Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “CARTILAGE”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,693 records · Page 94Linked to original sources
PubMed1968

Evidence for changes in protein polysaccharide associated with the onset of calcification in cartilage.

Past work has suggested that protein polysaccharide may play a role in the calcification of cartilage. Recent electron microscopic studies on noncalcified cartilage have indicated that protein polysaccharide in cartilage matrix is represented by granules associated with collagen fibers. The present work has been designed for comparison of the matrix of noncalcified cartilage to that of calcified cartilage, with particular reference to these granules. Small blocks of tibia from 16-day embryos were fixed in cacodylate-buffered glutaraldehyde and postfixed in either phosphate- or Veronal-buffered osmium tetroxide. Special care was taken to maintain the pH above 7.0 at all times. For electron microscopy the tissues were dehydrated, embedded in Epon 812, sectioned, and stained with uranyl acetate or lead citrate. A marked decrease in the size of granules in the matrix of calcified cartilage compared to noncalcified cartilage was noted. Associated with the decrease in the size of granules was a condensation of matrix components and the presence of an amorphous electron-opaque material that was not seen in noncalcified areas. These results are interpreted to represent either a drop in concentration or a change in state of protein polysaccharide with the onset of calcification in cartilage.

Animals↗
PubMed1960

The removal of cartilage matrix by papain. Factors affecting the distribution of crystalline papain in vivo.

In rabbits, the depletion of cartilage matrix which occurs following intravenous administration of papain treated with iodacetamide is attributable to a portion of the enzyme in the disulfide form which has not undergone alkylation. It is this portion that is reactivated in cartilage in vivo and initiates the enzymatic breakdown of the protein-polysaccharide complex which forms a major component of the matrix. Evidence presented in support of these conclusions indicates that, contrary to an earlier hypothesis, papain acetamide is not reactivated in vivo. Following intravenous injection in amounts up to 4 mg./kg., active and inactive papain leaves the circulation at a rate proportional to the concentration, and it is likely that the initial rate of disappearance represents equilibration with the extracellular space. Following injection in the active or inactive form, a high proportion of papain in serum is bound to protein in the alpha globulin fraction. It is believed that in the case of fully active papain, the proportion which is not bound to alpha globulin becomes attached to other proteins of serum in extracellular fluid, such as albumin, by a process of enzyme substrate combination, and is thus prevented from diffusing into cartilage. In the case of inactive papain, a comparable excess remains free to enter cartilage, where it initiates depletion of matrix following reactivation within the tissue. These conclusions provide an explanation for the failure of fully active papain to cause depletion of cartilage matrix in vivo; the widespread changes seen after the injection of papain inactivated by iodoacetamide or by simple reversible oxidation are attributable to a small proportion of the injected material which enters cartilage in the disulfide form in a concentration of approximately 2 micrograms/gm. wet weight. The possibility that such a small amount of protease, when reactivated, can produce changes in cartilage matrix has been confirmed by studies on the effects of papain on isolated cartilage and chondromucoprotein in vitro. It has been shown that severe local injury results when active papain is injected into the skin of a rabbit in low concentrations. Since a much higher concentration of papain can be attained in the circulation without obvious adverse effects, it is evident that binding of the protease by alpha globulin and possibly other serum proteins may exemplify a mechanism whereby the tissues are protected from injury following entry into the circulation of other potentially harmful agents, such as proteolytic enzymes derived from cells or bacteria.

Animals↗
PubMed1999

Characterization of enzymatically induced degradation of articular cartilage using high frequency ultrasound.

Ultrasound may provide a quantitative technique for the characterization of cartilage changes typical of early osteoarthrosis. In this study, specific changes in bovine articular cartilage were induced using collagenase and chondroitinase ABC, enzymes that selectively degrade collagen fibril network and digest proteoglycans, respectively. Changes in cartilage structure and properties were quantified using high frequency ultrasound, microscopic analyses and mechanical indentation tests. The ultrasound reflection coefficient of the physiological saline-cartilage interface (R1) decreased significantly (-96.4%, p < 0.01) in the collagenase digested cartilage compared to controls. Also a significantly lower ultrasound velocity (-6.2%, p < 0.01) was revealed after collagenase digestion. After chondroitinase ABC digestion, a new acoustic interface at the depth of the enzyme penetration front was detected. Cartilage thickness, as determined with ultrasound, showed a high, linear correlation (R = 0.943, n = 60, average difference 0.073 mm (4.0%)) with the thickness measured by the needle-probe method. Both enzymes induced a significant decrease in the Young's modulus of cartilage (p < 0.01). Our results indicate that high frequency ultrasound provides a sensitive technique for the analysis of cartilage structure and properties. Possibly ultrasound may be utilized in vivo as a quantitative probe during arthroscopy.

