**2. Synovial Joints**

Synovial joints, being the most common joints in mammals, are characterized by allowing movement in multiple planes. They allow for the articulation of long bones, ends of which are covered with articular cartilage (AC), within a fluid-filled cavity. AC,

incorporated with a viscous synovial fluid, is a biphasic tissue that provides extremely low friction [2]. It mitigates overstressing on the tissue's solid phase, while dissipating energy and enabling smooth joints movements. The synovial fluid consists of hyaluronic acid (HA), glycosaminoglycans (GAGs) containing chondroitin-4-sulfate, chondroitin-6-sulfate, keratan sulfate and mobile ions and is a dialysate of blood plasma without hemoglobin [3]. The synovial fluid is contained mainly within the molecular pore spaces of the cartilage cells [4]. AC incorporates the viscous synovial fluid to mitigate shock-loadings initiated by physiological activities and body weight [5]. Hence, AC supports smooth joint movements at an extremely low coefficient of friction (CoF) [6]. and enabling smooth joints movements. The synovial fluid consists of hyaluronic acid (HA), glycosaminoglycans (GAGs) containing chondroitin-4-sulfate, chondroitin-6-sulfate, keratan sulfate and mobile ions and is a dialysate of blood plasma without hemoglobin [3]. The synovial fluid is contained mainly within the molecular pore spaces of the cartilage cells [4]. AC incorporates the viscous synovial fluid to mitigate shock-loadings initiated by physiological activities and body weight [5]. Hence, AC supports smooth joint movements at an extremely low coefficient of friction (CoF) [6]. **3. The Structure of Articular Cartilage** 

Synovial joints, being the most common joints in mammals, are characterized by allowing movement in multiple planes. They allow for the articulation of long bones, ends of which are covered with articular cartilage (AC), within a fluid-filled cavity. AC, incorporated with a viscous synovial fluid, is a biphasic tissue that provides extremely low friction [2]. It mitigates overstressing on the tissue's solid phase, while dissipating energy

*Polymers* **2021**, *13*, x FOR PEER REVIEW 2 of 25

#### **3. The Structure of Articular Cartilage** The AC structure is complex, as the compositions of GAGs, chondrocytes and colla-

**2. Synovial Joints** 

The AC structure is complex, as the compositions of GAGs, chondrocytes and collagen are in random orientations and densities; with the main components of this composition contains water (60–85%), collagen type II (15–22%) and Proteoglycan (PG) (4–7%) [7]. Its deep zone includes hydroxyapatite (Hap) combined with collagen and chondrocyte in the vertical orientation [8], as illustrated in Figure 1. AC is a biphasic substrate categorized as a nonlinear, anisotropic, viscoelastic and inhomogeneous material [7,9]. gen are in random orientations and densities; with the main components of this composition contains water (60–85%), collagen type II (15–22%) and Proteoglycan (PG) (4–7%) [7]. Its deep zone includes hydroxyapatite (Hap) combined with collagen and chondrocyte in the vertical orientation [8], as illustrated in Figure 1. AC is a biphasic substrate categorized as a nonlinear, anisotropic, viscoelastic and inhomogeneous material [7,9].

**Figure 1.** Illustration of the AC structure: superficial, transition and deep zones. Reproduced from [10]. **Figure 1.** Illustration of the AC structure: superficial, transition and deep zones. Reproduced from [10].

.

#### *Zonal Categories of Articular Cartilage*

*Zonal Categories of Articular Cartilage*  AC is a soft avascular tissue with a 3–4 mm thickness and integrates three depthdependent layers of superficial, transition and deep zones. Each layer is responsible for minimizing either the imposing load or friction of the sliding movement, as described in AC is a soft avascular tissue with a 3–4 mm thickness and integrates three depthdependent layers of superficial, transition and deep zones. Each layer is responsible for minimizing either the imposing load or friction of the sliding movement, as described in the following sections.

