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PubMed1998

Wound healing of cartilage structures in the head and neck region.

This study was performed to determine the various processes involved in the behaviour of hyaline cartilage during the wound healing period after trauma or surgery of vulnerable structures like the nasal septal cartilage and the cricoid. The results of different procedures (perpendicular and parallel to the cartilage surface) in young and young-adult animals were analyzed: septal incision at different locations (young-old), cricoid split (young-old), suturing cartilage, closing defects with autologous cartilage (young), biomaterials (young) and newly engineered cartilage in 4- and 24-week-old rabbits (series of ten animals). Cartilage of the young rabbit and child have similar hyaline cartilage with a varying distribution in thickness. Thinner areas are more susceptible to malformations. Incisions through younger cartilage give rise to some new cartilage formation covered by a new layer of perichondrium: through older, differentiated cartilage the incision causes superficial but permanent necrosis. Edges of cut cartilage mostly do heal by formation of fibrous junctions. This forms a weak spot, sensitive to deviations. The same fate goes for the healing between the autologous graft and the surrounding pre-existent cartilage. Trauma parallel to the surface, leads to inconsistent quantity of neocartilage. With ageing the wound healing and regenerative capacities decrease. In general, biomaterials are less accepted by the surrounding tissues and would impede further growth. Only newly engineered, and thus less differentiated (younger) cartilage of hyaline nature, appeared to be well accepted at the interface with the edges of a cartilage defect. There are indications that the release of growth factors might play a role in cartilage wound healing. In the child as well as the adult, wound healing of hyaline cartilage structures is incomplete, and surgery remains 'experimental' surgery. The clinical implications of gradual loss of the regenerative capacity of hyaline cartilage should be further investigated.

Animals↗
PubMed2006

Urinary pentosidine does not predict cartilage loss among subjects with symptomatic knee OA: the BOKS Study.

OBJECTIVE: Age-related changes in articular cartilage are likely to play a role in the etiology of osteoarthritis (OA). One of the major changes in the extracellular matrix of cartilage is the age-related accumulation of advanced glycation end products (AGEs). Pentosidine, an AGE crosslink, is one of the few characterized AGEs and is considered an adequate marker for the many AGEs that are formed in vivo. We used data from a longitudinal observation study to determine if urinary pentosidine could serve as a marker to predict cartilage loss. METHODS: We conducted a prospective analysis of data from the Boston Osteoarthritis of the Knee Study (BOKS); a completed natural history study of knee OA. All subjects in the study met American College of Rheumatology (ACR) criteria for knee OA. Knee magnetic resonance (MR) images were scored for cartilage in 14 plates of the knee using the Whole Organ Magnetic Resonance Imaging Score (WORMS) semiquantitative grading scheme. Within the BOKS population, a nested sample of 127 subjects (39% of the whole sample) who had both baseline pentosidine and longitudinal magnetic resonance imaging (MRI) measurements (MRIs performed at baseline and 30 months later) was assessed. Urinary pentosidine was assayed and normalized to creatinine to account for differences in urine concentrations. We analyzed the data using three different methods to assess if baseline measures of pentosidine predicted subsequent cartilage loss on MRI. These were (1) analysis 1: logistic regression with the outcome cartilage loss in any plate; (2) analysis 2: proportional odds model where the outcome was defined as 0=no cartilage loss, 1=cartilage loss in one plate, 2=cartilage loss in two plates, and 3=cartilage loss in at least three plates; and (3) analysis 3: Poisson regression with the outcome the number of plates with cartilage loss. All analyses were adjusted for age, sex and Body Mass Index (BMI). RESULTS: At baseline the mean (standard deviation) age was 67 (9) years and 54% were male. The results for the three analytic steps are as follows: Analysis 1: the odds ratio for cartilage loss is 1.01 (95% confidence interval (CI) 0.93-1.09) with 1 unit increase in pentosidine. Analysis 2: the odds ratio for more cartilage loss is 0.99 (95% CI 0.92-1.06) with 1 unit increase in pentosidine. Analysis 3: the relative number of plates with cartilage loss decreased was 1.00 (95% CI 0.95-1.03) with a 1 unit increase in pentosidine. CONCLUSION: Urinary pentosidine does not predict knee cartilage loss. Previous studies have suggested that local content within cartilage of AGEs is elevated in persons at high risk for progression. Our data suggest that these changes are not measurable systemically. Alternatively, urinary pentosidine levels reflect cartilage degradation in all joints (thus whole body cartilage breakdown) and may therefore not relate to OA severity in a single knee joint.

Aged↗
PubMed2002

Candidate's thesis: Revision tympanoplasty utilizing fossa triangularis cartilage.

