AORF Textbook of Orthopaedics: African Orthopaedic Research Foundation (AORF) Edition

ORTHOPAEDICS; An Introduction

The Origin of Orthopaedic practice can be traced back to the 16th Century. NICHOLAS ANDRY (1658-1759), professor of Medicine at the University of Paris and Dean of the faculty of Physick, in 1741, at the age of 81, published a famous book entitled Orthopaedia or the Art of Correcting and Preventing Deformities in Children. In this book, the word Orthopaedic, which derives from the Greek words straight and child, is presented.

Long before the word orthopaedics was coined, the art of orthopaedics was practiced in line with other forms of medicine. In ancient Greece, the works of Hippocrates detail the treatment for dislocations of the shoulders, knees, and hips as well as treatments for infections resulting from compound fractures. In Egypt splints made of bamboo, reeds, wood or bark padded with linen have been found on mummies.

During the Greco-Roman period, there were also attempts to provide artificial prostheses. There are accounts of wooden legs, iron hands and artificial feet. There is a remarkable link between the origins of modern orthopaedics in the United Kingdom (and subsequently in North America) and the Anglesey bone setters of the 18th century.

Many developments in orthopedic surgery resulted from experiences during wartime. On the battlefields of the Middle Ages, the injured were treated with bandages soaked in horses’ blood which dried to form stiff, though unsanitary, splints. Traction and splinting developed during the 1st World War. Since the 2nd World War, orthopaedic treatment has evolved to include joint replacements, arthroscopy and a whole host of technologies.

Today the specialty is concerned with the following six broad areas;

a)The bones of:

•The extremities; the upper and lower limbs

•The axial skeleton; the bones of the spine

•The pelvic and shoulder girdles

b)The joints formed by the articulation of the bones mentioned above

c)The muscles and tendinous structures that move the joints

d)The ligaments that stabilize the joints

e)The spinal cord and the rest of the nervous tissue that control the movements and

f)The skin and other soft tissues that provide coverage to the bones.

An understanding of the entire body is essential in the diagnosis and management of orthopaedic diseases since all these systems are interrelated. Evaluation of any disease begins with general approach to the individual followed by review of the specific system involved and finally consideration of the other systems.

Musculoskeletal disorders arise from a variety of causes which can be congenital or acquired. These can be grouped as follows:

Traumatic disorders

Trauma is derived from the Greek word ‘traumata’ meaning body wound or shock produced by sudden physical injury, as from violence or accident. Today trauma is the sixth leading cause of death worldwide [in sub-Saharan Africa, it is third only to diarrhoea and malaria (Murray, 1996)]. Satics show that trauma accounts for 10% of all mortality and is a serious public health problem with significant social and economic costs. Trauma may draw attention to an underlying orthopaedic condition or worsen a pre-existing one. Trauma may also predispose to conditions that may present much later in life for example; trauma to the ankle joint may lead to osteoarthritis of the same joint.

Congenital disorders

Congenital causes are defined as conditions that have been present since birth. These may be as a result of:

Genetic abnormalities

Acquired abnormalities

Combination of both.

These conditions are commonly referred to as malformations when the abnormality is at structural level such as congenital club foot or as defects when the aberration is at molecular level for example osteogenesis imperfecta.

In as much as these conditions are present at birth, their presentation to the health care provider may occur at any chronicle age of the individual:

At birth, commonly, when a structural malformation is noticed, club foot is an example of one that is immediately evident at birth.

Later in life when the effect of the disorder may interfere with body functions; congenital Coxa vara is noted at about the age of one year when the child starts walking.

As a predisposing factor to a disorder of later life; evaluation of symptoms of osteoarthritis may reveal that a dysplastic hip had existed all along.

During screening; scoliosis may be evident during mass screening, it may also be apparent at the time when school age children undergo preschool medical examination.

As an incidental finding in the course of evaluation of other disorders, evaluation of back pain from other causes may reveal the presence of spina bifida occulta.