the following sections. The top layer (superficial zone) contains collagen fibrils cells in the horizontal orientation, which confers high tensile stiffness and strength. This layer is just 10–20% of the tissue's thickness [11]; both fibrils and chondrocytes are stretched along their length and surrounded at the surface with the finest size compared to the other layers' chondrocytes [12]. This feature also custodies the tissue against high tensile stresses and prevents interstitial fluid permeation, which plays a vital role in sliding on cartilage surface mates [13]. While this layer has high water content, it has the lowest PG [14]. The superficial zone is also called the surface amorphous layer (SAL) that is acellular with no fibril content [7]. Its thickness is a few micrometers, containing proteins, glycoproteins, PGs, hyaluronic acid-protein complexes, chondroitin/keratin sulfates and lipids [15]. In summary, the superficial zone is shear resistant because of the low content of PGs and low permeability [16,17]. This layer plays a crucial role in attaining smooth sliding contact, while controlling synovial fluid diffusion rate. The transition zone is the thickest part of the tissue, contributing to 40–60% of the total thickness of the AC [18]. Collagen fibrils and chondrocytes The top layer (superficial zone) contains collagen fibrils cells in the horizontal orientation, which confers high tensile stiffness and strength. This layer is just 10–20% of the tissue's thickness [11]; both fibrils and chondrocytes are stretched along their length and surrounded at the surface with the finest size compared to the other layers' chondrocytes [12]. This feature also custodies the tissue against high tensile stresses and prevents interstitial fluid permeation, which plays a vital role in sliding on cartilage surface mates [13]. While this layer has high water content, it has the lowest PG [14]. The superficial zone is also called the surface amorphous layer (SAL) that is acellular with no fibril content [7]. Its thickness is a few micrometers, containing proteins, glycoproteins, PGs, hyaluronic acidprotein complexes, chondroitin/keratin sulfates and lipids [15]. In summary, the superficial zone is shear resistant because of the low content of PGs and low permeability [16,17]. This layer plays a crucial role in attaining smooth sliding contact, while controlling synovial fluid diffusion rate. The transition zone is the thickest part of the tissue, contributing to 40–60% of the total thickness of the AC [18]. Collagen fibrils and chondrocytes are both ringed by an extracellular matrix (ECM) that includes GAGs [19]. Moreover, compared to the superficial zone, the transition zone has a higher PG content. The deep zone consists of orthogonally oriented collagen fibers in hydroxyapatite content and has the lowest water content. Its collagen structure is bundled together with fibers in the perpendicular direction to the articular surface. The deep zone forms an interface with the subchondral bone. The

stiffness of the whole structure varies gradually through the thickness. The PG, water content and cell density are the lowest in the deep zone [18].

#### **4. Osteoarthritis**

Osteoarthritis (OA) is the result of AC degeneration. The recovery process of the damaged lesions is prolonged because of tissue avascularity [7]. Therefore, degenerated tissue experiences high-pressure upon sliding of bones at the joints, which results in severe pain as well as movement disorders [20]. Factors that lead to OA are aging, musculoskeletal disordering and over-pressuring due to either physiological activities or obesity [21]. It is worth mentioning that joint immobilization yields to PG loss, contributing to AC thinning [22,23].

OA is categorized into two types, namely primary and secondary. Primary OA occurs in healthy AC without any abnormality of ligaments and menisci. The reason for primary OA in the elderly is repetitive loadings on thinned AC [20]. Secondary OA, however, is due to injury, trauma or inflammatory factors [24]. In the last decade, studies showed that OA does not result only from AC disease, but also from defects in the ligament, menisci, periarticular muscles and bone [25]. AC engrossed with any of the mentioned factors instigate knee instability and alteration in joint kinematics and consequently nonuniformly distributed stresses, which initiate OA [2].

#### *Treatment Methods for the Cartilage Subjected to OA*

The gold standard treatment for patients with OA are total knee/hip replacement (TKR/THR) or hemiarthroplasty. In hemiarthroplasty, only half of the joint in which cartilage deteriorated would be reamed, and either metallic or ceramic components are implanted. In case of hip joint damage, the acetabular cup is left intact, and damaged lesions of the femoral head cartilage would be reamed, and a metallic or ceramic cup is replaced. However, TKR or THR is not the practical solution at mid-adulthood ages due to the limitation of arthroplasty prostheses' life span [26]. Due to the short implant service life (15–20 years), THR/TKR procedures are only suitable for elderly patients [27].

