Synovitis
Stretching of the joint capsule
Periosteal elevation
Pain at tendon and ligament insertion sites (enthesopathy)
Muscular hypertonus
Increased intra-articular pressure
Bone microfractures
13.4 Risk Factors of OA Development
In addition to the pathobiochemical factors, the following risk factors may participate in the OA pathogenesis:
- 1.
Genetic factors
- 2.
Congenital and developmental defects
- 3.
Overloading of joints during physical work or sporting activities
- 4.
Obesity, reduction of body weight slows down the disease progression, e.g. in OA of the knee
- 5.
Impaired joint innervation (dysfunction of protective reflex mechanisms)
- 6.
Metabolic and endocrine diseases
- 7.
Hypermobility
A number of studies have described a family history of Heberden’s nodes inherited as a single autosomal dominant gene, with a strong female predominance. In the generalised nodal form, association has been revealed with HLA-A1 and B 8 and with α1-antitrypsin MZ phenotype. Early onset of OA was found also in familial diseases, such as chondrocalcinosis and ochronosis. The list of genetic associations with OA is quite broad, including the genes encoding molecules of extracellular matrix, collagen COL2A1 or COMP (cartilage proteoglycan), genes controlling skeletal development, such as BMP proteins (bone morphogenetic proteins; ASPN, BMP2) or Wnt signalling genes, as well as genes for inflammatory cytokines (IL-1, IL-6, IL-10 [9]). Meta-analysis of human genome-wide association studies has confirmed a susceptibility locus for knee osteoarthritis on chromosome 7q22 [10].
Factors contributing to OA development are also age-related involutionary changes of the musculoskeletal system, although the specific features of an ageing joint differ from the arthritic one in morphological, radiological as well as biochemical terms. In OA, cartilage fibrillation results in disintegration of chondrocytes and their general loss due to catabolic processes, while the ageing cartilage is characterised by loss of chondrocytes due to reduction of their replication ability [19].
13.5 Clinical Features
The main OA symptom is pain in the affected joint, occurring initially only after increased load. Tolerance to load gradually decreases. So-called start-up pain which usually works itself out after a few steps is typical of weight-bearing joints. At later OA stages, there occurs pain also during physical inactivity and at night, signalling further OA progression.
Sometimes it is impossible to move the joint through its full range of motion without any obvious cause, and sometimes the limited flexibility is caused by increasing pain. Morning stiffness, if any, subsides relatively quickly as compared to rheumatoid arthritis. A small effusion may be also present in certain cases.
Objective Symptoms of Osteoarthritis
Crepitus – popping and cracking sounds in joints indicating an uneven articular surface
Thickening and condensation of bone structures – joint deformation and remodelling (osteophytes)
Restricted range of motion – advanced OA stage
“Stretching” pain – in extreme ROM positions (periarticular structures)
Loss of axial alignment – varus/valgus deformity (knees, hips), deformities (DIP)
Joint instability – ligament injury
Pain at night often resulting from increased blood supply to the subchondral bone
Muscle atrophy – due to inactivity
13.6 Osteoarthritis Forms
13.6.1 Osteoarthritis of the Hip
OA of the hip is the most severe form of osteoarthritis [3], with pain concentrated initially in the groins, the region of greater trochanter and the buttocks. Most often the pain radiates through the anterior thigh and below the knee. Progression of the disease is potentiated by imbalance between muscle groups that stabilise the pelvic girdle, which results in flexion, adduction and external rotation of the lower extremity. Muscle weakness affects most of the hip extensors and abductors. As a rule, the first affected muscle is the gluteus medius, which is of an important diagnostic value (Trendelenburg sign).
Complaints are intermittent; in the active phase, all symptoms deteriorate, pain is more intensive and the range of motion of the joint is limited. However, the disease prognosis is not always poor, as its progression may be halted and the intensity of its symptoms may decrease (Figs. 13.1 and 13.2).