Infections

Infections may affect the musculoskeletal structures in a variety of ways: directly by eliciting an immunological response; by end functional tissue destruction and finally as an ever present real risk in every operative procedure. Various organisms cause infection directly depending on the virulence of the organism and the resistance of the host. The offending organisms can be categorized in the following ways:

Bacteria

The term Osteomyelitis, when not otherwise specified, conventionally refers to pyogenic bacterial infection of the bones such as that due to Staphylococcus spp. Other bacteria such as Mycobacterium spp, Treponema pallidum (causes chronic granulomatous infections that will be qualified specifically by mentioning the disease); tuberculous arthritis of the hip and syphilitic tabes dorsalis, as examples, respectively.

Fungi

Fungal infections are qualified specifically. For example, Madura foot is a fungal infection of the foot by madurella myecetoma. Fungi lead to an indolent response from the tissues of the affected person.

Parasites

Parasitic infections are referred to as infestations; hydatid infestation of the femur is the infection of the femur with echinococcus granulosus. Infestations may predispose to fractures.

Viral infections

Most viral infections in the body cause a limited illness then the body’s immune system destroys the virus, and the symptoms of the illness go away. Viruses are of interest in orthopaedics in a variety of ways. Polio is a contagious viral illness that in its most severe form causes paralysis, difficulty in breathing and sometimes death.

Several viruses are known to cause problems with joint inflammation and pain. Some of the most common are Parvovirus B-19, Hepatitis B infection, Rubella, and Human Immunodeficiency Virus. In viral arthritis, the immune system’s response to the virus causes inflammation in the joints. Even after the virus is eliminated from the body, the changes in the joint can continue to cause pain and swelling. The joint may even become permanently damaged. Some kinds of arthritis with unexplained causes may be the result of a virus.

In some cases, viruses that cause arthritis type symptoms can be carried by insects. Alpha viruses, one such family of viruses, are carried by mosquitoes in Africa, Australia, Europe, and Latin America. All can cause arthritis symptoms. Dengue fever and Chikungunya belong to this group.

The cause of myasthenia gravis is unclear. However, researchers suspect viruses or bacteria might trigger the autoimmune disease (Cavalcante et al, 2010, Robinson et al, 2010). Transient synovitis of the hip joint is a condition that occurs in childhood causing hip pain. Transient synovitis may be related to a viral illness.

Transmission of HBV, HIV, and HCV has been well-documented in health care settings. Transmission of these viruses has been reported from patient to health care providers, from health care providers to patient, and from patient to patient. Although much attention has focused on preventing HIV transmission, it is important for health care providers to be mindful of all of these common blood borne pathogens. Measures for preventing transmission are common to all three of these viruses.

Infections may affect the musculoskeletal system by direct destruction of the end functional tissue structures. In other situations the end tissues are involved by secondary effects. These can occur as:

Deformities secondary to motor neural damage such as those due to poliomyelitis.

Deformities secondary to sensory disturbances as in leprosy.

Kyphosis in tuberculosis as a consequence of destruction of bones due to the organism.

Whereas paraplegia may be caused by direct pressure on the spinal cord by inflammatory mass or compromise of the vascular supply by the inflammatory process.

Metabolic disorders

Bone has organic and inorganic components. To keep bone in optimum health, there is continuous physiological turnover of its mineral content with the rest of the systems of the body; the extra cellular fluid and blood taking a leading role. This continuous turnover is under the influence of hormones secreted by endocrine glands such as the thyroid and the parathyroid. Physical activity and mineral uptake and therefore by extension dietary availability also contribute to this balance. Conditions that disrupt this system are referred to as metabolic disorders. Rickets in children, Osteomalacia in the adults and osteoporosis in the elderly all belong to this class of diseases.

Immunological disorders

The body has an interacting combination of ways to recognize cells, tissues, objects and organisms that are not part of it and thus initiate the response to fight them. This immune response is often beneficial but at times it may malfunction and cause tissue damage leading to immunological diseases. The immune system may fail to recognize its own cells and tissues; it may over function or under function or even affect privileged compartments of the body. The joints of the body bear the brunt of these diseases. Rheumatoid arthritis and systemic lupus erythromatosis are examples of such immunological diseases. The trigger of this immune response may not be found. However, these diseases tend to run in families and different forms tend to affect the same individual. The presentations of these diseases are commonly medical chronic forms that show with deformities being the ones that present to the orthopaedic surgeon.