Animals↗
PubMed2001

Regeneration of hyaline cartilage by cell-mediated gene therapy using transforming growth factor beta 1-producing fibroblasts.

Transforming growth factor beta (TGF-beta) has been considered as a candidate for gene therapy of orthopedic diseases. The possible application of cell-mediated TGF-beta gene therapy as a new treatment regimen for degenerative arthritis was investigated. In this study, fibroblasts expressing active TGF-beta 1 were injected into the knee joints of rabbits with artificially made cartilage defects to evaluate the feasibility of this therapy for orthopedic diseases. Two to 3 weeks after the injection there was evidence of cartilage regeneration, and at 4 to 6 weeks the cartilage defect was completely filled with newly grown hyaline cartilage. Histological analyses of the regenerated cartilage suggested that it was well integrated with the adjacent normal cartilage at the sides of the defect and that the newly formed tissue was indeed hyaline cartilage. Our findings suggest that cell-mediated TGF-beta 1 gene therapy may be a novel treatment for orthopedic diseases in which hyaline cartilage damage has occurred.

3T3 Cells↗
PubMed2001

Cultured chondrocytes produce injectable tissue-engineered cartilage in hydrogel polymer.

The purpose of this study was to determine if chondrocytes cultured through several subcultures at very low plating density would produce new cartilage matrix after being reimplanted in vivo with or without a hydrogel polymer scaffold. Chondrocytes were initially plated in low-density monolayer culture, grown to confluence, and passaged four times. After each passage cells were suspended in purified porcine fibrinogen and injected into the subcutaneous space of nude mice while simultaneously polymerizing with thrombin to reach a final concentration of 40 million cells/cc. Controls were made by injecting fresh, uncultured cells with fibrin polymer and by injecting the cultured cells in saline (without polymer). All samples were harvested at 6 weeks. When injected in polymer, both fresh cells and cells that had undergone only one passage in culture produced cartilaginous nodules. Cultured cells did not produce cartilage, regardless of length of time spent in culture, when injected without polymer. Cartilage was also not recovered from samples with cells kept in culture for longer than one passage, even when provided with a polymer matrix. All samples harvested were subjected to histological analysis and assayed for total DNA, glycosaminoglycan (GAG), and type II collagen. There was histological evidence of cartilage in the groups that used fresh cells and cultured cells suspended in fibrin polymer that only underwent one passage. No other group contained areas that would be consistent with cartilage histologically. All experimental samples had a higher percent of DNA than native swine cartilage, and there was no statistical difference between the DNA content of the groups containing cultured or fresh cells in fibrin polymer. Whereas the GAG content of native cartilage was 8.39% of dry weight and fresh cells in fibrin polymer was 12.85%, cultured cells in fibrin polymer never exceded the 2.48% noted from first passage cells. In conclusion, this study demonstrates that porcine chondrocytes that have been cultured in monolayer for one passage will produce cartilage in vivo when suspended in fibrin polymer.

Animals↗
PubMedDate not supplied

Effects of basic fibroblast growth factor on the repair of large osteochondral defects of articular cartilage in rabbits: dose-response effects and long-term outcomes.

Articular cartilage possesses a limited capacity for self-renewal. The regenerated tissue often resembles fibrocartilage-like tissue rather than hyaline cartilage, and degeneration of the articular surface eventually occurs. The purpose of this study was to investigate the effect of basic fibroblast growth factor (bFGF) on the healing of full-thickness articular cartilage defects. bFGF (0, 10, 50, 100, 250, 500, or 1000 ng) was mixed with collagen gel and implanted into full-thickness articular cartilage defects drilled into rabbit knees. The repaired tissue was examined grossly and histologically, and was evaluated with the use of a grading scale at 4, 12, 24, and 50 weeks. At 4 weeks, treatment with 100 ng of bFGF had greatly stimulated cartilage repair both grossly and histologically in comparison with untreated defects (those filled with plain collagen gel). The average total scores on the histological grading scale were significantly better for the defects treated with bFGF than for the untreated defects. These improvements were evident as long as 50 weeks postoperatively, although slight deterioration was noted in the repaired cartilage. Immunohistochemical staining for type II collagen showed that this cartilage-specific collagen was diffusely distributed in the repaired tissue at 50 weeks. These findings suggest that bFGF may be a practical and important candidate for use in cartilage repair.

