long-term follow-up of meniscal allograft transplantation

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ABSTRACTS 393 Discussion: This non-thermal welding process pro- duces a covalent bond, that provides a secure stable biological scaffold for primary healing and tissue re- generation in meniscal tears and cartilaginous lesions. Long-Term Follow-Up of Meniscal Allograft Trans- plantation. George T. Stollsteimer and Walter R. Shel- ton. Jackson, Mississippi, U.S.A. Between February of 1991 and August of 1996, a total of 21 patients underwent meniscal transplantation with nonirradiated, cryopreserved allografts. Implanta- tion was arthroscopically assisted using bone plugs to preserve meniscal weight-bearing functional position. Average age was 31 years (range 20-42). Nineteen patients were male, 2 were female. Eleven lateral and 10 medial allografts were implanted. Complications included one hemarthrosis, one failure of bone plug fixation, one infection and 2 cases of synovitis. At an average of 37 months post-allograft, 17 of the 21 pa- tients were rated as successful and 4 as unsuccessful. Two of the 17 successful patients had grade 3/4 articu- lar cartilage damage. Two of the 4 unsuccessful pa- tients had grade 3/4 articular cartilage damage; a third required removal of the allograft due to infection and the fourth had a large tear in the graft on second-look arthroscopy at 14 months post-allograft. There were 8 second look arthroscopies, including 3 chondroplasties and 5 partial meniscectomies. At an average of 46 months post allograft, 2 of the previously successful patients were lost to follow-up. Of the remaining 19 patients, 14 continued to have no or mild pain only; with 8 of the 19 patients experiencing no effusion, 7 patients a minimal effusion and 4 patients experiencing a moderate effusion. Thirteen patients continued to be as active or more active than pre-operative levels. We obtained standing AP x-rays and lateral x-rays at 45 degrees flexion at a minimum of one year follow-up (range, 1-5 years). Sixteen patients had no change and 5 patients evidenced a mild increase in joint narrowing of 1 mm or less when compared to pre-operative films. No patient had moderate or severe increase in joint space narrowing. Magnetic resonance imaging (MRI) was preformed on both knees of ! 3 of the 17 successful patients at an average of 24 months post-allograft. One patient demonstrated l mm peripheral extrusion. Six patients had grade II signals in the meniscal allograft, possibly indicative of an early tear, but no patient had an obvious tear by MRI scan. On average, the allograft meniscus was 63% (range, 31-100%) of the size of the normal meniscus. Clinical results showed improve- ment of pre-operative pain in all 17 successful patients. One patient had a persistent effusion which resolved after a synovectomy at 12 months post-allograft. There was no decrease in range of motion in any patient. While patients continue to have good pain relief fol- lowing their meniscal allograft, the average shrinkage in size of the meniscus on MRI scan is a concern. Arthrofibrosis: A Potential Treatment Based on Growth Factor Manipulation. Mercedes D. yon Deck, John C. Richmond, and Benjamin A. Alman. Newton and Boston, Massachusetts, U.S.A., and To- ronto, Ontario, Canada. Introduction: Arthrofibrosis is a significant compli- cation of anterior cruciate ligament reconstruction and can lead to poor function, limited motion, and repeated surgical procedures. Histologic examination of arthrofibrotic tissue shows hypertrophic scar with fi- broblast proliferation. We hypothesize that arthrofi- brosis is a fibroproliferative disorder in which the growth factors involved in normal wound healing are expressed inappropriately. Blockade of these factors may control cell proliferation and excess collagen ma- trix formation and thus has potential as an adjuvent treatment for arthrofibrosis. Methods: Eight patients underwent excision of arthrofibrotic tissue in the knee. Control samples con- sisted of normal mature scar. Reverse-transcriptase polymerase chain reaction was used to detect mRNA expression of several growth factors implicated in nor- mal tissue repair using specific oligonucleotide primers for these factors. Once specifc growth factors were identified in arthrofibrosis tissue, neutralizing antibod- ies to these growth factors were added to primary cell cultures from arthrofibrosis and controls. The effects of growth factor blockade on cell proliferation were measured using incorporation of the thymidine ana- logue bromo-dioxy-uridine. Collagen gene expression was quantitated by extracting cellular RNA and sub- jecting it to slot-blot hypbridization analysis with Di- goxigenin-labelled collagen type IA oligonucleotide probes. Results: All of the arthrofibrosis specimens ex- pressed PDGF-A, PDGF-B, and IGF-I. None ex- pressed IGF-II or EGF. Three expressed TGF-beta and five expressed bFGF. Mature scar did not express any of the growth factors. Addition of neutralizing antibod- ies for PDGF-A, TGF-beta and IGF-I to culture media led to a significant decrease in proliferation in primary arthrofibrosis cell cultures. These blocking agents also inhibited the expression of collagen type IA by arthro- fibrosis cells. Arthroscopy, Vol 13, No 3, 1997

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ABSTRACTS 393

Discussion: This non-thermal welding process pro- duces a covalent bond, that provides a secure stable biological scaffold for primary healing and tissue re- generation in meniscal tears and cartilaginous lesions.