Neural disorders

An intact neuromuscular system is essential for optimal skeletal function. Disorders of the brain (such as cerebral palsy), the spinal cord and the peripheral nerves ultimately present as orthopaedic diseases. Other diseases can act through this pathway to produce disorders. Examples of such include poliomyelitis, leprosy and spinal cord trauma. Muscle weakness can occur as a primary disorder or as a consequence of innervations and hence belongs to this group.

Degenerative conditions

With the passage of time and continuous use of body structures, particularly joints, these structures undergo wear and tear. In this situation, degenerative musculoskeletal system disorders are said to be present. Osteoarthritis belongs to this group of disorders. This wear and tear may be accelerated in the presence of a predisposing condition.

Normal cell growth of the Tumours

musculoskeletal system, just as with the rest of the body, is closely regulated. In some instances, this regulation fails, resulting in uncontrolled proliferation of these cells resulting in neoplasms. If this happens to the cells at the site and system of origin it is referred to as primary neoplasia. If the cells have their origin from elsewhere within the body but have seeded in the musculoskeletal system these are referred to as secondary neoplasms. These neoplasm’s, also referred to as tumours, may be benign or malignant. The long bones and the spine are common sites of Secondary neoplasms.

Systemic illness

Systemic illnesses such as chronic renal failure, diabetes mellitus and sickle cell disease can result in orthopaedic problems. Definitive treatment and good control of those that are not totally curable will minimize the musculoskeletal effects of these diseases. Specific management of these complications depends on the individual presenting musculoskeletal complications.

Although we have classed the different possible types of afflictions separately, these conditions may present singly or in combinations thereof. An open traumatic injury can become infected; a child with developmental disorder of the hip may develop avascular necrosis of the femoral head requiring hip replacement.

In this manual, discussions of the musculoskeletal problems that may affect man are introduced, methods of diagnosis presented. The more common disorders are discussed in detail. Conservative, common, and relatively easier methods of management are presented whereas the more complicated usually operative methods are outlined. The reader is encouraged to refer to more specialized text books of orthopaedics for detailed information on a particular topic. Every effort is made to provide illustrations to enhance the application by the reader.

Bibliography and further reading

1.Cavalcante P., Serafini B., Mantegazza R. et al. Epstein-Barr virus persistence and reactivation in myasthenia gravis thymus. Ann Neurol; 2010; 67:726-738.

2.Fatal injuries in the slums of Nairobi and their risk factors of disease study. Results from a matched case-control study Injuries in Africa: a review. J Urban Health 2011

3.Garrett, W. E, et al. American Board of Orthopaedic Surgery Practice of the Orthopaedic Surgeon: Part-II, Certification Examination. The Journal of Bone and Joint Surgery (American). 2006;88:660-667

4.Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global burden of disease study. Lancet. 1997 May 3; 349(9061):1269-76

5.Murray, C.J.L. and Lopez, A.D. The global burden of disease. World Health Organization/Harvard School of Public Health/World Bank. Harvard University Press, 1996.

6.Nordberg E; Review Injuries in Africa: A review. East Afr Med J. 1994 Jun; 71(6):339-45.

7.Robinson, Richard Active Epstein-Barr Virus Found in Myasthenia Gravis Thymus Neurology Today 5 August 2010; Volume 10(15); pp 20-21

8.Sir Robert Jones; Great Teachers of Surgery in the Past: Br J Surg. 1967 Feb: 54(2):85-90.

Biology of the elements of the musculoskeletal system

Bone

Types of Bones

Cortical bone

This makes up 80% of the skeleton and is found in the outer shell of the bone. It is composed of tightly-packed osteons or Haversian canals made up of concentric lamellar (layers) of cylinders and surrounding systems up made up of a central co-vascular channel, connected by Haversian (Volkmann’s) canals.

