1. Anatomy of cartilage
1.1. Note: Cartilage is similar to bone but stronger
1.2. Functions:Resists compression because of the large amounts of water held in the matrix Functions to cushion and support body structures
1.3. Types of cartilage:
1.3.1. Hyaline cartilage: Firm amorphous matrix; Imperceptible complex network formed by collagen fibres; chondroblasts produce the matrix and later mature (chondrocytes), whence they lie in lacunae.
1.3.1.1. Function:Supports; Reinforces; Serves as resilient cushion that is able to resists compressive stress.
1.3.1.2. Location:Embryonic skeleton; Surface of the ends of long bones in joint cavities; Costal cartilages of the ribs; Cartilages of the trachea, nose, and larynx.
1.3.2. Elastic cartilage:Similar to hyaline cartilage but with greater elasticity.
1.3.2.1. Function:Maintains shape of structure along with great elastic flexibility.
1.3.2.2. Location:External ear (pinna); Epiglottis.
1.3.3. Fibrocartilage: Dominated by thick collagen fibres. Matrix is similar to that of hyaline cartilage but less firm.
1.3.3.1. Function: Tensile strength; Compressive shock absorbance.
1.3.3.2. Location:ntervertebral discs; pubic symphysis; discs of knee joint.
1.4. Components: Simple component;Firm flexible tissue; No blood vessels or nerves; Matrix(80% H20);
1.5. Cell components:
1.5.1. Chondrocytes(mature bone cell)
1.5.2. Chondroblasts(Responsible for forming the cell matrix)
1.6. Matrix components(Ground substance+fibers):
1.6.1. Gel-like ground substance( secreted by chondroblasts):
1.6.1.1. Composed of large sugar and sugar- protein molecules (proteoglycans and glycosaminoglycans) that are able to absorb fluid much like a sponge. The sponginess allows cartilage to withstand compressive stresses.
1.6.2. Fibers: collagen, elastic fibers in some
1.6.2.1. Elastic fibres: Contain elastin protein which contribute/allow for the fibres elasticity and ability to recoil.
1.6.2.2. Collagen fibres: Composed of amino acids (Glycine, Proline, Hydroxyproline and Arginine). Fibres contribute to the strength of tissue, this strength is derived from the bundling and cross linking of fibrils within bundles, again within larger bundles.
2. Bone
2.1. Growth: Embryonic; Post natal
2.1.1. Post-natal growth:focusing on puberty, the effect of hormones, and remodeling
2.1.1.1. Bones lengthen by the growth of epiphyseal plates. During lengthening process cartilage is replaced with bone connective tissue at a approximate that of growth.
2.1.1.1.1. Epiphyseal plates: Initially promote growth while retaining a constant thickness. Nearing the end of adolescence the chondroblasts divide less often, as a result the plates begin to thin and are eventually gone, at which the diaphysis and epiphyses fuse and the bone stops lengthening.
2.1.1.2. Bone widening is the result of osteoblasts through appositional growth where bone tissue is added to the surface of bones, specifically the diaphysis.
2.1.1.3. Growth hormones:
2.1.1.3.1. Thyroid hormone: Ensures that proper proportions are retained within the skeleton as it grows.
2.1.1.3.2. Sex hormones(estrogen and testosterone): Promote growth and growth termination
2.1.1.3.3. Pituitary gland:Contains hormone that stimulates epiphyseal plates.
2.1.1.4. Bone remodelling: Deposition and removal occurs at the periosteal and edosteal surfaces, which are the result of osteoblasts and osteoclasts.
2.1.1.4.1. Cancellous bone: replaced every 3-4 years
2.1.1.4.2. Compact bone: Replaced every 10 years
2.1.1.4.3. In children and adolescents deposition outweighs removal. in young adults deposition and removal approximate each other and in old age removal predominates deposition.(bone mass inversely proportional to age).
2.1.2. Osteogenesis: The formations of bone.
2.1.2.1. Intramembranous ossification: Form membrane bones(skull+clavicles) directly from mesenchyme.
2.1.2.1.1. Ossification centers appear in the fibrous connective tissue membrane, derived from mesenchymal cells differiating into osteoblasts
2.1.2.2. Endochondral ossification: Form all non membranous bones from hyaline cartilage. Formation begins in month 2 of embryonic development and continues throughout early adulthood.
2.1.2.2.1. Hyaline cartilage model is formed and at it's diaphysis a bone collar begins to form.
2.2. Anatomy of bone
2.2.1. Note: Bone is similar to cartilage but stronger
2.2.2. Functions: Organ support/protection; Acts as lever/attachement(trunk) for muscles; Storage of Calcium, minerals, and fat; Provides marrow for blood formation; Hard tissue able to resist both compression and tension.
2.2.3. Cell components:
2.2.3.1. Osteocytes(mature cell-located in the lacunae).
2.2.3.2. Osteoblasts(secrete collagen fibres and ground substance of matrix).
2.2.3.3. Osteogenic cells: Stem cells that later differentiate into osteoblasts.
2.2.3.4. Osteoclasts: Multinucleate cells responsible for the resorption of bone.
2.2.4. Types of bone:
2.2.4.1. Compact bone:
2.2.4.1.1. Function/composition: Dense outer layer of bone present for protection/support. Contain passage way for blood vessels and nerves. Contain osteons (long cylindrical structures functioning in support).
2.2.4.1.2. Location: surrounding all bones.
2.2.4.2. Spongy bone:
2.2.4.2.1. Location: Within short, flat, irregular bones. At the epiphyses of long bones.
2.2.4.2.2. Function/composition: Internal honeycomb of small needle-like/ flat pieces, composed of trabeculae. The trabeculae helps bone resist stress and stores red(produces blood cells) and yellow blood marrow(stores energy as fat).