OBJECTIVES/HYPOTHESIS: A small percentage of fascia graft tympanoplasties fail. Cartilage tympanoplasty has a reputation for excellent graft healing but potentially sacrifices maximum hearing improvement and creates difficulty in postoperative follow-up resulting from opacity and immobility. We sought to use a tissue thicker than fascia but thinner than tragal cartilage to repair tympanic membranes that had failed previous fascia grafting. Our hypothesis was that use of the thinner cartilage would maintain the excellent healing rate and resistance to chronic negative pressure while improving hearing and mobility. STUDY DESIGN: The study is a retrospective review of all patients who received a total cartilage graft tympanoplasty after experiencing a failed standard fascia graft tympanoplasty. No previous operative series on impedance testing following cartilage grafting was identified in the literature. Standard audiologic and tympanometric parameters were obtained in all patients. METHODS: Tragal and fossa triangularis cartilage were statistically analyzed for thickness and weight. Surgical indications included patients who had chronic otologic disease that resulted in recurrent tympanic membrane perforation, atelectasis, or cholesteatoma. The tympanic membrane and any posterior canal wall defect were completely replaced with cartilage. Preoperative and postoperative audiometric and impedence tympanometry measurements were compared. RESULTS: Triangularis fossa cartilage is thinner and has less mass than tragal cartilage. Complete data were obtained on 83 of 159 patients to make up this study. The success rate for tympanic membrane integrity measured by tympanometry was 100% at a minimum 2-year follow-up in all ears included in the study. Hearing results are reported collectively and include all types of ossiculoplasty. The largest closure of air-bone gap was at 1000 Hz, followed by 2000, 500, and 4000 Hz. The patient's best hearing level was most frequently at 2000 Hz. Impedence testing showed a large shift in tympanogram configuration from B to C, indicating that cartilage grafts heal with integrity and measurable mobility although stiffened compared with normal. CONCLUSIONS: Fossa triangularis cartilage is thinner and has less mass than tragal cartilage. This creates a relatively mobile neotympanic membrane that can be monitored postoperatively by standard tympanometry, and allows for excellent hearing results. Recurrent tympanic membrane perforation or atelectasis with or without bony canal erosion that has failed standard fascia graft tympanoplasty can be successfully repaired with fossa triangularis cartilage graft tympanoplasty. Primary surgical use of cartilage graft tympanoplasty should be considered in patients with high-risk otologic disease, since fossa triangularis cartilage is thick enough to resist prolonged negative middle ear pressure and the hearing results with fossa triangularis cartilage shield graft tympanoplasty are comparable to those reported with fascia grafting. In patients with type A or C tympanogram results following successful fossa triangularis cartilage grafts, standard impedance testing can be used to clinically evaluate tympanic membrane mobility and help identify the presence of middle ear disease. However primary placement of a tympanostomy tube should be performed in patients with granulation tissue in the middle ear at time of tympanoplasty. Further study is needed to determine the ideal thickness of cartilage for tympanic membrane reconstruction.

Audiometry↗
PubMed2006

Histological analysis of human diced cartilage grafts.

BACKGROUND: Grafting the radix and dorsum of the nose has been controversial and the plastic surgery community has recently revisited diced cartilage grafts. Previous articles by the authors reported clinical failures of diced cartilage-Surgicel-wrapped grafts and the successful implementation of diced cartilage-fascia-wrapped grafts for rhinoplasty procedures. This article investigates four means of radix and dorsum augmentation, including banked and fresh septum. METHODS: Twenty-seven human specimens were taken from rhinoplasty patients: six failed diced cartilage-Surgicel-wrapped grafts, eight diced cartilage-fascia-wrapped grafts, and 13 specimens of fresh cartilage or previously placed cartilage grafts. All were stained with hematoxylin and eosin, Masson's trichrome, safranin-O, glial fibrillary acidic protein, and Evans' van Gieson stains and analyzed for chondrocyte viability, matrix proteins, and regenerative potential of the cartilage. RESULTS: The diced cartilage-Surgicel-wrapped grafts showed disorganized fibrosis, loss of nuclei in chondrocyte lacunae, and negative glial fibrillary acidic protein staining. All specimens contained remnants of Surgicel and evidence of foreign body reaction. The diced cartilage-fascia-wrapped grafts showed normal histologic characteristics, healthy cartilage pieces with viable chondrocytes in their lacunae, positive glial fibrillary acidic protein staining, and organized capsule of fibrosis surrounding the cartilage pieces. The fascia was viable and showed an organized architecture distinctly different from the disorganized scar tissue of the diced cartilage-Surgicel-wrapped grafts. CONCLUSIONS: Given the histologic findings, diced cartilage-Surgicel-wrapped grafts absorbed due to foreign body reaction. Diced cartilage-fascia wrapped grafts survived and demonstrated normal cartilage viability. According to the clinical performance and analysis of these grafts, diced cartilage-fascia is the most reliable way to augment the nasal dorsum and radix with autologous diced cartilage.

Cartilage↗
PubMed1994

Characterisation of articular and growth plate cartilage collagens in porcine osteochondrosis.