Fig 2.1: The structure of cortical bone

These Haversian canals contain capillaries, arterioles, venules, nerves and possibly lymphatic’s. Lying between these osteons are interstitial lamellae. Fibrils often connect lamellae but do not cross the cement lines that form the outer border of osteons. The intraosseous circulation provides for homeostasis of the bone including nutrition and hormonal balance. Cortical bone has a slow turnover rate and a high resistance to bending and torsion.

Figure 2.2: Diagram of compact bone from transverse section of a long bone’s cortex demonstrating Osteon

Spongy or cancellous bone

This is less dense and more elastic than cortical bone and has a higher turnover rate. It is organized in trabecular struts, with lamellae running parallel to the trabeculae. It is found in the epiphyseal and metaphyseal regions of long bones and throughout the interior of short bones.

Fig 2.3: Illustration of a typical long bone showing the location of cancellous bone, Osteon, lamellae, Haversian canal, canaliculi and Volkmann’s canal

Immature or developing bone

This is woven and more random with more osteocytes than lamellar bone. It is the product of rapid bone formation resulting in an irregular, disorganized pattern of collagen orientation and osteocytes distribution. It is found in embryonic and foetal development and in healthy adults at ligament and tendon insertions. It also occurs in response to bone injury and dramatic changes in mechanical stimulation. It provides a temporary mechanical adjunct to allow bone to maintain or return quickly to its role as a structural support.

Cellularity of Biology

Osteoblasts

Osteoblasts form osteoid, the non mineralized component of bone matrix. They differentiate from mesenchymal progenitor cells and contain extensive endoplasmic reticulum with multiple cisternae, well-developed Golgi bodies, numerous ribosomes and mitochondria allowing for their abundant synthesis and secretion of matrix. They initiate mineralisation of osteoid material possibly by modulating electrolyte fluxes between the extracellular fluid volume and osseous fluid spaces.

Fig 2.4: Plenty of osteoblast - They are basophilic, more or less cuboidal shaped, arranged in rows along the pieces of bone and the inner surface of the marrow spaces. They are close to the bone they are making, which is usually less densely stained than the cells.

Bone-lining cells

They are narrow, flattened cells which differentiate from Osteoblasts but have fewer active organelles. They envelop quiescent bone surfaces including endosteal, periosteal and intra-cortical surfaces. Their function is to encase the bone surface and moderate site-specific mineralisation or resorption on activation by parathrohormone (PTH).

Osteocytes

Osteocytes maintain bone and comprise 90% of all cells in the mature skeleton. They originate as Osteoblasts which have been trapped within osteoid, formed by surrounding Osteoblasts, forming a lacuna. They have a single nucleus, and an increased nucleus to cytoplasm ratio. Osteocytes are smaller in size and have fewer numbers of organelles than Osteoblasts therefore are not as active in matrix production. Osteocytes play a role in controlling the extracellular concentration of calcium and phosphate; they are directly stimulated by calcitonin and inhibited by PTH.

Osteoclasts

Osteoclasts act in opposition to Osteoblasts and their role is to resorb bone providing for coupling of bone formation and resorption. They are multinucleated, irregularly-shaped giant cells which arise from haematopoietic cell lines through the fusion of monocyte progenitor cells.

Fig 2.5 Three big Osteoclasts are sitting on a piece of bone in the center of the field Osteoclasts are multinucleated: one shown here has at least nine nuclei, which is not a very unusual situation. Some have fewer and some have more, depending on the requirements of the time and place where they’re formed.

Matrix

Bone matrix is made up of organic components (40% dry weight of mature bone) and inorganic components (60% dry weight).

Organic Components

Collagen

Collagen, mainly of type I, forms 90% of the bone matrix and provides the bone’s tensile strength.

Proteoglycans

Proteoglycans contribute to the compressive strength of bone. Their function is unclear, but they are thought to play a role in the reservation of space for bone development, the binding and availability of local growth factors, and the deposition and structuring of collagen fibrils. Proteoglycans inhibit mineralisation.

Osteocalcin

Osteocalcin is produced by Osteoblasts and makes up 10-20% of the collagenous protein of bone. It attracts Osteoclasts; therefore its function is associated with bone remodeling. Synthesis is induced by 1, 25 Dihydrocholecalciferol (Vitamin D3) and inhibited by PTH. Serum and urine levels are elevated in Paget’s disease, renal osteodystrophy and hyperparathyroidism.