Animals↗
PubMed1997

Tissue-separating capacity of growth cartilages.

The tissue-separating capacity of chondral structures has been debated for more than 30 years, and one aspect that has particularly been questioned is whether the secondary cartilage of the mandibular condyle is comparable to primary growth cartilage, e.g. the epiphyseal growth plate. The present report summarizes information gained by using a specific interosseal transplantation method. These findings lead to the conclusion that all the structures examined, i.e. the proximal epiphyseal cartilage of the tibia, the cartilage of the costochondral junction of the ribs, the basicranial synchondroses, the medial cartilage of the clavicle and the mandibular condyle, have the capacity to separate adjoining skeletal structures. The changes induced by the transplanted structures in the recipient area vary, however, suggesting a hierarchial arrangement of cartilages with regard to their tissue-separating capacity. It is suggested that the tissue-separating capacity is a basic phenomenon in the function of growth, not only of primary growth cartilages, but of secondary cartilages as well.

Animals↗
PubMed2000

Cartilage turnover in embryonic chick tibial explant cultures.

Growth plate cartilage regulates the rate of growth and ultimate length of several bones in the skeleton. Chondrocytes within the growth plate proliferate, differentiate, enlarge, and die. The extracellular matrix undergoes synthesis, reorganization, and eventually degradation. The majority of research in growth plate physiology has focused on the proliferation and differentiation of chondrocytes as well as proteins they produce for the extracellular matrix. However, little is known about the transition from hypertrophic to apoptotic chondrocytes or the regulation of terminal degradation of cartilage prior to bone formation. An explant culture has been developed to study cartilage differentiation using 12-d-old embryonic chick tibiae. We have modified the explant culture and are using it to further elucidate mechanisms involved in the regulation of growth plate cartilage turnover. In our cultures, chondrocytes mature and then die, completely degrading the cartilage in approximately 16 d. The matrix undergoes a predictable pattern of degradation in which proteoglycans followed by collagen are removed. Increases in matrix metalloproteinase activity and nitric oxide production are detected in cartilage concurrently with release of proteoglycans into media. Inhibitors of nitric oxide inhibit nitric oxide production and proteoglycan degradation, suggesting that nitric oxide, at least in part, regulates growth plate cartilage turnover in the explant culture. Information gained from using this explant culture will aid in understanding the regulation of growth plate cartilage turnover in vivo and potentially help determine the cause of bone growth diseases such as tibial dyschondroplasia.

Animals↗
PubMed1992

Susceptibility of normal and arthritic human articular cartilage to degradative stimuli.

Recombinant interleukin-1 (IL-1) alpha and beta stimulated significant loss of glycosaminoglcan (GAG) content from normal (non-arthritic) articular cartilage explants but only after incubation for 14 days and only in specimens from 8/21 (38%) individuals. By contrast, all cartilage specimens but one from patients with osteoarthritis (OA) and rheumatoid arthritis (RA) were degraded (as judged by their reduced GAG content) by the recombinant cytokines but again only after 14 days' incubation. The reduction in GAG induced by IL-1 was also greater for both OA and RA cartilage than normal cartilage. Synovial fluids (SFs) from RA patients stimulated greater loss of GAG content from OA cartilage explants than normal explants although in both cases the loss was evident within 2 days. It is concluded that cartilage explants from some individuals are susceptible to the degradative effects of IL-1 whereas others are refractory and that arthritic cartilage is more susceptible to degradation by both IL-1 and RA SFs than non-arthritic cartilage.

Aged↗
PubMed1992

Intermittent hydrostatic compressive force stimulates exclusively the proteoglycan synthesis of osteoarthritic human cartilage.