The articular and growth plate cartilages of osteochondrotic pigs were examined and compared with those from clinically normal animals. Both types of osteochondrotic cartilage showed considerable localised thickening apparently due to a lack of ossification. Histological examination of cartilage lesions demonstrated a breakdown in the normal pattern of chondrocyte maturation. Articular cartilage lesions lacked mature clones of chondrocytes in the calcifying region. Growth plate cartilage showed an accumulation of disorganised hypertrophic chondrocytes rather than the well-defined columns seen in normal tissue. The overall percentages of collagen in osteochondrotic lesions from both articular and growth plate cartilage were significantly reduced compared with levels in unaffected cartilage. There were substantial increases in the proportion of type I collagen in lesions from both osteochondrotic articular and growth plate cartilages and a reduction in the proportion of type II collagen. Type X collagen was detected in osteochondrotic but not normal articular cartilage. The proportion of type X collagen was unchanged in osteochondrotic growth plate cartilage. The levels of the collagen cross-links, hydroxylysylpyridinoline, hydroxylysyl-ketonorleucine and dehydrohydroxylysinonorleucine were radically reduced in samples from osteochondrotic growth-plate cartilage lesions when compared with normal tissue. Less dramatic changes were observed in articular cartilage although there was a significant decrease in the level of hydroxylysylketonorleucine in osteochondrotic lesions. Immunofluorescence examination of osteochondrotic lesions showed a considerable disruption of the organisation of the collagenous components within both articular and growth-plate cartilages. Normal patterns of staining of types I and VI collagen seen at the articular surface in unaffected tissue were replaced by a disorganised, uneven stain in osteochondrotic articular cartilage lesions. Incomplete removal of cartilage at the ossification front of osteochondrotic growth plate was demonstrated by immunofluorescence staining of type IX collagen. Type X collagen was produced in the matrix of the calcifying region of osteochondrotic articular cartilage by small groups of hypertrophic chondrocytes, but was not detected in normal articular cartilage. The distribution of type X collagen was unchanged in osteochondrotic growth plate cartilage.

Animals↗
PubMed2001

Immunolocalization of matrix metalloproteinases in partial-thickness defects in pig articular cartilage. A preliminary report.

BACKGROUND: Partial-thickness defects in mature articular cartilage do not heal spontaneously. Attempts at repair often result in limited integration between the repair tissue and the surrounding cartilage, with formation of chondrocyte clusters adjacent to a zone of cartilage necrosis. In wound repair, spatially and temporally controlled expression of matrix metalloproteinases and their inhibitors have been implicated in proteolytic degradation of damaged extracellular matrix components, but the sequence of events following damage to cartilage is unknown. To determine this sequence, we studied the distribution of matrix metalloproteinases and their inhibitors during early in vivo repair of partial-thickness defects in pig articular cartilage. METHODS: With use of a model that elicits the ingrowth of mesenchymal cells into partial-thickness defects, partial-thickness defects were created in knee joint cartilage. The distributions of matrix metalloproteinase-1, 2, 3, 9, 13, and 14; tissue inhibitors of metalloproteinase-1 and 2; and the neoepitope DIPEN341 specifically generated following matrix metalloproteinase cleavage of aggrecan were determined by immunolocalization of repair tissue and surrounding cartilage excised from immature pigs during the first eight weeks of repair and from adult minipigs at eight days and three weeks. RESULTS: Synthesis of matrix metalloproteinase-13 was usually confined to hypertrophic chondrocytes in immature cartilage and to the radial zone in adult cartilage. Following injury, strong induction of matrix metalloproteinase-13 synthesis was observed in chondrocyte clusters surrounding lesions in all of the animals. The migration of macrophages into defects was prominent at two and eight days, with synthesis and deposition of matrix metalloproteinase-9 onto damaged cartilage matrix and newly synthesized matrix in the defect. The DIPEN341 neoepitope was localized to damaged cartilage matrix at eight days and six weeks, indicating partial degradation of aggrecan. Focal synthesis of matrix metalloproteinase-1, 3, and 14 and of tissue inhibitor of metalloproteinase-1 occurred at later times, suggesting continuous remodeling of the increasingly compact repair tissue. CONCLUSIONS: The expression of matrix metalloproteinase-13 by normal hypertrophic chondrocytes and the induction of synthesis in chondrocyte clusters adjacent to the zone of cartilage necrosis suggest that this enzyme participates in the pericellular proteolysis required for lacunar expansion. The localization of matrix metalloproteinase-9 to damaged cartilage matrix suggested matrix proteolysis, which was confirmed with DIPEN341 localization. Reduced matrix metachromasia persisted and was colocalized with DIPEN341 at six weeks. However, under the conditions investigated, there was only limited proteolytic degradation in the zone of cartilage necrosis. This may render the zone mechanically weakened, thereby contributing to subsequent instability of the region, and may form a barrier to integration of repair tissue with viable cartilage. CLINICAL RELEVANCE: Osteoarthritis initially involves the superficial layers of cartilage. The development of procedures to promote the healing or repair of early defects will have major advantages in terms of disease alleviation as well as economic importance. Identification of the enzymes involved in the early repair of partial-thickness defects in articular cartilage is clinically relevant because proteolysis of damaged matrix has to take place in order for repair tissue to integrate with surrounding healthy cartilage.