Osteonectin

Osteonectin is secreted by platelets, Osteoblasts and Osteoclasts. It is thought to either play a role in the regulation of calcium or the organisation of material within the matrix, as it binds with collagen. It also has a high affinity for both calcium and Hydroxyapatite, and localises to crystal-producing matrix vesicles.

Osteopontin

Osteopontin mediates the attachment of cells to bone matrix, similar to integrins.

Growth factors and cytokines

These occur in small amounts in bone matrix.

Bone Morphogenic Proteins (BMPs)

BMPs are members of the TGF-b super family of growth factors. They act on progenitor cells to induce differentiation into Osteoblasts and chondroblasts. They are responsible for ectopic bone formation by certain tumour cells, epithelial cells and demineralised bone. BMPs appear to be stored within the bone matrix and released during the resorptive activity that often follows injury.

Inorganic components

Calcium Hydroxyapatite (Ca10 (PO4)6(OH) 2)

Calcium Hydroxyapatite provides the compressive strength of bone. It makes up most of the inorganic matrix, and is responsible for mineralisation of the matrix (the transformation of Hydroxyapatite from a soluble to a solid form).

Osteocalcium Phosphate (Brushite)

Osteocalcium phosphate comprises the remainder of inorganic matrix.

Fluid is also an important component of bone and its distribution in the various compartments of bone is as follows:

Extra vascular 65%

Lacuna 6%

Haversian 6%

Red blood cells 3%

Bone Remodeling

Wolff’s Law states that bone grows and remodels in response to the forces that are placed upon it (Wolff 1896); the architecture and the mass of the skeleton are adjusted to withstand the prevailing forces imposed by functional need or deformity. Bone remodeling is affected by mechanical function, according to Wolff’s Law, which attempts to predict bone adaptation in the face of an altered loading environment.

Generally, remodeling occurs in response to stress and responds to piezoelectric charges. Crystals which acquire a charge when compressed, twisted or distorted are said to be piezoelectric. This provides a convenient transducer effect between electrical and mechanical oscillations. (Compression causes negative potential, which stimulates Osteoblastic activity & bone formation while tension causes positive potential, leading to Osteoclasts stimulation). Bone is dynamic hence coordinated Osteoblast and Osteoclast activity results in continuous remodeling of both cortical and cancellous bone throughout life.

Cortical bone remodeling occurs by Osteoclasts which tunnel through to the bone forming cutting cones, followed by sheets of Osteoblasts which deposit osteoid in lamellae. Cancellous bone remodeling involves Osteoclasts resorption of bone, followed by the deposition of osteoid by Osteoblasts.

Bone Circulation

Bones are well-supplied with arteries, receiving 5% of cardiac output under basal conditions. Long bones receive blood from:

Periosteal arteries

Nutrient arteries,

Metaphyseal and

Epiphyseal arteries.

Periosteal arteries enter the bone at various points and supply the outer third of the cortex of the diaphysis. This is a low pressure system. Nutrient arteries are branches of major systemic arteries and pass obliquely through the diaphyseal cortex to reach the medullary canal. Here they divide into longitudinally directed branches which supply at least the inner two-thirds of mature diaphyseal cortex. This endosteal supply is a high pressure system.

Fig 2.6: Diagrammatic representation of the Blood supply to the long bones

Metaphyseal and epiphyseal arteries supply the ends of bone and arise mainly from the periarticular vascular plexus. In growing bones they supply growth plates, so significant disruptions of blood flow disturb bony growth.

Direction of flow

In mature bone, arterial blood flows centrifugally from the high pressure nutrient arteries to the low pressure periosteal arteries. If a displaced fracture causes interruption of the nutrient artery system, the flow reverses as the periosteal system now predominates, so blood flow becomes centripetal.

In developing bone, arterial flow is centripetal because the periosteum is highly vascularised and is the major component of blood flow in bone. In mature bone, venous flow is centripetal; cortical capillaries drain to venous sinusoids, which then drain to emissary veins. As with other tissues and organs, hypoxia, such as at a high altitude, causes an increase in blood flow to bone, as does hypercapnia and sympathectomy.

