Orthopedics Hyperguide Review | Dr Hutaif General Ortho -...

The three articular cartilage collagens that form cross bands are types II, IX, and XI. Of particular note:
Type XI binds to type II.
Type IX binds to the cross-banded fibrils in the superficial layer. Type VI attaches to the matrix around the chondrocytes.
Type X is near the calcified layer and is probably involved in mineralization of the calcified layer.

Decorin and fibromodulin bind to type II collagen and likely stabilize the type II collagen network. The other responses refer to:
Biglycan: Binds with type VI collagen
Anchorin C II: Helps attach chondrocytes to the collagen fibrils
C OMP: Binds to chondrocytes

The superficial zone has a number of important characteristics: Thinnest articular cartilage layer
Two layers:
Most superficial – fine collagen fibrils (lamina splendens)
Deep layer – flattened fibroblast-like chondrocytes (parallel to joint surface) Forms a cartilage skin
Important chemical properties:
High collagen and low proteoglycan concentration
Fibronectin and water concentrations are highest in this zone
Great tensile stiffness and strength
Seals off the cartilage from the immune system

The superficial zone has a number of important characteristics: Thinnest articular cartilage layer
Two layers:
Most superficial – fine collagen fibrils (lamina splendens)
Deep layer – flattened fibroblast-like chondrocytes (parallel to joint surface) Forms a cartilage skin
Important chemical properties:
High collagen and low proteoglycan concentration
Fibronectin and water concentrations are highest in this zone
Great tensile stiffness and strength
Seals off the cartilage from the immune system

The superficial zone has a number of important characteristics: Thinnest articular cartilage layer
Two layers:
Most superficial – fine collagen fibrils (lamina splendens)
Deep layer – flattened fibroblast-like chondrocytes (parallel to joint surface) Forms a cartilage skin
Important chemical properties:
High collagen and low proteoglycan concentration
Fibronectin and water concentrations are highest in this zone
Great tensile stiffness and strength
Seals off the cartilage from the immune system

The transitional zone lies between the superficial and middle zones of the articular cartilage. The following important points should be remembered:
The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
The collagen fibers are larger than in the superficial zone.
The proteoglycan concentration is higher than the superficial zone.

The chondrocytes in the calcified cartilage zone show the least metabolic activity. In contrast, the chondrocytes of the other areas are very active:
Superficial zone
Fine collagen fibrils (lamina splendens)
High collagen and low proteoglycan concentration
Fibronectin and water concentrations are highest in this zone
Transitional zone
The chondrocytes have a high concentration of synthetic organelles such as rough endoplasmic reticulum and Golgi apparatus.
The collagen fibers are larger than in the superficial zone.
The proteoglycan concentration is higher than the superficial zone. Middle (radial or deep) zone
Largest diameter collagen fibrils
Highest proteoglycan content

Interleukin I has the potential to increase expression of matrix metalloproteinases that can dissolve the extracellular matrix. The other responses are anabolic factors:
Insulin-dependent growth factor I Transforming growth factor beta Bone morphogenetic protein 2
Bone morphogenetic protein 7

Type II collagen fibers resist tensile and shear deformation forces in the articular cartilage.
In contrast, the glycosaminoglycan aggregates resist articular cartilage compression and fluid flow.

Type II collagen fibers resist tensile and shear deformation forces in the articular cartilage.
In contrast, the glycosaminoglycan aggregates resist articular cartilage compression and fluid flow.