Moreover, any failure after primary surgery yields to a revision surgery. The revision surgery can be implemented for patients just once in their treatment life, since the second revision may result in the implant's loosening [28]. Other procedures that have been developed for damaged cartilage are microfracture [29], autologous-matrix induced chondrogenesis [30], autologous chondrocyte implantation, autologous cultured chondrocytes on porcine collagen membrane (MACI) [31]. However, long-term clinical follow-ups have revealed durability issues with all the above-mentioned procedures [32]. Therapeutically, nonsteroidal drugs, corticosteroids and hyaluronic acid just relieve the pain in short-term and are pushed out of the joint within a few days [32].

Therefore, TKR/THR is the only clinical solution for older patients. However, there is not much attention for developing procedures and treatments suitable for younger patients suffering from dysfunctional cartilage, to eliminate or at least postpone the need for TKR/THR. Young patients between the age of 20–25 years old have reported the highest incidence of joint injury [3]. It turns into OA by 35–40 years old and implementing TKR/THR is high-risk at this age. If TKR, for instance, is performed at the age of 35–40 years, then based on 15–20 years' service life of prosthesis, patients may need revision surgery at the age of 55–60 years. Revision surgery could potentially lead to disability at this age due to the loosening of the prosthesis. In this case, a novel orthopedics implant with minimally invasive surgery that could mimic the mechanical and biological behavior of the native cartilage has been highlighted among researchers as a better alternative to TKR surgery for younger patients [33].

#### **5. Mechanical Characteristics of Articular Cartilage**

AC can withstand imposed load under its lifetime which is estimated at 100–200 million loading cycles [34]. AC is categorized as viscoelastic due to variations of its deformation

under various strain-rates [35]. It is anisotropic, since the tensile stiffness varies with the direction of loadings [36]. Furthermore, AC is inhomogeneous and performs diverged mechanical functions of tension and compression through the thickness from the superficial to the deep zone [37]. AC incorporation with the synovial fluid, which is incompressible and pressurizes noticeably, supports the significant portion of joint contact pressure [5]. These mentioned properties provide a unique cartilage structure to withstand cyclic loading from the body and transfer those loads smoothly to the bones.

AC tolerates contact pressures in the range of 3–5 MPa during the walking state in hip and knee joints [38]. Moreover, cartilage compressive and shear modulus are reported to be less than 1.5 MPa and 0.5 MPa, respectively. Its Poissons's ratio also ranges from 0.34 to 0.48 [7,39]. AC is also classified as a poroelastic material as its stiffness is highly dependent on strain-rate [40]. Oloyede et al. [41] have reported that at low strain-rates (0.01 > ε (t)) AC response is consolidation-type deformation, which is stiffness-dependent. In contrast, at higher strain-rates (0.01 ≤ ε (t)) hyperelastic deformation mechanism is dominant that results in high stiffness according to the classical elastic deformation process [41]. Eric et al. [42] studied correlation of cartilage stiffness and strain rate and reported that strain rate increases from 2.7 <sup>×</sup> <sup>10</sup>−<sup>3</sup> s −1 to 3.5 <sup>×</sup> <sup>10</sup>−<sup>2</sup> s <sup>−</sup><sup>1</sup> by increasing stiffness. Their studies employing a wide range of strain rates, showed two primary mechanical responses for AC. At low strain rates, stiffness increases considerably by a minimum increase in strain rate. In contrast, at the upper strain rates regime, stiffness does not vary significantly when the strain-rate increases. Moreover, there is a critical point beyond which the stiffness does not change much by high-strain rate loading [41]. It indicates that the compressive response of AC is strain-rate dependent at low strain-rate regime.

ECM significantly affects the mechanical properties of AC. AC exhibits time-dependent responses with viscoelasticity, poroelasticity or the combination of both phenomena [43]. Research studies demonstrate that AC responds to the loads based on PGs and chondrocyte arrangement [12,44]. However, cartilage's viscoelastic properties support the continuity of the inner tissue interactions by solid and fluid phase incorporation and fluid migration rates through the solid architecture [45]. Therefore, categorizing AC as viscoelastic or poroelastic material is highly dependent on several test factors, such as the size of the indenter, indentation depth and strain rates. Joseph et al. [43] demonstrated that the AC neither follows the classical poroelastic nor the viscoelastic model; In fact, the best model characterizing AC is a nonlinear biphasic material.