After an injury to a bone, blood flow to the site initially decreases due to disruption of vascular structures. Blood flow then gradually increases over the following hours and days, peaking at around 2 weeks. By 3-5 months, flow has returned to normal. Fracture healing is largely reliant on bone blood flow - reaming of bone devascularises the central 50-80% of cortex, and thus is associated with delayed vascularisation with all types of fixation.

Regulation

Blood flow to bone is regulated by humeral, metabolic and autonomic signals. The osseous vessels express various vasoactive receptors. These provide an avenue which has potential for exploitation by pharmacological agents for the treatment of bone diseases related to circulatory disturbances such as osteonecrosis, and fracture nonunions.

The tissue surrounding bone, Periosteum, is a dense connective tissue membrane which covers bone. It is composed of an outer fibrous layer, which is contiguous with joint capsules, and an inner, or cambium, layer which is loose, more vascular, and contains cells; Osteoblasts (if bone formation is in progress on the surface) and Osteoblast precursors (If bone formation is not occurring). The outer layer is the main component of periosteum, and cells in this layer are sparse.

Fig 2.7: Stages in endochondral bone formation.

Bone marrow

Red marrow is the tissue in which blood cells develop and is 40% water, 40% fat and 20% protein. In later stages of growth and in the adult, when the rate of blood cell formation has decreased, red marrow slowly changes to yellow marrow. Yellow marrow is made up mostly of fat cells (80% fat, 15% water, 5% protein). Under the appropriate stimulus, yellow marrow can revert to red marrow.

Endochondral bone formation/mineralisation

Cartilage model

Human bones are mostly preformed from hyaline cartilage. This originates as condensed mesenchyme beginning at 6 weeks gestational age. This model is gradually invaded by vascular buds which bring in osteoprogenitor cells that differentiate into Osteoblasts and form primary centers of ossification at around 8 weeks. The cartilage model grows through appositional growth (new bone is applied to the surface of existing bone leading to an increase in width of bone) and interstitial growth (growth and replacement by bone of deeper layers of epiphyseal growth plate, pushing the epiphysis and its overlying articular cartilage away from the metaphysis and diaphysis leads to increased length of bone). Ossification thus spreads to replace the cartilage model. Marrow is formed by the resorption of the central cancellous bone and invasion by myeloid precursor cells, brought in by capillary buds.

Secondary centers of ossification develop at the ends of bone, to form epiphyseal centers of ossification which allow increase in bone length until the adult dimensions are attained. During the developmental stage, the epiphyses enjoys a rich arterial supply composed of an epiphyseal artery, metaphyseal arteries, nutrient arteries and perichondral arteries.

Regions of growing long bone

Physis

In immature long bones there are 2 growth plates:

Horizontal (the physis)

Spherical (allowing for the growth in the girth of the epiphysis; it has the same arrangement as the physis but is less organised).

Physeal cartilage is classified into zones according to growth and function. They include:

Reserve zone - Here there is no evidence of cellular proliferation or active matrix production. There is decreased oxygen tension. Cells here store lipids, glycogen and proteoglycan aggregates for later growth. Therefore diseases such as lysosomal storage diseases (Gaucher’s) can affect this zone.

Proliferative zone - The cartilage cells undergo division and actively produce matrix, and longitudinal growth occurs with chondrocytes forming columns. The oxygen tension here is increased, and there is also increased proteoglycan in the surrounding matrix which inhibits calcification. Defects in this zone (affecting chondrocyte proliferation and column formation) occur in achondroplasia.

Hypertrophic zone - This may be subdivided into 3 zones:

•Maturation

•Degeneration and

•Provisional calcification.

Here the cartilage cells are greatly enlarged (up to 5 times normal size), they have clear cytoplasm as a result of the glycogen accumulated, and the matrix is compressed into linear bands between the columns of hypertrophied cells. The cartilage cells accumulate calcium in mitochondria, then undergo aptosis (death), releasing calcium from matrix vesicles. Sinusoidal vessels bring Osteoblasts, which use the cartilage as a template for bone formation.