Aggrecans↗
PubMed1999

Expression of matrix metalloproteinases in normal and damaged articular cartilage from human knee and ankle joints.

The objectives of this study were the following: (a) describe the appearance of histopathologic changes observed in human articular cartilage from the knee and ankle joints of organ donors with no symptomatic joint disease; (b) compare by in situ hybridization mRNA expression of six matrix metalloproteinases (MMP) in these cartilages; (c) compare MMP mRNA expression with the histology of the cartilage; and (d) test whether the effect of interleukin-1beta (IL-1beta) on the MMP mRNA expression could be detected with in situ hybridization. Human articular cartilages from the knee (tibiofemoral) and ankle (talocrural) joints of 41 different donors (aged 18 to 84 years) were obtained through the Regional Organ Bank of Illinois. The microscopic appearance of the cartilages was graded on a histopathologic scale from 0 to 13 with the highest grade representing severely damaged cartilage. In situ hybridization was performed using oligonucleotide probes to three collagenases (MMP-1, MMP-8, MMP-13), gelatinase A (MMP-2), stromelysin (MMP-3), and matrix type-1 metalloproteinase (MMP-14). Cartilages from some donors were cultured with IL-1beta and then analyzed for MMP expression using in situ hybridization. The histopathology grades of the cartilages from the asymptomatic donors covered the entire scale even in the ankle. Based on their grades, the cartilages were described as either normal (grades 0 to 5) or damaged (grades 6 to 13). The cartilages contained message for all six MMP tested with no detectable differences in expression of MMP-1, -2, -13, and -14 between the normal and damaged cartilages. However the expression of MMP-3 and MMP-8 was elevated in the damaged cartilages. In normal knee cartilage, mRNA expression of MMP-3 and MMP-8 was low, whereas in normal ankle cartilage, MMP-8 expression was below the detection limit. MMP-3 and MMP-8 message was up-regulated in the damaged cartilage from both joints, or if the tissue was cultured in the presence of IL-1beta. From this study we conclude the following: (a) similar histopathologic changes occur in both knee and ankle cartilages; (b) MMP-1, -2, -13, and -14 are constitutively expressed in adult human cartilage; and (c) only up-regulation of mRNA expression of MMP-3 and MMP-8 could be detected with naturally occurring cartilage damage and IL-1beta induction.

Adolescent↗
PubMed1995

Experimental assessment by high frequency ultrasound of articular cartilage thickness and osteoarthritic changes.

OBJECTIVE: Osteoarthritis (OA) is characterized by progressive loss of articular cartilage in the involved joint. Accurate, reproducible measurement of the thickness of the cartilage in vivo, however, is difficult. Because development of an ultrasonic imaging device for intraarticular use is feasible and would permit acquisition of information that could complement the assessment of articular cartilage made at arthroscopy, we evaluated the efficacy of high frequency ultrasound in assessing the thickness and subsurface characteristics of normal and OA cartilage. METHODS: Blocks of human femoral cartilage and subchondral bone and chips of cartilage alone were examined in vitro with an experimental 25 MHz pulse-echo ultrasound scanner that portrayed cross sections of the cartilage as B-mode images. The gross and histologic appearance of the articular surface was used to identify specimens of unblemished, normal cartilage and OA cartilage. The speed of sound in cartilage, determined from measurements of cartilage thickness and sound transmission, was related to its biochemical composition. RESULTS: The speed of sound in normal cartilage (1658 +/- 185 m/s, n = 27) was greater than that in OA cartilage (1581 +/- 148 m/s, n = 40, p = 0.06), but was not related to the cartilage water content or the concentration of uronic acid or hydroxyproline. Images of normal cartilage showed a smooth echo band at the tissue surface with a hypoechoic matrix; in scans of fibrillated cartilage the width of this band was proportional to the depth of fibrillation (r = 0.78). Ultrasonic and histologic measurements of OA cartilage thickness were closely correlated (r = 0.87) and the mean coefficient of variation for repeated measurements was 2%. CONCLUSION: High frequency ultrasonic images obtained in vitro provide highly accurate and reproducible measurements of the thickness and subsurface characteristics of normal and OA articular cartilage.

Arthroscopy↗
PubMed1998

Expression of proteoglycan epitopes in articular cartilage repair tissue.