Fig. 13.1
Pelvis: OA of the hip, degree III, bilateral, with a thick concentric osteoplastic lining of the rims of articular surfaces of both femoral heads, subchondral sclerosis, geodes and central joint space narrowing in both hips, thinning of the acetabular floor with initial protrusion and bilateral varus deformity of both hips, SI joints intact
Fig. 13.2
Pelvis – right hip: deformity of the right femoral head after osteonecrosis with secondary osteoarthritic changes, shortening and varus deformity of the femoral neck, left hip intact, SI joints intact, calcified formation in the small pelvis, probably a calcified myoma
13.6.2 Osteoarthritis of the Knee
OA of the knee is the most prevalent form of arthritis [11]. In younger age groups, it affects more men, while with advancing age, its incidence is higher in women. As a rule it occurs bilaterally and is often associated with obesity. Clinical manifestations of OA of the knee depend on the prevailing locations of osteoarthritic changes in the knee joint. It involves more frequently the medial tibiofemoral compartment and results in a typical varus deformity of the knee joint. The frequency of involvement of the patellofemoral compartment is almost the same. Typical pain in the knee joint gets worse during climbing up and down the stairs and walking on uneven ground. Short-term pain may be experienced with the transition from sitting to standing or with passive motion, forced hyperextension in particular. OA of the knee lasting for a longer time results in atrophy of the quadriceps, mainly the vastus medialis, and there develop painful enthesopathies of the patellar tendon and the pes anserinus. OA of the knee is often associated with the generalised OA form, and its prognosis is worth than in OA of the hip (Figs. 13.3, 13.4, 13.5, 13.6, 13.7 and 13.8).
Figs. 13.3, 13.4 and 13.5
Knee joints: varus deformity in both knee joints, subchondral sclerosis and osteophytosis of the rims of articular surfaces particularly on both femurs – degree III arthritis, bilateral, necrosis of medial tibial condyle and periarticular ossification
Figs. 13.6, 13.7 and 13.8
Knee joints: degree III OA of the knee, bilateral, varus deformity, bilateral subchondral sclerosis of both tibiofemoral and patellofemoral joints with marginal osteophytes; on the right, necrosis of the medial tibial condyle and probably calcified enchondroma in distal femoral metaphysis
13.6.3 Arthritis of the Joints of the Hand
The joints commonly affected by the disease are DIP joints (Heberden’s nodes) or PIP joints (Bouchard’s nodes), when bony nodules develop on their posterior and lateral borders of IP joints. These nodules are usually preceded by gelatinous cysts. Occasionally the pain in the joint may get worse, with swelling and reddening of the joint. Gradually there develop typical deformities, such as lateral subluxations and deviations primarily of the DIP joints. Arthritis of both the DIP and PIP joints has a good prognosis, and the function of the affected joints is not usually affected (Figs. 13.9, 13.10, 13.11 and 13.12).
Fig. 13.9
Hands, prevalence of arthritis in the PIP joints: Degree III arthritis both in the DIP and PIP joints of both hands, with progressive marginal osteoproductive changes dominating mainly in the PIP joints bilaterally, degree I rhizarthrosis, bilateral
Fig. 13.10
Hands, prevalence of arthritis in the DIP joints: joint space narrowing in the PIP but mainly in the DIP joints of both hands, subchondral sclerosis, marked marginal osteoproduction, semi-flexion and initial ulnar drift – degree III arthritis bilaterally, degree II rhizarthrosis bilaterally
Fig. 13.11
Hands, erosive osteoarthritis: Degree III polyarthritis in the DIP and PIP joints of both hands with marked deformities, ulnar drift, in some of the PIP joints arthritis is almost of erosive nature, in PIP3 on the right and PIP4 on the left even ankylosis – degree IV arthritis, degree III rhizarthrosis on the right, degree II rhizarthrosis on the left, degree II arthritis of the trapezioscaphoideal joint bilaterally
Fig. 13.12
Hands: degree II arthritis in the DIP joints bilaterally and in PIP2 on the right, degree III rhizarthrosis on the left, degree I on the right
Arthritis of the first carpometacarpal joint – rhizarthrosis – is characterised by pain and tenderness at the base of the thumb, mainly during pinching or grasping objects. Mobilisation of the thumb is associated with crepitus; at later stages there occurs thumb adduction contracture, often with hyperextension of the proximal phalanx, and the base of the thumb squared in shape. Unlike arthritis of the DIP and PIP joints, this OA type has a marked and permanent negative impact on the function of the hand. The condition may be improved by surgery.
A rare disorder of small joints of the hand (PIP and DIP joints) is erosive osteoarthritis. It is characterised by inflammatory manifestations, particularly painful swelling of these joints. Radiological examination shows subchondral erosions. The disease occurs in episodes and may result even in ankylosis of one or more joints [17]. Clinical examination of OA should be combined with radiological examination which reflects pathological processes in the cartilage and the subchondral bone.
Radiological Findings in Osteoarthritis
Osteophytes – marginal bony outgrowths (remodelling)
Joint space narrowing as a result of reduction of the cartilage height
Subchondral bone sclerosis – manifestation of pathological processes in the subchondral bone
Subchondral cysts proving the impaired cartilage integrity
Remodelling of the bone surface and change of the bone shape
Relevant radiographic visualisation of the relationships in the joint depends on accuracy of the techniques used. Even the smallest deviations may distort the information about the width of the joint space and consequently about the height of the articular cartilage. It may be stated that typical OA symptoms in bones and joints already prove an advanced stage of the disease (Figs. 13.13, 13.14, 13.15, 13.16, 13.17, 13.18, 13.19, 13.20 and 13.21). In order to obtain more information about the condition of the cartilage, radiographic images may be magnified, or digital analysis may be made of the images stored in digital form.