C yclic compressive loads have the ability to stimulate matrix synthesis â aggrecan core protein and the glycosaminoglycans. The other responses are catabolic toward the cartilage â break the cartilage down:
Tumor necrosis factor
Interleukin I
Matrix metalloproteinases
C hronic compressive loads outside the physiologic range
Static compression (eg, putting a patient in a cast)

The characteristic findings in osteoarthritis are:
Asymmetric loss of the joint space Subchondral sclerosis and cysts Osteophyte formation
As the cartilage degenerates, progressive bone remodeling occurs. The other responses refer to other synovial proliferative disorders:
Pigmented villonodular synovitis: Synovial proliferation, cysts/erosions on both sides of the joint
Rheumatoid arthritis: Synovial proliferation with lymphocytic infiltration, periarticular osteopenia, symmetric joint space loss
C harcot neuropathy: Subluxation, bone fragmentation, dissolution of the articular surfaces
Gout: Periarticular erosions, soft tissue masses, preservation of the articular surfaces

The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
C onstant type II collagen content
Decreased proteoglycan concentration and decreased chain length
Increased water content
The decreased proteoglycan content results in increased permeability of the cartilage. A reduction of the stiffness makes the articular cartilage less able to bear loads.

The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
C onstant type II collagen content
Decreased proteoglycan concentration and decreased chain length
Increased water content
In the second stage, there is a cellular response â chondrocyte proliferation. C lusters of chondrocytes producing new matrix are visible.
In this stage, there is nitric oxide and interleukin I production. These are catabolic factors that increase matrix metalloproteinase activity. Degradative enzymes break down types IX and XI collagen, which may compromise the stability of the type II collagen framework.

The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
C onstant type II collagen content
Decreased proteoglycan concentration and decreased chain length
Increased water content
In the second stage, there is a cellular response â chondrocyte proliferation. C lusters of chondrocytes producing new matrix are visible.
In this stage, there is nitric oxide and interleukin I production. These are catabolic factors that increase matrix metalloproteinase activity. Degradative enzymes break down types IX and XI collagen, which may compromise the stability of the type II collagen framework.

The cause of osteoarthritis is unknown. From a chemical standpoint, one of the earliest findings is a decrease in the proteoglycan and an increase in the water content. One should remember:
C onstant type II collagen content
Decreased proteoglycan concentration and decreased chain length
Increased water content
In the second stage, there is a cellular response â chondrocyte proliferation. C lusters of chondrocytes producing new matrix are visible.
In this stage, there is nitric oxide and interleukin I production. These are catabolic factors that increase matrix metalloproteinase activity. Degradative enzymes break down types IX and XI collagen, which may compromise the stability of the type II collagen framework.

In the last stage of osteoarthritis, there is reduced chondrocyte proliferation and function, which may be secondary to reduced ability to respond to anabolic factors (down regulation). There may be accumulation of molecules that bind to the anabolic factors (and keep the factors from the chondrocytes) such as decorin and insulin-dependent growth factor binding protein.

The recurrence rate of a previously resected neuroma is approximately 15%. The deep transverse metatarsal ligament is involved in the pathogenesis of a primary, but not a recurrent, neuroma. None of the present symptoms suggests tarsal tunnel syndrome, although this may exist concurrently with a neuroma. Phenol has ablative neural properties, but it cannot be injected due to the local effect on tissue necrosis.

In the presence of metatarsalphalangeal joint arthritis, either resection arthroplasty or arthrodesis is recommended. However, with this degree of intermetatarsal deformity, a resection arthroplasty may lead to a high recurrence rate of hallux valgus deformity.

The abductor hallucis muscle attaches to the tibial sesamoid and resection without repair of the abductor and medial capsule may lead to hallux valgus. Hallux varus may occur after resection of the fibular sesamoid, and a cock-up extension hallux deformity occurs after resection of both sesamoids or with a rupture of the volar plate.

Although the woman may wish to wear shoes of varying height, there is sufficient plantarflexion occurring through the transverse tarsal joint to permit the wearing of high-heel shoes. Any plantarflexion of the fusion will cause arthritis of the transverse tarsal joint, particularly the talonavicular joint. Dorsiflexion of an ankle arthrodesis is associated with a calcaneus position and heel pain. The ankle should be fused in a similar position for both male and female patients.

The presence of posterior tibial tendonitis in a young individual should raise the concern for seronegative arthritis. Although a stress fracture of the medial malleolus may be present, pain is not exacerbated with resisted inversion.