To determine if expression of specific proteoglycan epitopes distinguishes articular cartilage repair tissue from normal articular cartilage, we used seven monoclonal antibodies to examine normal articular cartilage and cartilage repair tissue from osteochondral defects 3.2 mm in diameter and 4.0 mm deep in the medial femoral condyles of 27 New Zealand white rabbits and seven cynomolgus monkeys. Following creation of the osteochondral defects, one limb of each animal was treated with cast immobilization while the other limb was treated with passive motion for two weeks. Rabbit knees were examined at eight (13 animals, 26 knees) and 36 weeks (14 animals, 28 knees) and monkey knees at eight weeks (seven animals, 14 knees) following surgery. Staining for six of the antibodies did not differ between repair cartilage and normal articular cartilage, but an antibody that recognizes atypical glycosaminoglycan structures in developing tissues (MAb 7D4) consistently distinguished repair cartilage from normal cartilage in rabbits and monkeys. Repair tissue consisting of hyaline toluidine blue-staining matrix containing chondrocytic cells uniformly showed strong 7D4 staining. In contrast, normal articular cartilage and fibrous repair tissue showed inconsistent weak 7D4 staining. At eight weeks following surgery, rabbit cartilage repair tissue stained more intensely for 7D4 than monkey cartilage repair tissue; in rabbits, cartilage repair tissue stained more intensely for 7D4 at eight weeks than at 36 weeks following surgery. Repair tissue staining for 7D4 did not differ between osteochondral defects treated with passive motion and those treated with immobilization in rabbits and monkeys. These results indicate that expression of a high level of proteoglycan epitope 7D4 distinguishes hyaline articular cartilage repair tissue from normal articular cartilage and fibrous cartilage repair tissue in the early stages of osteochondral healing, and that as hyaline articular cartilage repair tissue matures expression of 7D4 decreases. The ability to characterize repair cartilage proteoglycans with monoclonal antibodies may aid in the evaluation of the quality and maturity of cartilage repair tissue and thereby facilitate improvements in procedures for resurfacing joints.

Animals↗
PubMed1993

Characteristics of anti-type II collagen antibody binding to articular cartilage.

OBJECTIVE: Previous studies suggested that it was possible to characterize the intact surface of articular cartilage by probing it with antibodies against matrix macromolecules. The present studies were undertaken to investigate type II collagen (CII) epitope availability on the intact surface of articular cartilage. METHODS: Normal bovine, rabbit, and human cartilage specimens were used to measure binding of anti-CII antibodies to the articular and cut surfaces of cartilage. Antisera were raised against the material obtained after brief extraction of the cartilage surface with 4M guanidine solution. RESULTS: Anti-CII did not bind to the intact surface of rabbit articular cartilage when compared with control rat sera, but did bind significantly to the cut surface. With normal human articular cartilage, the cut surfaces bound approximately 4 times as much anti-CII antibody as the intact articular surfaces. These findings suggested that the CII epitopes are normally protected by the superficial cartilage layer. In experiments carried out to characterize this layer, binding of anti-CII antibodies was unchanged after exhaustive washing of bovine or rabbit cartilage with phosphate buffered saline or 1M NaCl solution, whereas it was significantly increased after brief exposure to 4M guanidine solution or after incubation with neutrophil elastase. No restoration of the protection of CII epitopes in guanidine-treated cartilage could be achieved by incubation with undiluted normal bovine synovial fluid; however, 8-day culture of elastase-treated cartilage explants resulted in partial restoration of protection of the CII epitopes. Rat and rabbit antisera raised against the cartilage surface material extracted with 4M guanidine contained antibodies that bound to the cartilage surface. By Western blotting, rat antibodies identified 50-65-kd protein bands present in the guanidine extract, but not present either in the material obtained from brief digestion of cartilage with neutrophil elastase or in synovial fluid. The rabbit antisera identified a broad 70-95-kd band. Exposure of elastase-treated cartilage to the guanidine-extracted material resulted in a partial decrease of anti-CII antibody binding. CONCLUSION: These results suggest that CII on intact cartilage is protected from antibody binding, and that the protective material is at least partly proteinaceous in nature, is unlikely to be derived from synovial fluid, is noncovalently bound to the underlying intercellular matrix, and is synthesized by resident chondrocytes. Further characterization of the protective material may provide important information on the mechanisms of early cartilage damage in inflammatory arthritis.

Animals↗
PubMed2001

Establishment and characterization of chondrocyte cell lines from the costal cartilage of SV40 large T antigen transgenic mice.