In paired observations the in vitro proteoglycan turnover was studied of human normal and osteoarthritic cartilage in the absence and presence of intermittent hydrostatic compressive force. Shortly after collection, osteoarthritic cartilage showed a higher proteoglycan synthesis rate than normal cartilage, whereas after culture the reverse was found. Exposure during culture to hydrostatic intermittent compression of a low physiological magnitude enhanced the proteoglycan synthesis rate for osteoarthritic cartilage, whereas normal was unaffected by this hydrostatic intermittent compression. This enhancing effect was reversible. We conclude that human osteoarthritic cartilage is in vivo synthetically more active than normal cartilage, but loses this increased activity in vitro. Enhanced sensitivity of osteoarthritic cartilage to compressive forces may contribute to the increased proteoglycan synthesis of osteoarthritic cartilage.

Adult↗
PubMed1996

In vitro effects of methotrexate on human articular cartilage and bone-derived osteoblasts.

Conflicting data have been published on whether low-dose methotrexate (MTX) treatment of rheumatoid arthritis (RA) is able to slow down radiological joint damage, i.e. retard the destruction of articular cartilage and (subchondral) bone. We studied the effects of MTX on proteoglycan (PG) turnover and interleukin-1 (IL-1)- and RA mononuclear cell (RA-MNC)-induced cartilage damage in human articular cartilage tissue cultures, and the effects of MTX on basal and RA-MNC-influenced proliferation and differentiation of osteoblasts in cultures of human bone-derived osteoblasts. MTX exerted no direct effect on cartilage nor did MTX influence IL-1- or RA-MNC-induced cartilage damage, despite strong suppression of basal as well as mitogen- and antigen-induced RA-MNC proliferation. MTX induced strong inhibition of osteoblast proliferation, but did not significantly interfere with osteoblast differentiation (i.e. alkaline phosphatase activity). RA-MNC-enhanced proliferation and differentiation of osteoblasts were abolished by MTX. These results suggest that if MTX is able to induce retardation of radiological progression in RA, this is not based on an initial direct effect of MTX on cartilage as measured by PG turnover, nor on an initial inhibition of IL-1- or RA-MNC-induced cartilage damage. However, longstanding MTX-induced inhibition of RA-MNC proliferation may lead to reduction of the catabolic activity involved in cartilage destruction. On the other hand, long-term inhibition of osteoblast proliferation may eventually lead to decreased bone formation and osteopenia. Whether this will turn out to be a problem of clinical importance in the treatment of RA has to be established.

Adult↗
PubMed2004

Longitudinal study of the relationship between knee angle and tibiofemoral cartilage volume in subjects with knee osteoarthritis.

OBJECTIVES: There is emerging evidence that knee alignment is associated with progression of osteoarthritis (OA). The aim of this study was to examine the relationship between baseline knee angle and the rate of cartilage loss in subjects with knee OA. METHODS: One hundred and seventeen subjects with knee OA had standing radiographs and MRI on their symptomatic knee at baseline and at the 1.9+/-0.2 yr follow-up. Knee cartilage volume was measured at baseline and follow-up. Knee angle was defined as the angle subtended by a line drawn through the mid-shaft of the femur with respect to one drawn through the mid-shaft of the tibia. RESULTS: At baseline, in the medial compartment, as the angle decreased (i.e. was less varus) the tibial and femoral cartilage volume increased. In the lateral compartment, as the angle became more valgus, there was a reduction in tibial and femoral cartilage volume. In the longitudinal study, for every 1 degrees increase in baseline varus angulation there was an average annual loss of medial femoral cartilage of 17.7 micro l [95% confidence interval (CI) 6.5-28.8]. Although not statistically significant, there was a trend for a similar relationship between loss of medial tibial cartilage volume and baseline knee angle. In the lateral compartment, there was an average loss of tibial cartilage volume of 8.0 micro l (95% CI 0.0-16.0) for every 1 degrees increase in valgus angle. CONCLUSIONS: Baseline knee angle is associated with the rate of cartilage loss in the knee. Further work will be needed to determine whether therapies aimed at modifying the knee angle will reduce the progression of knee OA.

Aged↗
PubMed2004

Repair of articular cartilage defects in rabbits using CDMP1 gene-transfected autologous mesenchymal cells derived from bone marrow.