Metaphysis

Here Osteoblasts from progenitor cells accumulate on cartilage bars formed by Physeal expansion. Mineralization of primary spongiosa (calcified cartilage bars) occurs, forming woven bone which is remodeled to form secondary spongiosa and a cutback zone at the metaphysis. Cortical bone is formed when Physeal and intramembranous bones are remodeled in response to stress along the periphery of growing long bones.

Periphery of the Physis

This has two main components:

Groove of Ranvier - allow chondrocytes to travel to the periphery of the growth plate, resulting in lateral growth.

Perichondral Ring of LaCroix - dense fibrous tissue which anchors and supports the physis mineralization.

Collagen whole zones (between ends of molecules) are seeded with calcium Hydroxyapatite crystals, through branching and accretion.

Fig 2.8: Growth and parts of an immature long bone.

Fig 2.9: Frontal bone, the ossified areas are stained rather darkly compared to the rest.

Hormone and growth factor effects on the growth plate

Hormones and growth factors affect the growth plate either directly or indirectly, through their effects on chondrocytes and matrix mineralisation. Some factors are produced and act within the growth plate, while others are produced at a distant site.

Intramembranous ossification

The flat bones of the skull, the mandible and the clavicle ossify at least partly by intramembranous ossification. This occurs without a cartilage model by aggregation of layers of connective tissue cells at the site of future bone formation, and their differentiation into Osteoblasts. The Osteoblasts then form a centre of ossification which expands by appositional growth.

The irregular structures in the center of the image will form the spongy bone of the sandwich a typical flat bone displays in gross sections. The outer compact bone - the tables will be formed by ossification of the dense areas top and bottom in this field. Even though one region in this field will produce spongy bony and one compact bone, both arise via the intramembranous mode.

Bone injury and repair.

General principles

Bone response to injury consists of overlapping phases of inflammation, repair (soft callus then hard callus formation) and remodeling. Fracture healing is affected by systemic factors such as age, hormones and nutrition and local factors such as degree of local trauma, type of bone affected and infection.

a.Inflammation (Haemorrhage/Granulation Tissue-minutes/hours)

This begins immediately after the fracture, and is characterized by bleeding from the fracture site and surrounding tissues, causing haematoma formation, accompanied by edema and pain.

b.Cellular Proliferation

Lysosomal enzymes are released and tissue necrosis occurs - Osteoclasts and macrophages remove necrotic bone and tissue debris from the fracture site. This is followed by the stimulation of proliferation of reparative cells such as Osteoblasts and endothelial cells.

c.Repair (Immature Callus/Mature Callus-weeks/months)

Within 2 weeks, primary callus response occurs. If the bone ends are not in apposition to one another, soft (bridging) callus is formed around and between the fragments, reducing their mobility. This soft callus contains fibroblasts, proliferating Osteoblasts and often chondroblasts, embedded in a matrix rich in collagen and glycoprotein, into which new blood vessels grow.

d.Consolidation

Hard (medullary) callus supplements the bridging callus – the soft callus is gradually converted into woven bone, mainly by endochondral ossification. This stage is reached about 3 or 4 weeks after injury and continues until firm bony union occurs (around 2 or 3 months later for most adult bones). The amount of callus formation is indirectly proportional to the degree of immobilization of the fracture.

e.Remodeling (years)

This stage overlaps with hard callus formation and may continue for up to 7 years. It involves the gradual conversion of the woven bone of the hard callus to lamellar bone. It is considered complete when the site of the fracture can no longer be identified either structurally or functionally. It allows the restoration of bone to its normal configuration and shape, according to the stresses placed on it (Wolff’s Law).

Joints

Skeletal structures are connected to one another in many ways. These junctions are referred to as articulations, arthroses or joints. Joints are classified based on the extent of movements or the type of articular cartilage.

a.The classification of articulations based on the extent of joint movements: Using this criteria, articulations can be classified as follows:

Synarthroses: Fixed or rigid joints.

Amphiarthroses: Slightly movable joints.