Complete understanding of the physiology and pathology of the cartilage is essential to establish treatments for a variety of cartilage disorders and defects such as rheumatoid arthritis, congenital malformations, and tumors of cartilage. Although synthetic materials have been used in many cases, they possess inherent problems including wear of the materials and low mechanical strength. Autograft has been considered very effective to overcome these problems. However, the limitation of the transplant volume is a major problem in autograft to be overcome. The costal cartilage is the most serious candidate for donor site transplantation, since it is the largest permanent hyaline cartilage in the body. To investigate the possibility using the costal cartilage as a transplant source, we have established and characterized three mouse chondrocyte cell lines (MCC-2, MCC-5, and MCC-35) derived from the costal cartilage of 8-week-old male SV40 large T-antigen transgenic mice. At confluence, all the cell lines formed nodules that could be positively stained with alcian blue (pH 2.5). The size of nodules gradually increased during culturing time. After 2 and 6 weeks of culture, RT-PCR analysis demonstrated that all three cell lines expressed mRNA from the cartilage-specific genes for type II collagen, type XI collagen, aggrecan, and link protein. Furthermore, type X collagen expression was detected in MCC-5 and MCC-35 but not in MCC-2. Any phenotypic changes were not observed over 31 cell divisions. Immunocytochemistry showed further that MCC-2, MCC-5, and MCC-35 produced cartilage-specific proteins type II collagen and type XI collagen, while in addition MCC-5 and MCC-35 produced type X collagen. Treatment with 1alpha, 25-dihydroxyvitamin D(3) inhibited cell proliferation and differentiation of the three cell lines in a dose-dependent manner. These phenotypic characteristics have been found consistent with chondrocyte cell lines established from cartilage tissues other than costal cartilage. In conclusion, costal cartilage shows phenotypic similarities to other cartilages, i.e., articular cartilage and embryonic limbs, suggesting that costal cartilage may be very useful as the donor transplantation site for the treatment of cartilage disorders. Furthermore, the cell lines established in this study are also beneficial in basic research of cartilage physiology and pathology.

Alkaline Phosphatase↗
PubMed2006

Survival of diced cartilage grafts: an experimental study.

BACKGROUND: Use of diced cartilage grafts in rhinoplasty surgery has recently undergone a dramatic resurgence. Some authors recommend wrapping diced cartilage with oxidized methylcellulose (i.e., Surgicel). Others prefer wrapping diced cartilage with autogenous deep temporal fascia. This study was designed to compare the behavior of diced cartilage grafts as an isolated entity or when wrapped with either Surgicel or deep temporal fascia. METHODS: Septal cartilage and deep temporal fascia were obtained from five patients in this institutional review board-approved study. The cartilage was diced into 0.5-mm pieces and implanted into subcutaneous dorsal skin pockets of Rowlett nude rats as isolated diced cartilage grafts, or wrapped in Surgicel or deep temporal fascia. Pieces of Surgicel and fascia were implanted alone as controls. The specimens were harvested at 8 weeks; processed by thin-section histology; stained with hematoxylin and eosin, Masson's trichrome, glial fibrillary acidic protein, safranin-O, and Evans van Gieson; and evaluated to determine cartilage viability and architectural characteristics. RESULTS: Diced cartilage wrapped in Surgicel yielded the lowest percentage viability and minimal staining with hematoxylin and eosin, trichrome tissue, safranin-O, and Evans van Gieson stains. Diced cartilage grafts wrapped in fascia had the greatest percentage of viable cartilage. The grafts wrapped in deep temporal fascia also demonstrated the strongest staining with the aforementioned stains. Differences in uptake of glial fibrillary acidic protein were not noticeable between the three groups. However, absolute numbers of nucleated lacunae and basophilic lacunae were significantly higher for grafts wrapped in deep temporal fascia. CONCLUSIONS: Diced cartilage grafts have reemerged as a viable method for nasal reconstruction in both primary and secondary rhinoplasty. Wrapping diced cartilage specimens contains the individual pieces and facilitates graft placement. Surgicel wraps appear to incite an inflammatory response and subsequent absorption of the cartilage. Fascia wraps appear to minimize inflammatory responses to the cartilage, thereby preserving healthy cartilage. This study demonstrates that deep temporal fascia is the preferred envelope with which to facilitate graft containment and maintain chondrocyte viability of diced cartilage grafts.

Animals↗
PubMed2002

Immunochemical and mechanical characterization of cartilage subtypes in rabbit.

Cartilage is categorized into three general subgroups, hyaline, elastic, and fibrocartilage, based primarily on morphologic criteria and secondarily on collagen (Types I and II) and elastin content. To more precisely define the different cartilage subtypes, rabbit cartilage isolated from joint, nose, auricle, epiglottis, and meniscus was characterized by immunohistochemical (IHC) localization of elastin and of collagen Types I, II, V, VI, and X, by biochemical analysis of total glycosaminoglycan (GAG) content, and by biomechanical indentation assay. Toluidine blue staining and safranin-O staining were used for morphological assessment of the cartilage subtypes. IHC staining of the cartilage samples showed a characteristic pattern of staining for the collagen antibodies that varied in both location and intensity. Auricular cartilage is discriminated from other subtypes by interterritorial elastin staining and no staining for Type VI collagen. Epiglottal cartilage is characterized by positive elastin staining and intense staining for Type VI collagen. The unique pattern for nasal cartilage is intense staining for Type V collagen and collagen X, whereas articular cartilage is negative for elastin (interterritorially) and only weakly positive for collagen Types V and VI. Meniscal cartilage shows the greatest intensity of staining for Type I collagen, weak staining for collagens V and VI, and no staining with antibody to collagen Type X. Matching cartilage samples were categorized by total GAG content, which showed increasing total GAG content from elastic cartilage (auricle, epiglottis) to fibrocartilage (meniscus) to hyaline cartilage (nose, knee joint). Analysis of aggregate modulus showed nasal and auricular cartilage to have the greatest stiffness, epiglottal and meniscal tissue the lowest, and articular cartilage intermediate. This study illustrates the differences and identifies unique characteristics of the different cartilage subtypes in rabbits. The results provide a baseline of data for generating and evaluating engineered repair cartilage tissue synthesized in vitro or for post-implantation analysis.