2.2.5. Categories: The bones within these grouping are classified within long bones,short bones, flat bones, irregular bones.
2.2.5.1. Axial:80 bones
2.2.5.2. Appendicular:206 bones
2.2.6. Matrix components(Ground substance+fibers):
2.2.6.1. Gel-like ground substance( secreted by osteoblasts):(Occupy 35%)
2.2.6.1.1. Gel-like ground substance calci ed with inorganic salt making the matrix hard and able to contribute to it's function in supporting the body.
2.2.6.2. Fibers: collagen(Occupy 65%)
2.2.6.2.1. Collagen fibres: Composed of amino acids (Glycine, Proline, Hydroxyproline and Arginine). Fibres contribute to the strength of tissue, this strength is derived from the bundling and cross linking of fibrils within bundles, again within larger bundles.
2.2.7. *Week4*Surface markings(3 types): Projections fo muscle and ligament attachment; Surface that form joints; Depressions and openings.
2.2.7.1. Projections fo muscle and ligament attachment: Tuberosity, crest, trochanter, line, tubercle, epicondyle, spine, process.
2.2.7.2. Surface that form joints: Head, facet,condyle.
2.2.7.3. Depressions and openings: Foramen, groove, fissure, notch, fossa, meatus, sinus.
2.2.8. Tissues housed/used: Bone connective tissue; Nevous tissue; Blood connective tissue; Cartilage; Epithelial tissue
2.3. 3 disorders of bone. Outline the underlying defect, the symptoms, the treatment and current day clinical trials (gene therapy, stem cell research) that are being done.
2.3.1. Clubfoot, Hip dysplasia, Bone fractures,Scoliosis,Kyphosis, Lordosis,Stenosis, Cleft palate, rickets; Osteoporosis
2.3.2. Rickets: Skeletal disorder resulting in weakened bones due to inadequate mineralization; Occurs in children (6-24 months) ; Malformation of the child’s head + rig cage are common.** Osteomalacia is essentially the same disease only it occurs in adults. bot of which are the result of a vitamin D efficiency.
2.3.2.1. Symptoms in children under 5 years old: Forehead perspiration during sleeping and breastfeeding; pungent urine; occipital alopecia; soft fontanel; craniatabes; olympic forehead; cranial deformation; rosary of rickets; Harrison's groove; pigeon chest; symptom of bracelet; frog abdomen; spinal deformation; bowing of the legs; X leg; hard swollen joints of knee; hard swollen joints of anklebone; unclosed fontanel.
2.3.2.2. Treatment+clinical trials:
2.3.2.2.1. Stoss therapy: Use of high doses of vitamin D given in single dose/split doses over several weeks.
2.3.2.2.2. Doses between 1000 and 10,000iu of ergocalciferol (vitamin D2)/cholecalciferol (vitamin D3) given on a daily basis for several weeks.
2.3.2.2.3. Treatment+clinical trials:Trials done in Turkey, India, Northern Nigeria showed good results for stops therapy(India). The study northern Nigeria showed improved result for children prescribed a combination of calcium and vitamin D rather than vitamin D on it's own. The conclusions of these studies showed a daily 2000iu dose of D2 or D3 dose for 12 weeks along with a 500mg oral dose of calcium daily in conjunction with vitamin D for treatment stood out.
2.3.3. Pagets disease:
2.3.3.1. Treatment+clinical trials:
2.3.3.1.1. Medications: Bisphosphonates(alendronate, pamidronate, risedronate, and zoledronic acid)+Amniobiphosphonates or calcitonin(Regulates calcium and bone metabolism). Calcitonin is seldom used but it can improve bone pain.
2.3.3.1.2. Surgery: Fracture repair; joint repair/replacement;
2.3.3.1.3. Antiresorptive therapy: Reduces bone pain but often requires analgesic agents, antiinflammatory drugs, and antineuropathic agents to more greatly do so.
2.3.3.2. Symptoms: Bone deformity; warmth of the skin overlying an affected bone; elevated serum alkaline phosphatase level; abnormal radiograph; bone pain; Deafness(If skull is affected); osteosarcoma(Rare but expected for those with sudden increase in bone pain/swelling); Also rare/seen in mobile patients:obstructive hydrocephalus, high-output cardiac failure, hypercalcemia.
2.3.4. Osteoporosis: A disease in which bone reabsorption outpaces bone deposition, as a result one affected by the disease has low bone density.
2.3.4.1. Symptoms: Back pain(acute, chronic), for- ward-bulge of the abdomen, spinal shrinkage, back rounding,teeth loosening and falling out, thin/transparent skin, premature greying of the hair. Rare:persistent nerve root pain or spinal cord syndromes)
2.3.4.2. Treatment+clinical trials: The overall goal is to prevent fractures through medicating, where the medication used optimally is well tolerated/safe; has minimal side effects; has oral and intravenous bioavailability; is proven to increase bone mass, improve bone quality, reduce fractures at all sites.
2.3.4.2.1. Bisphosphonates:Reduce bone turnover by 80–90%; causes a gain in bone mineral density; reduces bone remodelling; increase mineralization/mean tissue age of bone.
2.3.4.2.2. PTH and tetraparatide therapy: Shown to have outstanding effects in both men and women with minor/severe osteoporosis, including those non-responsive to antiresorptive therapies. Also tetriparatide was safely administered over the course of 5 years to men and women in the Us and several European countries. PTH is still in it's testing process.