OBJECTIVE: Cartilage-derived morphogenetic protein 1 (CDMP1), which is a member of the transforming growth factor-beta superfamily, is an essential molecule for the aggregation of mesenchymal cells and acceleration of chondrocyte differentiation. In this study, we investigated whether CDMP1-transfected autologous bone marrow-derived mesenchymal cells (BMMCs) enhance in vivo cartilage repair in a rabbit model. METHODS: BMMCs, which had a fibroblastic morphology and pluripotency for differentiation, were isolated from bone marrow of the tibia of rabbits, grown in monolayer culture, and transfected with the CDMP1 gene or a control gene (GFP) by the lipofection method. The autologous cells were then implanted into full-thickness articular cartilage defects in the knee joints of each rabbit. RESULTS: During in vivo repair of full-thickness articular cartilage defects, cartilage regeneration was enhanced by the implantation of CDMP1-transfected autologous BMMCs. The defects were filled by hyaline cartilage and the deeper zone showed remodelling to subchondral bone over time. The repair and reconstitution of zones of hyaline articular cartilage was superior to simple BMMC implantation. The histological score of the CDMP1-transfected BMMC group was significantly better than those of the control BMMC group and the empty control group. CONCLUSION: Modulation of BMMCs by factors such as CDMP1 allows enhanced repair and remodelling compatible with hyaline articular cartilage.

Animals↗
PubMed2004

COOH-terminal heparin-binding fibronectin fragment induces nitric oxide production in rheumatoid cartilage through CD44.

OBJECTIVES: To examine the mechanism of nitric oxide (NO) production by a COOH-terminal heparin-binding fibronectin fragment (HBFN-f) in rheumatoid arthritis (RA) cartilage. METHODS: Articular cartilage slices from RA knee joints and normal hip joints were cultured with HBFN-f. Secreted NO levels in conditioned media were determined. Cultures were pretreated with anti-CD44 antibody or HBFN-f-derived synthetic peptide (peptide V; WQPPRARI) to evaluate the role of CD44 in HBFN-f action. Immunofluorescence histochemistry was performed using fluorescein isothiocyanate-conjugated anti-CD44 antibody. RESULTS: HBFN-f stimulated NO production in a dose-dependent manner. Whereas CD44 expression was up-regulated in RA cartilage, anti-CD44 antibody blocked HBFN-f-stimulated NO production. Peptide V with heparin-binding ability significantly reduced NO levels elevated by HBFN-f. Compared with normal cartilage, cartilage response to HBFN-f and the blocking effects of anti-CD44 antibody on HBFN-f action were stronger in RA cartilage. CONCLUSIONS: The present study clearly demonstrated that HBFN-f stimulated NO production through CD44 in RA cartilage. Increased expression of CD44 in RA cartilage may play a pathological role in joint destruction through enhanced NO production by binding to fibronectin fragments such as HBFN-f.

Aged↗
PubMed2006

Retinoic acid and oncostatin M combine to promote cartilage degradation via matrix metalloproteinase-13 expression in bovine but not human chondrocytes.

OBJECTIVES: Retinoic acid (RetA) and oncostatin M (OSM) have both been shown to mediate potent effects with respect to extracellular matrix integrity. This study assesses the effects of a RetA + OSM combination on cartilage catabolism. METHODS: Animal and human cartilage samples were used to assess the ability of RetA + OSM to promote the release of collagen and proteoglycan fragments, which was determined by measuring glycosaminoglycan and hydroxyproline, respectively. Total collagenolytic and tissue inhibitor of metalloproteinases (TIMP) inhibitory activities were determined by bioassay, whilst gene expression of matrix metalloproteinases (MMPs) and TIMP-1 were determined by northern blotting. Immunohistochemistry was used to assess the presence of MMP-1 and -13 in resorbing cartilage explants. RESULTS: Both agents alone induced proteoglycan release from bovine cartilage, whilst RetA-induced collagen release was variable. Reproducible and synergistic collagenolysis was observed with RetA + OSM, which appeared to be due to MMP-13. Similar collagen release was observed from porcine cartilage. Conversely, no collagen release was seen with human articular cartilage. In primary human chondrocytes, RetA + OSM failed to induce MMP-1 or -13 but caused a significant increase in TIMP-1 expression. CONCLUSIONS: These novel observations show that the combination of RetA + OSM has profound effects on cartilage matrix turnover, but these effects are species-specific. A better understanding of the mechanism by which this combination differentially regulates MMP and TIMP expression in human chondrocytes could provide valuable insight into new therapeutic strategies aimed at the prevention of cartilage destruction.

Animals↗
PubMed2006

A longitudinal study of the effect of sex and age on rate of change in knee cartilage volume in adults.