As AC is a heterogeneous, anisotropic and multiphasic biomaterial, the mechanical properties depend on its different zones. AC with three main zones and variation of collagen fibrils, PG and water contents in different layers show different responses based on the structure depth or thickness. AC with its relative strength through its thickness is in accordance with its non-homogeneity [46]. Therefore, to analyze the AC responses under loadings, the non-homogeneous poroelastic model has been recommended [47]. This model presented that the collagen fibril reinforces the cartilage through its thickness resulting in stress-strain ranges. This range is not limited just to the axial-loading direction, but also to the radial direction due to the pressurized pores by the interstitial fluid.

Hydration and dehydration are factors that affect the dissipation of pressure energy [48]. AC dissipation response is analyzed by uncoupling poroelastic and intrinsic viscoelastic mechanisms. In the dehydration state, energy dissipation reduction presents the essence of hydration in both poroelastic and viscoelastic functionality [48]. Several elements affect the mechanical properties of AC; however, researchers have circumnavigated through the complexities using customized techniques. For example, the sample-specific tissue composition has been used to predict the compressive mechanical behavior [49].

Depth-dependent mechanical properties of cartilage were also attained with optical imaging techniques such as relaxometry by MRI, which has demonstrated that under similar loading, different deformation patterns at different anatomical sites [50]. Cartilage degeneration is associated with deformation and its mechanics patterns before morphological symptoms. This finding complies with the depth-dependent mechanical properties under contact loading [50].

The cyclic loading effect on cartilage compaction was highlighted when its relaxation time was altered [40]. Moreover, static and dynamic loadings are other factors that significantly affect stress distribution over the cartilage. By dynamic loading, more uniform deformation across cartilage depth occurs, and this is because of substantial synovial fluid pressure in dynamic loading imposed on the cartilage compared to static loading. Thus, it exemplifies cartilage characteristics in reducing local strains in daily high intense physiological activities [51].

A novel method, known as Principle Component Analysis (PCA), has been developed to characterize cartilage mechanical properties with more abilities than conventional methods. This method is based on the surrounding tissue of the loaded area (L) and the transient strain (TS) of the AC during loading and unloading. L would be a benchmark to differentiate healthy and PG-depleted cartilage under loadings (deformation) and unloading (recovery) modes [52]. This framework is proving how PGs play a significant role in mechanical functioning.

#### **6. Tribological Properties of Articular Cartilage**

#### *6.1. Wear and CoF of Articular Cartilage Components*

Human knee or hip joints are subjected to up to one million cycles of loading per year during daily activities [53]. The rupture of the anterior cruciate ligament (ACL), or meniscal tears, is attributed to joints' misalignment, consequently affecting the joint kinematics, which increases the OA risk [54]. ACL and meniscus deficiency also cause excess tribological contact stresses due to instability of the joint and immediate fibrillation on the tibial plateau [55]. Several studies have presented that cartilage properties vary as the function of local contact stresses and mechanical environment; however, tribological properties have been reported to be location-independent [56,57]. Moore et al. [58] have shown that cartilage properties are location-independent and claimed that tribological properties also vary with respect to the local mechanics of the healthy joint. They found four primary tribological responses of the healthy cartilage: first, different regions have different damage tolerances. Secondly, material properties vary remarkably due to OA diseases. Third, different properties are the results of the healthy tibial plateau and OA cartilage. Fourth, OA tissues demonstrate different tribological performances that increase the shear stresses due to mechanical failure or biomechanical degradation [58]. Since cartilage is avascular, degenerated cartilage initiated from the superficial zone and propagated to the deep zone causes destruction of the layers through the thickness, resulting in gradual material loss. Cyclic loading induces stress through the entire cartilage structure yielding microscopic damage [59]. The superficial zone in AC experiences shear stresses and cracks within its collagen fibers. Therefore, AC damage occurs when the fibers crack rate exceeds the cell repair rate [60], and this phenomenon is called AC wear-off. AC presents a rubbery surface with a meager wear rate and CoF [6] but can be escalated by the absence of lubrication, abnormal loading due to varus or valgus knee alignment, aging and excess physiological activities [61].