Long-Term Follow-Up of Meniscal Allograft Trans- plantation. George T. Stollsteimer and Walter R. Shel- ton. Jackson, Mississippi, U.S.A.

Between February of 1991 and August of 1996, a total of 21 patients underwent meniscal transplantation with nonirradiated, cryopreserved allografts. Implanta- tion was arthroscopically assisted using bone plugs to preserve meniscal weight-bearing functional position. Average age was 31 years (range 20-42). Nineteen patients were male, 2 were female. Eleven lateral and 10 medial allografts were implanted. Complications included one hemarthrosis, one failure of bone plug fixation, one infection and 2 cases of synovitis. At an average of 37 months post-allograft, 17 of the 21 pa- tients were rated as successful and 4 as unsuccessful. Two of the 17 successful patients had grade 3/4 articu- lar cartilage damage. Two of the 4 unsuccessful pa- tients had grade 3/4 articular cartilage damage; a third required removal of the allograft due to infection and the fourth had a large tear in the graft on second-look arthroscopy at 14 months post-allograft. There were 8 second look arthroscopies, including 3 chondroplasties and 5 partial meniscectomies. At an average of 46 months post allograft, 2 of the previously successful patients were lost to follow-up. Of the remaining 19 patients, 14 continued to have no or mild pain only; with 8 of the 19 patients experiencing no effusion, 7 patients a minimal effusion and 4 patients experiencing a moderate effusion. Thirteen patients continued to be as active or more active than pre-operative levels. We obtained standing AP x-rays and lateral x-rays at 45 degrees flexion at a minimum of one year follow-up (range, 1-5 years). Sixteen patients had no change and 5 patients evidenced a mild increase in joint narrowing of 1 mm or less when compared to pre-operative films. No patient had moderate or severe increase in joint space narrowing. Magnetic resonance imaging (MRI) was preformed on both knees of ! 3 of the 17 successful patients at an average of 24 months post-allograft. One patient demonstrated l mm peripheral extrusion. Six patients had grade II signals in the meniscal allograft, possibly indicative of an early tear, but no patient had an obvious tear by MRI scan. On average, the allograft meniscus was 63% (range, 31-100%) of the size of the normal meniscus. Clinical results showed improve- ment of pre-operative pain in all 17 successful patients.

One patient had a persistent effusion which resolved after a synovectomy at 12 months post-allograft. There was no decrease in range of motion in any patient. While patients continue to have good pain relief fol- lowing their meniscal allograft, the average shrinkage in size of the meniscus on MRI scan is a concern.

Arthrofibrosis: A Potential Treatment Based on Growth Factor Manipulation. Mercedes D. yon Deck, John C. Richmond, and Benjamin A. Alman. Newton and Boston, Massachusetts, U.S.A., and To- ronto, Ontario, Canada.

Introduction: Arthrofibrosis is a significant compli- cation of anterior cruciate ligament reconstruction and can lead to poor function, limited motion, and repeated surgical procedures. Histologic examination of arthrofibrotic tissue shows hypertrophic scar with fi- broblast proliferation. We hypothesize that arthrofi- brosis is a fibroproliferative disorder in which the growth factors involved in normal wound healing are expressed inappropriately. Blockade of these factors may control cell proliferation and excess collagen ma- trix formation and thus has potential as an adjuvent treatment for arthrofibrosis.

Methods: Eight patients underwent excision of arthrofibrotic tissue in the knee. Control samples con- sisted of normal mature scar. Reverse-transcriptase polymerase chain reaction was used to detect mRNA expression of several growth factors implicated in nor- mal tissue repair using specific oligonucleotide primers for these factors. Once specifc growth factors were identified in arthrofibrosis tissue, neutralizing antibod- ies to these growth factors were added to primary cell cultures from arthrofibrosis and controls. The effects of growth factor blockade on cell proliferation were measured using incorporation of the thymidine ana- logue bromo-dioxy-uridine. Collagen gene expression was quantitated by extracting cellular RNA and sub- jecting it to slot-blot hypbridization analysis with Di- goxigenin-labelled collagen type IA oligonucleotide probes.

Results: All of the arthrofibrosis specimens ex- pressed PDGF-A, PDGF-B, and IGF-I. None ex- pressed IGF-II or EGF. Three expressed TGF-beta and five expressed bFGF. Mature scar did not express any of the growth factors. Addition of neutralizing antibod- ies for PDGF-A, TGF-beta and IGF-I to culture media led to a significant decrease in proliferation in primary arthrofibrosis cell cultures. These blocking agents also inhibited the expression of collagen type IA by arthro- fibrosis cells.

Arthroscopy, Vol 13, No 3, 1997