Animals↗
PubMed1987

Articular cartilage blood vessels in swine osteochondrosis.

Perfusion studies in swine with early lesions of osteochondrosis demonstrated that lamellar areas of chondrocyte necrosis within reserve zones of growth areas occurred only in regions of nonperfused articular cartilage. Articular cartilage with a similar anatomical location was perfused in some animals. Occasionally, nonperfused articular cartilage showed vascular alterations within cartilage canals without evidence of significant perivascular or lamellar necrosis. By light microscopy, some vessels within or adjacent to nonperfused articular cartilage had normal morphology; however, ultrastructural abnormalities were found in some vessels of all cartilage canals adjacent to necrotic cartilage lamella. Minimal alterations were in the few cartilage canal vessels that appeared normal by light microscopy, and the surrounding chondrocytes showed only minimal alterations. Early cartilage canal alterations were seen in the endothelium of cartilage canal capillaries, and ultrastructural changes in these vessels were similar to those described with experimentally induced, direct vascular injury. Vascular injury was followed by leakage of plasma and cells into the interstitial space of the cartilage canal. Necrosis of the vessel wall and interstitial tissue caused the cartilage canals to appear empty or to be filled with fibrin-like material. Although the vascular changes could be considered as part of the normal process of cartilage maturation and cartilage canal chondrification, observations suggest that in domestic swine the attendant cartilage necrosis and chondrolysis is exuberant. It is suggested that alterations in cartilage canal vessels play a major role in the pathogenesis of articular cartilage lesions that are found in osteochondrosis of swine.

Animals↗
PubMed1995

Quantification of the volume of articular cartilage in the metacarpophalangeal joints of the hand: accuracy and precision of three-dimensional MR imaging.

OBJECTIVE: Cartilage loss is central to the development of joint failure in arthritis. However, radiographic assessment of cartilage loss is highly unreliable. This study examined the accuracy and reproducibility of a noninvasive technique for quantifying the volume of articular cartilage in the metacarpophalangeal joints of the hand by use of three-dimensional (3D) MR imaging. SUBJECTS AND METHODS: Eight metacarpophalangeal joints (four normal, one rheumatoid arthritic, and three normal cadaveric) each were imaged three times with a 1.5-T clinical MR imaging scanner with a small partial volume coil and a fat-saturated 3D spoiled gradient-echo sequence optimized for delineating articular cartilage. The volumes of cartilage over the metacarpal and phalangeal surfaces were quantified by summing the voxels within segmented 3D reconstructions of the images. Cartilage volumes in the three cadaver joints also were estimated by scraping cartilage off the articular surfaces and measuring water displacement in graduated cylinders. These values were used as the gold standard for assessing the accuracy of cartilage volume quantification by MR imaging. RESULTS: The fat-saturated sequence discriminated the articular cartilage from adjacent joint structures with high contrast and high spatial resolution. Cartilage volumes determined by MR imaging for the different subjects ranged from 115 microliters to 222 microliters for metacarpal cartilage and from 34 microliters to 86 microliters for proximal phalangeal cartilage. Accuracy errors for quantifying cartilage volume by MR imaging were -1.8% (95% confidence interval, -3.5% to -0.7%) for metacarpal cartilage and 9.1% (4.3% to 14.7%) for proximal phalangeal cartilage. Reproducibility errors were 5.2% (95% confidence interval, 2.9% to 7.6%) and 9.9% (5.4% to 15.1%), respectively. CONCLUSION: Fat-suppressed T1-weighted 3D MR imaging provides sufficient contrast and spatial resolution to allow accurate and reproducible quantification of articular cartilage volume in the metacarpophalangeal joints of the hand. This technique may be useful for monitoring cartilage loss in patients with arthritis.

Adult↗
PubMed2003

[Allograft antigenicity of human ear cartilage and effect of cell extraction on antigenicity].