Wear is the amount of material loss from the surfaces due to contacting asperities and friction. In AC, the wear mechanism is categorized as adhesive, abrasive and fatigue wear [62]. Cartilage wear is because of PGs loss and alterations in the collagen network [63]. Cartilage wear could be initiated due to biochemical degradation and biomechanical factors such as knee misalignment, which induces higher pressure on either the medial or lateral side of the knee joint [64]. Most of the studies have fallen short of quantifying wear mechanism due to its complex nature; hence only frictional properties have been investigated. Several studies used metal abrader against AC to quantify wear depth, and their results demonstrated that synovial fluid incorporation with trypsin effectively protects the cartilage surface against wear [65,66]. Other studies showed that the wear rate increases with increased contact pressure, area of contact, and sliding speed [67,68]. Wear rate can be

quantified by biochemical characterization of collagen and GAGs content [69]. Another method to capture wear depth and wear scar is surface topography, using scanning electron microscopy (SEM), transmission electron microscopy (TEM), atomic force microscopy (AFM), contact and non-contact profilometric methods [70,71]. Quantifying wear in AC is complex because of the deficient wear volume of soft tissues. An experiment was conducted to assess wear in AC and cartilage specimens loaded against stainless steel ball by steady sliding motion with 4.62 MPa contact pressure. Collagen loss was monitored as the wear rate indicator, and the results showed a low wear rate (0.5 µg/h at 4.62 MPa) in AC [7].

McCutchen [72] worked on the interstitial fluid and hypothesized that this fluid is the most load-bearing element in AC functioning. The author highlighted that since AC has deformable architecture, the interstitial fluid withstood most of the compressive state load. After this theory, Mow et al. [73] studied the biphasic structure and categorized it as incompressible and immiscible tissue. Katta et al. [56] then assessed that fluid could migrate through the porous AC architecture with tiny pore sizes in the range of 2.0–6.5 nm. In addition, Lai et al. [74] presented the triphasic theory, which considers monovalent ions in the interstitial fluid as the third phase. It showed three elements of fluid, solid and ion concentration are vital in identifying compressive stiffness of cartilage. Joint under compressive loading pressurize the interstitial fluid in the tissue. Such a pressure gradient in the tissue supports a significant contribution of the applied loads until the fluid is exuded away at the very beginning of the unloading period [75]. By the fluid pressurizing phase, the applied load is gradually transferred to the soft cartilage tissue, while the imposed load on the fluid is also gradually dissipated. At the equilibrium state, however, the load is tolerated by the soft cartilage tissue. Therefore, the solid phase of cartilage incorporated with interstitial fluid deprives CoF between cartilage mates. It can be maintained at a very low level as long as sufficient interstitial fluid is lubricating superficial layers of the cartilage [57].

Rehydration, contact stress, sliding contact materials and speeds are proportionally related to AC lubrication [76]. The sliding speed and stroke length are primary factors for controlling CoF and rehydration time. These factors control the wear in the cartilage surface as fluid carries the maximum load and results in a very low CoF in AC [77]. Contact stress was also reported to impact CoF significantly; increasing contact stress resulted in the reduction of CoF [78]. On the other hand, it has been shown that experimental parameters and rehydration would change the trend of decreasing CoF by increasing contact stress [57]. Consequently, Katta et al. [78] demonstrated that with increased contact stresses from 0.2 to 0.5 MPa, CoF decreased upon regular rehydration. Most of the cartilage frictional studies conducted have been based on the linear relationship between the applied load and CoF; however, further study is needed to investigate this relationship by a nonlinear trend.

Krishnan et al. [79] investigated friction in AC under cyclic compressive loading with various frequencies (0.05, 0.5 and 1 Hz). They reported that cyclic loading does not decrease CoF by increasing the interstitial fluid's pressurization compared to the static loading. Their study showed that relocation of contact areas effectively lowered CoF rather than the cyclic loading. On the other hand, another study showed that contact stress and stroke length (for rehydration process time) affect CoF detrimentally [80].

While fluid lubrication has been highlighted as a critical element of CoF variations in experimental studies [58,81], boundary lubrication shows a remarkable improvement since cartilage is biphasic and retains fluid in its superficial layer [82]. By lubricant depletion, the CoF is mostly altered as a function of surface chemistry [56]. Boundary lubrication has been recognized for its usefulness in tissue engineering purposes, joint lubrication, cartilage substitution therapies and several other applications [75].