OBJECTIVE: To describe the association between sex, age and rate of change in knee cartilage volume in adults. METHODS: A total of 325 subjects (mean age 45 yrs, range 26-61) was measured at baseline and approximately 2 yrs later. Knee cartilage volume and bone size were determined using T1-weighted fat saturation magnetic resonance imaging (MRI). Height, weight, body mass index and radiographic osteoarthritis (ROA) were measured by standard protocols. RESULTS: Knee cartilage volume decreased by 1.5-4.2% per annum. In multivariable analysis, females had higher rates of change per annum in knee cartilage volume than males (medial tibia: -3.5%, P < 0.001; lateral tibia: -2.6%, P < 0.001 and patella: -0.8%, P = 0.053). The sex difference first appeared at age 40 and became more marked with increasing age at the medial tibial site only (P = 0.039). Age was significantly associated with annual change in knee cartilage volume at all three sites (beta = -0.06 to -0.12%/yr, all P < 0.05), and these associations were stronger in females. With the exception of the medial site (beta = -0.05/yr, P = 0.117 for ROA exclusion, and beta = -0.06%/yr, P = 0.056 for ROA adjustment), the association with age did not change when subjects with ROA were excluded from analyses or after further adjustment for ROA. CONCLUSIONS: Within the age range we studied, knee cartilage volume declines at a faster rate with increasing age. This is partly mediated by ROA at the medial tibial site only. Furthermore, women have substantially higher knee cartilage loss than men, and these sex differences first appear at age 40 and become more marked with increasing age, which has implications for prevention of cartilage loss from middle age.

Adult↗
PubMed1991

Unique fatty acid composition of normal cartilage: discovery of high levels of n-9 eicosatrienoic acid and low levels of n-6 polyunsaturated fatty acids.

We report here the finding that normal, young cartilages, in distinction from all other tissues examined, have unusually high levels of n-9 eicosatrienoic (20:3 cis-delta 5,8,11) acid and low levels of n-6 polyunsaturated fatty acids (n-6 PUFA). This pattern is identical to that found in tissues of animals subjected to prolonged depletion of nutritionally essential n-6 polyunsaturated fatty acids (EFA). This apparent deficiency is consistently observed in cartilage of all species so far studied (young chicken, fetal calf, newborn pig, rabbit, and human), even though levels of n-6 PUFA in blood and all other tissues is normal. The n-9 20:3 acid is particularly abundant in phosphatidylethanolamine, phosphatidylinositol, and the free fatty acid fractions from the young cartilage. Several factors appear to contribute to the reduction in n-6 PUFA and the appearance of high levels of the n-9 20:3 acid in cartilage: 1) limited access to nutritional sources of EFA due to the impermeability and avascularity of cartilage, 2) rapid metabolism of n-6 PUFA to prostanoids by chondrocytes, and 3) a unique fatty acid metabolism by cartilage. Evidence is presented that each of these factors contributes. Previously, EFA deficiency has been shown to greatly suppress the inflammatory response of leukocytes and rejection of tissues transplanted into allogeneic recipients. Because eicosanoids, which are derived from EFA, have been implicated in the inflammatory responses associated with arthritic disease, reduction of n-6 PUFA and accumulation of the n-9 20:3 acid in cartilage may be important for maintaining normal cartilage structure.

8,11,14-Eicosatrienoic Acid↗
PubMed2002

Cartilage shaping with the Er:YAG laser: an in vivo experimental study.

Reshaping and preserving the new shape of cartilage grafts is important for reconstruction of congenital or acquired deformities. In this in vivo study the authors investigated the effect of the Er:YAG laser on cartilage reshaping in comparison with scalpel stripping. The study consisted of two groups (N = 9). After measuring the angle between two margins of the ear, the cartilage in the right ear in rabbits was reshaped using the Er:YAG laser in group I, and scalpel incisions were used to reshape the left-ear cartilage in group II rabbits. Changes in the shape of the ears were evaluated at 10 days, and 1 and 6 months. The laser-reshaped ears were flattened and preserved the new flattened shape at the end of 6 months. The ultrastructural changes in the cartilage were evaluated based on the results from histopathological examination and electron microscopy. The authors conclude that cartilage can be reshaped using the Er:YAG laser. The mechanical effect of laser ablation and the thermal effect of laser radiation caused ultrastructural changes in the cartilage tissue, resulting in permanent changes in cartilage shape.

Animals↗