OBJECTIVE: To study the allograft antigenicity of human ear cartilage and the effect of the cell extraction on antigenicity. METHODS: The human ear cartilage was acellular by cell extraction with Triton X-100. Then the cartilage and the acellular cartilage were analyzed by anti-MHC-I immunohistochemical staining, the reaction of the peripheral blood mononuclear(PBM) cells to the cartilage and the acellular cartilage and the migration of the PBM cells toward the cartilage and the acellular cartilage. RESULTS: The result of human ear cartilage was positive for the anti-MHC-I immunohistochemical staining, whereas that of the acellular cartilage was negative for the staining. The reactive proliferation of the PBM cells was more when they were co-cultured with human ear cartilage than that when they were cultured alone in vitro(P < 0.05), but the acellular cartilage did not show the same phenomena (P > 0.05); when the cartilage and the acellular cartilage were co-cultured with the PBM cells, the PBM cells migrated to the cartilage much more than that to acellular cartilage(P < 0.01). CONCLUSION: Human ear cartilage has allograft antigenicity and its antigenicity can be removed by cell extraction with Triton X-100.

Cell Separation↗
PubMed1994

[Involvement in morphological changes of the articular cartilage of rat temporomandibular joint induced by experimental malocclusion].

The effect of malocclusion induced by increase in unilateral occlusal vertical dimension on the articular cartilage of rat mandibular condyle was histologically and immunohistologically examined. WKA rats (8 weeks) were divided into three group A: untreated (control) rats, group B: rats forced to mouth open just for 20 min, and group C: rats given malocclusion by putting the 1 mm diameter wire on the right upper molar continuously. After treatment, each rat was sacrificed periodically up to 9 weeks, and the morphological changes of condylar cartilage (articular, embryonic and transitional zones of cartilage layer) were histologically investigated. The thickness of articular cartilage in all groups was decreased in a time-dependent manner (up to 9 weeks after treatment). In group C rats, whose articular cartilage was thinnest in three groups, the reduced thickness of cartilage in the non-treated side (the left side) was same as that in the treated side which was presented with excessive molar contact. But, its occurrence in the treated side was seen 2 weeks earlier than that in the non-treated side. Even in group B rats which were only forced to open the mouth for 20 min without setting of permanent malocclusion, the thickness of condylar cartilage was decreased more than that of group A rats. When the condylar cartilages of all three groups were immunohistologically examined with anti-interleukin-1 (IL-1) antibody in order to investigate the pathophysiological involvement of IL-1, which is well-known catabolic factor to cartilage, some chondrocytes in articular cartilage were positively stained. The ratio of IL-1 positive cells increased time-dependently. IL-1-producing cells in group B and the non-treated side of group C reached to the maximal ratio at the same time when the condylar cartilage markedly decreased in thickness. However, the ratio of IL-1-positive chondrocytes in the treated side of group C was maximal four weeks after the decrease of cartilage thickness. In respect with the size of cells in cartilage, the occurrence of decreased thickness in condylar cartilage corresponded to that of the reduction of cellular size, especially in the embryonic zone of group C. These results described above suggest that malocclusion, unilateral immature occlusion, can induce the thinning of condylar cartilage which may result from the reducing size of articular chondrocytes (differentiated chondrocytes) and the accompanying decreased cartilage matrix. This change of cartilage may be caused by IL -1 that articular chondrocyte seemed to produce.(ABSTRACT TRUNCATED AT 400 WORDS)

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PubMed1997

Transforming growth factor-beta predominantly stimulates phenotypically changed chondrocytes in osteoarthritic human cartilage.

OBJECTIVE: One of the most prominent alterations that characterizes osteoarthritic cartilage damage is a reduction of proteoglycan content, reflecting an imbalance between synthesis and release of proteoglycans. Both synthesis and release depend on the activity of cartilage cells. Chondrocytes in the upper layer of moderately osteoarthritic human knee cartilage appear to be phenotypically altered, including diminished proteoglycan synthesis. Transforming growth factor-beta (TGF-beta) as a multifunctional growth factor has differential effects believed to depend on the differentiation stage of the target cells. We tested the effect of TGF-beta on phenotypically altered chondrocytes in osteoarthritic cartilage. METHODS: Human articular cartilage was cultured 4 days with or without TGF-beta. Proteoglycan synthesis was determined by (35)SO4(2-) incorporation (biochemically and by autoradiography) for the upper and deep layer separately. RESULTS: Osteoarthritic cartilage proved more sensitive to TGF-beta than normal cartilage. Proteoglycan synthesis of osteoarthritic cartilage was stimulated significantly more by 5 ng/ml TGF-beta than normal cartilage. For normal cartilage this increase was equally divided among the upper and deeper layer of the explants. For osteoarthritic cartilage the increase in proteoglycan synthesis could largely be attributed to the upper layer. Autoradiography revealed that the relative (35)SO4(2-) incorporation in the cell clusters, present in the upper layer of osteoarthritic cartilage, was significantly increased upon the addition of TGF-beta. CONCLUSION: Osteoarthritic cartilage is more sensitive to TGF-beta than normal cartilage because phenotypically changed chondrocytes in the damaged upper layer of osteoarthritic cartilage are more sensitive to TGF-beta than chondrocytes in the more intact deep layer and are more sensitive than the chondrocytes of normal cartilage. TGF-beta appears to redifferentiate the phenotypically altered chondrocytes in osteoarthritic cartilage.

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