH, Nikaein A, et al: HLA-I? loci associated with connective tissue diseases and TMD. J Oral Maxillofac Surg 52:131, 1994 (suppl 2) (abstr) 14. Sanger JR, McDonald AH: Development of murine models of silicone-induced autoimmunity. Research in progress at Medical College of Wisconsin, Milwaukee, Wisconsin.