Subtalar instability is not common, although a component of instability may be present in conjunction with ankle instability. If symptoms are suggestive of ankle instability but cannot be verified upon clinical or radiographic examination, then subtalar instability is likely to be present. The clinical diagnosis of subtalar instability is difficult.

With the exception of physical therapy and a rigid orthotic support, most of the treatment alternatives would be helpful in the initial treatment of plantar fasciitis. Achilles stretching combined with a soft, gel-type heel cushion is consistently the most successful modality.

Ankle replacement is a treatment alternative that is widely recommended today, although it is still not as reliable as an ankle arthrodesis in terms of predictability and absence of complications. One must consider the option of arthrodesis and replacement carefully with each patient.

Although arthrodesis has proved reliable with respect to managing tarsal coalition in the adult, resection of a calcaneonavicular coalition should be performed whenever possible. This procedure is preferable to a triple arthrodesis. A subtalar arthrodesis would be applicable as treatment for a middle facet coalition in the adult.

Planing or shaving of the sesamoid is a reliable procedure for treatment of a specific focal keratosis beneath the tibial sesamoid. Resection of the tibial sesamoid is a reasonable alternative, although it should be used only for pathology of the sesamoid itself. In this individual, the position of the first metatarsal is normal. Since no plantarflexion is present, an osteotomy is not indicated.

The patientâs history and clinical findings indicate an injury to the tarsometatarsal joint complex, specifically between the middle and the medial columns. Although surgery may become necessary, initial treatment should consist of support. Physical therapy will worsen foot pain and injection is not indicated.

Preservation of the joint and maintaining range of motion are important to any active individual. Any procedure, such as resection or implant arthroplasty, is contraindicated in this age group. Arthritis has not progressed to the degree that arthrodesis is necessary.

If there is a contraindication to performing surgery, nonoperative methods of treatment for an acute C harcot neuroarthropathy may be acceptable. This patientâs midfoot is dislocated and is likely to result in a worsening deformity over time, with ulceration and infection possible. Open reduction with internal fixation has not proven sufficient in patients presenting with the symptoms indicated in the scenario. Arthrodesis is most likely to yield a satisfactory outcome.

This patient has a rupture of the posterior tibial tendon. Repair of the tendon will not work because there is a degenerative elongation of the tendon that will not heal. Because the foot is flexible, arthrodesis is not necessary. Flexor digitorum longus transfer with calcaneal osteotomy is a reliable procedure for treatment of Stage II posterior tibial tendon insufficiency.

The deep transverse metatarsal ligament passes between the undersurface of the metatarsal heads and connects the volar plate
to the adjacent soft tissue structures. The common digital nerve becomes irritated under the sharp edge of the distal portion of the ligament, resulting in nerve swelling and formation of the neuroma.

It is unusual for an adolescent to require surgical correction of a flatfoot deformity, however, when the deformity is markedly symptomatic, surgery is a reasonable treatment option. Arthrodesis should not be considered as treatment of the flexible flatfoot in the adolescent. There is no indication of an accessory navicular bone being present. Lateral column lengthening (Evans Procedure) is a reliable procedure in this age group. The most common correction in kids with severe flexible pes planus is a lateral column lengthening. This is because most children, such as in this case, have severe forefoot abduction with significant talo-navicular uncoverage. (The description stated that the patient had a callus under the talar head, which means the talus is
protruding beyond the navicular medially.) Medial slide calcaneal osteotomy would only correct the heel valgus, whereas a lateral column lengthening has the potential to correct both heel valgus and forefoot abduction.

The gold standard surgical treatment for rheumatoid patients with severe forefoot deformities is first metatarsophalangeal fusion with second through fifth metatarsal head resections.

Each of the possible answers may occur following triple arthrodesis. In numerous studies, ankle arthritis is the complication most likely to occur regardless of the underlying disease process.

A pantalar arthrodesis is the combination of an ankle and triple arthrodesis. It should not be confused with an ankle and subtalar arthrodesis (tibiotalocalcaneal).