Fig. 13.13
Feet: hallux valgus, asymmetrical lateral joint space narrowing to minimum and marginal osteophytes – degree III arthritis in the MTP1 joint on the left
Figs. 13.14 and 13.15
Left elbow: degree II arthritis with joint space narrowing and marginal osteophytes mainly in the humeroulnar articulation, varietal small bones below the ulnar epicondyle of the humerus
Figs. 13.16 and 13.17
Shoulders: joint space narrowing in both glenohumeral joints – more progressive pronounced on the left, deformed humeral head and reduction of subacromial space, with a large inferior osteophyte, subchondral sclerosis and small geodes – degree II omarthritis on the right, degree III on the left
Fig. 13.18
The right acromioclavicular articulation: large osteophytes and joint line narrowing – degree II–III arthritis of AC joint on the right
Fig. 13.19
(a) C spine: cervical lordotic compensation, polydiscopathy of the type of osteochondrosis of degree II to III in the entire C segment, anterior contours of vertebral bodies with a hyperostotic lining reaching the maximum on the anterior part of C4 vertebral body. (b) C spine: uncarthrosis of degree II to III in the entire C segment
Fig. 13.20
Th spine: sinistro-convex scoliosis, degree II osteochondrosis of Th6–8, degree III osteochondrosis of Th9–12, with vacuum phenomenon and pronounced anterior and lateral spondylosis, in Th8–9 segment synostosis of vertebral bodies, reduced and wedge-shaped deformity of Th7 vertebral body at the apex of kyphotic curve. (a) LL view (b) AP view
Fig. 13.21
LS spine: dextroscoliosis with a slight rotation of vertebral bodies, in L1–5 segments degree III osteochondrosis with vacuum phenomenon, subchondral sclerosis of endplates and marked spondylosis, the most prominent changes in the L3–L4 segment, L3 vertebral body causes impression of the anterior part of L4 vertebral body, degree I retrolisthesis of L5. (a) AP view (b) LL view
Ultrasonography is increasingly used, which reveals even a small joint effusion and provides valuable information about the condition of periarticular structures.
Discrepancies may be found between the radiological and clinical findings as progressive radiological changes do not necessarily have a clinical response and vice versa [3].
13.7 Classifications
- 1.
Idiopathic OA may involve:
Hands (Heberden’s and Bouchard’s nodes, CMC I) erosive form
Feet (MTP 1)
Hip joints
Knee joints
Spine (C and L segments)
Generalised OA affects at least three joints.
- 2.
Secondary OA results from:
Trauma (fractures, mainly intra-articular, soft tissue injuries)
Microtraumas (overload caused by practising intense physical exercise or work)
Anatomical changes
Epiphysiolysis, developmental dysplasia of the hip
Hypermobile syndrome, unequal limb length
Metabolic diseases (Gaucher’s disease, hemochromatosis and others)
Endocrinopathy (acromegaly, diabetes mellitus, hypothyroidism, hyperparathyroidism)
Crystal deposits (calcium pyrophosphate, hydroxyapatite, uric acid)
Inflammatory diseases (rheumatoid arthritis, infectious arthritis)
Arthritis may affect all joints, with prevalence in small joints of the hand and the spine. A severe complication is involvement of weight-bearing joints, knees and hips, which restricts the patients’ general mobility, permanently decreases their quality of life and quite often results in total disability.
13.8 Diagnostic Criteria
Criteria for establishment of OA diagnosis have been developed by ACR (the American College of Rheumatology; 2000; 13).
Diagnosis of Osteoarthritis of Small Joints of the Hand Is Confirmed if the Following Symptoms Are Present
- 1.
Pain, aching or stiffness in the hands for the majority of days during the last month
- 2.
Hard tissue enlargement involving at least two of ten selected joints
- 3.
Swelling of two or more metacarpophalangeal (MCP) joints
- 4.
Hard tissue enlargement of at least two distal interphalangeal (DIP) joints
- 5.
Deformity of at least one of the ten selected joints
The ten selected joints include bilateral DIP II, III; PIP II, III; CMS I.
OA is diagnosed if the criteria 1, 2, 3 and 4 or 1, 2, 3 and 5 have been met.
Diagnosis of OA of the Hip
- 1.
Hip pain for the majority of days during the last month
- 2.
ESR less than 20 mm/h
- 3.