Biological factors also have a significant impact on CoF in cartilage. GAGs/PGs formation and existence result in fluid pressurization and consequently variation in tribological properties [83]. These materials exhibit resistance against the interstitial fluid flow, leading to a low permeability rate (~10–15 to 10–16 m4/Ns) [84]. Aging or joint disease leads to a

reduction of GAG [85], which effectively increases the CoF rate [86]. Chondroitin sulfate is recommended in case of GAGs depletion; however, lubrication conditions must be considered [87]. Diffusing chondroitin sulfate into the cartilage reported results in a deficiency of ECM integration with chondroitin sulfate, and after imposing load, it is exuded out [56]. Collagen, another major component of cartilage, has also been reported to be effective in reducing CoF, and the lower level of collagen could exacerbate friction [88] and reduce water contents [89]. The SAL contains sulfated sugars, glycoproteins and lipids, which can be removed by wiping, resulting in higher friction than the unwiped surface [84].

#### *6.2. Boundary Lubrication*

Transition time in joint is shifting of dynamic to static loading or vice versa. When dynamic loading is gradually transformed to static loading, dissipating energy is mitigated by the interstitial fluid, and it permeates into the cartilage. At this stage, cartilage components absorb the synovial fluids, which initiate the boundary lubrication process [90]. Therefore, it yields to cartilage-on-cartilage contact that increases CoF.

Several studies have demonstrated the role of synovial fluid in minimizing CoF drastically under boundary lubrication regime [91,92]. Radin et al. [93] demonstrated that the proteinaceous layer has a load-bearing duty and not hyaluronic acid (HA) in the synovial fluid. In contrast, other researchers have shown that HA significantly supports the interstitial fluid in withstanding load [88,94,95]. Tests using HA on healthy and dysfunctional cartilage for both humans and bovine showed a remarkable decrease in CoF [88]. This effect is limited to lowering CoF in dynamic loading, even under static pressure, while boundary lubrication occurs. HA penetrates into the cartilage structure and surrounds the chondrocytes, which preserves the CoF levels [95].

Lubricin, a mucinous glycoprotein, is another component of synovial fluid has been reported that lack of lubricin in synovial fluid resulted in inadequate boundary lubrication and increases wear in cartilage [70]. This research showed that in the presence of lubricin, adhesion between contacting cartilage is minimized, and this process yields to decreased friction upon boundary lubrication [70].

As another component of synovial fluid, phospholipids contributed significantly to boundary lubrication due to the hydrophobic nature of its fatty acid [96]. Hills and Crawford [97] reported that phospholipids are a component of lubricin in the boundary lubrication, whereas lubricin and HA only supported the phospholipids. Furthermore, Pickard et al. [98] demonstrated that elimination of phospholipid from the cartilage increases the CoF of cartilage minimally. Their study was just limited to the short time; however, no remarkable effect was reported at a prolonged time regarding the cartilage friction properties.

According to the literature, all mentioned components of synovial fluid effects boundary lubrication, and isolating any component can compromise the boundary lubrication process. Moreover, the biomechanical and biochemical synergies may also be insufficiently controlled, as it is in a synovial joint. Nevertheless, all these findings are the expedient benchmark to characterize wear and CoF in AC.

#### **7. Tissue Engineering of Articular Cartilage**

Cartilage tissue engineering has been investigated extensively by researchers since this tissue is avascular, and confined migration of chondrocyte reduces its self-recovery considerably. Therefore, the essence of artificial cartilage motivates researchers to design and manufacture materials mimicking mechanical and tribological responses of the native cartilage. Polymeric hydrogels have been highlighted as candidates for this application as they resemble the biomechanical, biochemical and architectural properties of native cartilage [99]. Hydrogels have also appealed to researchers due to their biocompatibility [100], nontoxicity effects and no stimuli on the immune system [101]. Hydrogels are categorized as natural and synthetic and can be modulated with cell-free or cell-laden scaffolds. Some of the cell-free scaffolds have been presented with the use of bacterial nano-cellulose [102], polyethylene glycol (PEG) in combination with HA [103], collagen-hydroxyapatite hybrids [104], aragonite-hyaluronate membranes [105], acrylamide (AAm) hydrogels [106], alginate (Alg)/chitosan compounds, agarose/polyglycolic acids (PGA) [107], and porous polycaprolactone (PCL) [108]. The mentioned scaffolds were used clinically; however, after clinical follow-up in the longer term, they were rejected due to the lack of strength and durability. The following sections describe some of the common materials used in the manufacture of hydrogels.