By history, this patient has hereditary sensorimotor neuropathy (C harcot-Marie-Tooth disorder). Historically referred to as peroneal muscular atrophy, this condition initially affects the peroneus brevis, followed by the intrinsic and anterior tibial muscles. Other patterns of deformity and muscle loss are occasionally present.

Although resection arthroplasty (Keller procedure) may be a reasonable alternative, arthrodesis of the hallux metatarsophalangeal joint is required in the presence of arthritis. Other alternatives, such as osteotomies, are impractical.

The first branch of the lateral plantar nerve (occasionally referred to as the nerve to the abductor digiti quinti) is occasionally involved in pathologic painful heel syndrome and plantar fasciitis.

A foot salvage amputation, including the transarticular ankle amputation (Symeâs amputation), will not work in the presence of a disrupted heel pad (with or without ulceration) and infection of the heel.

By history and physical examination, this patient has a Stage III flatfoot deformity. Due to the rigidity, only an arthrodesis will correct this abnormality. Although a transverse tarsal arthrodesis (C hopartâs arthrodesis) may adequately correct the deformity, a triple arthrodesis will correct all of the components including heel valgus, forefoot abduction, and midfoot pronation.

Management of the non-infected plantar neuropathic ulcer is nonoperative, with the exception of refractory recurrent ulceration. In this case, surgery may be indicated. The most reliable means of healing the ulcer is with the use of a total contact cast that
permits immediate ambulation and protection for the rest of the foot. Shoe modifications are required following healing of the ulcer but are insufficient as part of the initial treatment program.

Because of his history, this patient may have a compartment syndrome of the foot. Although other studies may be relevant as part of his evaluation, a compartment syndrome mandates emergency treatment. Vascular evaluation, including laser Doppler flowmetry is unreliable in diagnosing compartment syndrome. Imaging studies may be performed as part of the surgical work-up, but they are not indicated at this time.

This patient presents with symptoms of a tarsal tunnel syndrome, specifically involving the medial plantar nerve. Because she did not experience any initial pain relief from her surgery, one may suspect that an inadequate release was initially performed. C ortisone injection and physical therapy have no role in the management of a recurrent tarsal tunnel syndrome, although desensitization treatments with neuroleptic medication and manual massage are beneficial following surgery. It is important to rule out a sympathetically mediated pain syndrome prior to embarking on repeat surgery.

For athletes, particularly those involved in activities that require repetitive proprioceptive and balance activities of the foot and ankle, an anatomic repair (Brostrom procedure) with addition of the extensor retinaculum (Gould modification) is the only procedure that will allow this individual to return to athletic activity. Surgeons must not sacrifice the peroneal tendon, or part thereof, since this may unnecessarily weaken the foot.

This patient has an osteochondral defect of the talus. According to most classification systems, the grade of the defect is not severe. Retrograde drilling of the defect through the sinus tarsi is possible for a posteromedial lesion of the talus for which the cartilage surface is intact. An autogenous osteochondral bone graft is indicated for a severe lesion with bone loss or following failure of previous attempts at arthroscopic drilling. The ideal procedure is arthroscopic debridement and drilling of the subchondral bone.

Although pigmented villonodular synovitis (PVNS), infection, or gout may cause inflammatory changes on both sides of the ankle joint, the most likely cause of this inflammatory arthropathy is rheumatoid arthritis. Note the cystic changes, the synovial hypertrophy, and the joint inflammation.

It is imperative that any diastasis of the tibiofibular joint is repaired to prevent the late sequelae (e.g., arthritis), particularly in the athlete. Arthroscopy is not sufficient, other than evaluation for additional joint pathology, and syndesmosis arthrodesis would
rarely be indicated for this condition. There is no evidence of a high fibula fracture, although this must be a concern and should always be considered.

The reported recurrence rate following excision of a primary interdigital neuroma is approximately 15%. The recurrence rate should always be communicated to the patient preoperatively.