Diarthroses: Freely movable joints.

b.The classification of joints on the basis of histology emphasizes the type of tissue that characterizes the junctional area. These are categorized as follows:

Fibrous articulations

Apposed bony surfaces are fastened together by fibrous connective tissue. These are further subdivided into three types: sutures, syndesmoses, and gomphoses. Sutures are limited to the skull and allow no active motion. They exist where broad osseous surfaces are separated only by a zone of connective tissue. This connective tissue, along with two layers of periosteum on the outer and inner surfaces of the articulating bone, is termed the sutural membrane or ligament. A syndesmosis may demonstrate minor degrees of motion related to stretching of the interosseous ligament or flexibility of the interosseous membrane. Gomphosis is a special type of fibrous joint located between the teeth and maxilla or mandible. At these sites, the articulation resembles a peg that fits into a fossa or socket.

Cartilaginous articulations

Apposed bony surfaces initially or eventually are connected by cartilaginous tissue. There are two types of cartilaginous joints, symphysis and synchondrosis. In symphyses adjacent bony surfaces are connected by a cartilaginous disc, which is composed of fibro cartilaginous or fibrous connective tissue, although a thin layer of hyaline cartilage usually persists, covering the articular surface of the adjacent bone. Examples are the symphysis pubis and the intervertebral disc. They allow a small amount of motion, which occurs through compression or deformation of the intervening connective tissue.

Synchondroses are temporary joints that exist during the growing phase of the skeleton and are composed of hyaline cartilage. Typical synchondroses are the cartilaginous growth plate between the epiphysis and metaphysis of a tubular bone, the neurocentral vertebral articulations and the unossified cartilage in the chondrocranium and the spheno-occipital synchondrosis. With skeletal maturation, synchondroses become thinner and eventually are obliterated by bony union or synostosis. Two synchondroses that persist into adult life are the first sternocostal and the petro basilar joints.

Synovial articulations

Apposed bony surfaces are separated by an articular cavity that is lined by synovial membrane. A synovial joint is a specialized type of joint that is located primarily in the appendicular skeleton. Synovial articulations generally allow unrestricted motion. The inner portion of the articulating surface of the apposing bones is separated by a space; the articular or joint cavity. Articular cartilage covers the ends of both bones. Motion between these cartilaginous surfaces is characterized by a low coefficient of friction. The inner aspect of the joint capsule is formed by the synovial membrane which secretes synovial fluid into the articular cavity. This synovial fluid acts both as a lubricant encouraging motion and as a nutritive substance, providing nourishment to the adjacent articular cartilage.

Parts of a synovial joint

The synovial joint is the commonest joint found in the body and may comprise of: Cartilage, Articular Capsule, Fibrous Capsule, Synovial Membrane, Intra-articular Disc (Meniscus), Labrum, Fat Pad, and Synovial Fluid.

Fig 2.10: Diagrammatic representation of a synovial joint; the hip joint.

Articular cartilage

The articulating surfaces of the bone are covered by a layer of glistening connective tissue, the articular cartilage. Its unique properties include:

Transmission and distribution of high loads

Maintenance of contact stresses at acceptably low levels

Enabling movement with little friction

Shock absorption

Articular cartilage is devoid of lymphatic vessels, blood vessels and nerves. A large portion of the cartilage derives its nutrition through the synovial fluid.

Articular capsule

The articular capsule is connective tissue that envelops the joint cavity. It is composed of a thick, tough outer layer, the fibrous capsule, and a more delicate thin inner layer, the synovial membrane.

Fibrous capsule

The fibrous capsule consists of parallel and interlacing bundles of dense white fibrous tissue. At each end of the articulation, the fibrous capsule is firmly adherent to the periosteum of the articulating bones.

Synovial membrane

The synovial membrane is the delicate, highly vascular inner membrane of the articular capsule. It lines the non-articular portion of the synovial joint and any intra-articular ligaments or tendons. The synovial membrane also covers the intracapsular osseous surfaces, which are clothed by periosteum or perichondrium but are without cartilaginous surfaces.

Intra-articular Disc (Meniscus), Labrum, and Fat Pad

A fibro cartilaginous disc or meniscus may be found in some joints, such as