In vitro reversal of the load-bearing properties of lipid-depleted articular cartilage following exposure to phospholipid surfactant solutions.

BACKGROUND: A microscopic layer of surface active phospholipids overlays the articular cartilage of the knee. Its depletion in osteoarthritic joints results in loss of lubrication and load-bearing efficiency. We hypothesize that exposure of articular cartilage to the dominant unsaturated phospholipid component of knee surfactant can regenerate the load-bearing properties of the tissue. This was evaluated by studying the stress-strain and stiffness characteristics of normal intact and lipid-depleted cartilage exposed to lipid-based surfactants for known durations. METHODS: Normal intact, lipid-depleted and surfactant-treated bovine articular cartilage specimens were compressed at 0.5mm/min to a maximum strain of 40% and their stress-strain and stiffness data were compared. FINDINGS: The stiffness of lipid-depleted samples increased by 40% on average relative to the normal; after exposure of the same samples to saturated surfactant for one and 24h, the average stiffness decreased by 25% and 62%, respectively from this high value. On the other hand, exposure of delipidized specimens to a mixture of selected unsaturated surfactant species for one and 24h resulted in a reduction of 85% and 90% in the stiffness of the depilidized samples respectively, largely reversing the effect of lipid removal to a level much closer to that of the normal intact cartilage and therefore better than that obtained with incubation in the saturated surfactant. INTERPRETATION: Lipid loss in articular cartilage results in a consistent increase in stiffness relative to normal tissue stiffness. This consequence of lipid loss can be partially reversed by the reintroduction of surface active phospholipids. The results of this study show that the lipid components of cartilage play an important role in determining the compliance of the loaded tissue.

The influence of lipid-extraction method on the stiffness of articular cartilage.

BACKGROUND: One of the known characteristics of osteoarthritis is the loss of articular cartilage lipids. Therefore, it is important to study how lipids influence the functions of the tissue. This can only be done successfully by indirect analysis involving the extraction of lipids and subsequent assessment of the delipidized matrix. Therefore, for accuracy, the procedure for lipid extraction must not induce any other modification in the samples to be assessed. Hence, we compare three rinsing agents and methods in this study. METHODS: Normal and delipidized articular cartilage samples were tested under compressive loading at 4 loading velocities to obtain and compare their stiffness values. FINDINGS: Chloroform rinsing resulted in a 45% decrease in the stiffness of cartilage at low strain-rates (10(-2)/s and 10(-1)/s) on average with a corresponding increase of 55% at higher strain-rate of 10/s relative to the normal. Ethanol rinsed cartilage exhibited a corresponding decrease of 40% at the low strain-rates while exhibiting an increase of about 20% at the highest loading rates. Propylene glycol rinsing resulted in a decrease of approximately 20% in stiffness, while an increase of up to 5% at high rates of loading. INTERPRETATION: The loss of lipids modifies the stiffness of articular cartilage at all loading rates. The relatively larger deviation of the stiffness of chloroform-rinsed samples relative to the normal is probably a consequence of the drying process involved in rinsing protocol. It is probable that the results of milder rinsing agents, used without vacuum drying, are more reflective of physiological delipidization effects on the tissue. Consequently, we recommend propylene glycol and its associated protocol for extracting lipids from articular cartilage.

Consolidation responses of delipidized articular cartilage.

OBJECTIVE: To determine the role of articular cartilage lipids in its load-bearing function. DESIGN: Normal and delipidised, bovine articular cartilage specimens were statically loaded and both the hydrostatic excess pore pressure and creep strain were measured. From this the compression stiffness of the skeletal structures of both types of matrices was determined. BACKGROUND: It has been hypothesized that surfactant injection could relief osteoarthritis, but there is no study in the literature relating to the influence of lipids, the main ingredients of such products, on cartilage load-carriage. METHODS: Articular cartilage specimens were obtained from the patellar grooves of 2-3 year old bovine animals. When required specimen delipidization was carried out using chloroform/methanol rinsing. Both normal and delipidised samples were loaded in the consolidometer and the hydrostatic excess pore pressure and strain were measured. RESULTS: The transient patterns of the hydrostatic excess pore pressure were similar for both types of tissue, with a relatively insignificant increase of 2% in the maximum hydrostatic excess pore pressure of the delipidized samples relative to the normal intact specimens. The maximum creep strain of the delipidised specimens decreased by 10% on average relative to their normal intact counterparts, thereby indicating that delipidization causes stiffening of the cartilage matrix. CONCLUSION: The delipidized fluid-saturated articular cartilage is stiffer than its intact counterpart with consequence for cartilage compliance during function. RELEVANCE: Because osteoarthritis can be accompanied by lipid loss in cartilage, this study contributes to the further understanding of the disease with potential benefit for treatment.

Biomechanical responses of normal and delipidized articular cartilage subjected to varying rates of loading.

In alignment with the proposition that a lipid layer overlays the superficial zone of the articular cartilage, this study presents the consequence of the removal of lipids on the load-bearing characteristics of the tissue. Both normal unmodified and delipidized cartilage matrices were loaded at four different strain-rates of 1.3 x 10(-4)/s, 1.3 x 10(-3)/s, 1.3 x 10(-2)/s, and 1.3 x 10(-1)/s to strains of no more than 40%, to compare their stress-strain and stiffness-strain-rate characteristics. Our results demonstrate that at the lowest strain-rate of 1.3 x 10(-4)/s, the stiffness of the delipidized matrix was lower in comparison to that of the normal unmodified tissue. This response was reversed at higher strain-rates of 1.3 x 10(-2)/s and above. We conclude, therefore, that in general, at physiological rates of loading, the depletion of lipids from the articular cartilage reduces its compliance by at least 25%. We infer from the present study that this degenerative stiffening is an important contributing factor in impairing the tissue's load processing function in osteoarthritic joints.