Radiographic femoral or acetabular osteophytes
- 4.
Axial joint space narrowing
OA of the hip is diagnosed if criteria 1 and 2 or 1, 3 and 4 have been met.
Diagnosis of OA of the Knee
- 1.
Knee pain for the majority of days during the last month
- 2.
Osteophytes along articular edges
- 3.
Non-inflammatory joint effusion
- 4.
Age over 40 years
- 5.
Morning stiffness for less than 30 min
- 6.
Crepitus on active motion
OA of the knee is diagnosed if criteria 1 and 2 or 1, 3, 5 and 6 or 1, 4, 5 and 6 have been met.
13.9 Therapy
The aim of all therapeutic interventions is to reduce or resolve pain, maintain the joint mobility and slow down the disease progression [13, 14]. In order to be efficient, OA treatment requires a timely diagnosis, examination of the scope of functional involvement and knowledge of the patient’s activities of daily living. Patients should follow certain general measures that will allow them to overcome more easily the OA-related complications.
General Measures in the Management of Osteoarthritis
Weight loss (for persons who are overweight)
Observance of principles of well-balanced diet
Maintenance of general physical fitness
Load-bearing exercises without overusing the affected joint
More frequent bed rest in the active phase of the disease
The use of appropriate assistive devices
Treatment should always begin with non-pharmacological therapy.
Therapeutic Programme Includes
Patient education
Physical therapy
Physical medicine
Appropriate footwear, braces, crutches and assistive devices
Pharmacological treatment
Surgical treatment
Patient Education
Patients with OA should be appropriately informed about the nature and course of the disease, its treatment options and the need for their active cooperation, particularly in terms of observance of general recommendations [15].
Rehabilitation Therapy
The aim of physical therapy in OA treatment is maintenance of the range of motion, muscle strength, muscle balance and improvement of the patient’s general condition [16, 17]. Physical therapy is required in the spine involvement and is inevitable in the management of hip and knee OA. Imbalance of the hip and knee joints developed already at early stages of OA of weight-bearing joints results in incorrect movement patterns. Of great importance is maintenance of the strength of the quadriceps and the gluteus maximus that are often considerably weakened, but their adequate cooperation allows the patient to perform activities of daily living (rising from a chair, stair climbing). Low-impact exercises in suspension or aquatic physical therapy are highly efficient in this respect. Aerobic exercises, preferably walking, are indicated in stabilised periods of the disease. Physical therapy in the management of OA of the spine should focus on achievement of balance between the chest and back muscles and abdominal muscles.
Physical Therapy
Physical therapy may help relieve pain, improve local metabolism or reduce inflammatory manifestations [18]. Thermotherapy (paraffin wax, hot wet pack) and electrothermotherapy are used during stabilised periods of the disease activity, while in its active phase, cryotherapy and electroanalgesia (TENS and medium frequency currents) are locally applied. Pain in OA of the knee is successfully managed also by acupuncture. Both reflexive and classic massage techniques may be used to manage muscle spasms and reflexive mechanisms, mainly in osteoarthritis of the spine. Spa therapy is in OA indicated as a priority together with other forms of physical therapy.
Orthopaedic (Orthotic) Devices
In OA of the weight-bearing joints and the spine, it is necessary to correct abnormal position. Transverse and longitudinal flat foot should be addressed by appropriate insoles or orthopaedic footwear. Of great importance is correction of the limb length prior to the use of insoles. Varus or valgus deformity of the knee or its instability should be treated with custom-made braces. In case of more progressive OA of the knee or hip joints, the patients must use forearm walking crutches. Patients are recommended to adjust their home setup by raising chairs or toilet seat, installation of hand rails in the bathtub, etc. Radicular pain in OA of the spine may be relieved by a lumbar support belt to treat low back pain or a cervical collar to support the cervical spine.
13.10 Pharmacological Treatment of Osteoarthritis
Breakdown of pharmacological OA treatment is shown in Table 13.2.
Table 13.2
Pharmacological treatment of osteoarthritis
(a) Symptomatic drugs |
1. With a short-term rapid-onset effect: |
Non-steroidal anti-inflammatory drugs |
Analgesics |
Intra-articular glucocorticoids |
Local treatment |
2. With a long-term slow-onset effect of glucosamine sulphate: |
Chondroitin sulphate |
Hyaluronic acid |
Diacerein |
ASU (unsaponifiable extract from avocado and soybean oil) |
(b) Structure-modifying drugs |
(c) Experimental treatment |
13.11 Rapid-Onset Drugs
Their rapid onset of action within a few hours terminates after discontinuation of the therapy. These drugs do not influence the course of the disease, but have analgesic and anti-inflammatory effect [3, 19].
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