Rehab 521 Autumn 2024 Lecture 26 Intro Bone and Soft Tissue PDF

Intro Skeletal-Soft Tissue module Overview of bone and soft osteomyelitis tissue pathophysiology Overview of normal bone physiology Bone pathology including: Infectious diseases (osteomyelitis) Keloid scar Fracture Soft tissue and b...

Intro Skeletal-Soft Tissue module Overview of bone and soft osteomyelitis tissue pathophysiology Overview of normal bone physiology Bone pathology including: Infectious diseases (osteomyelitis) Keloid scar Fracture Soft tissue and bone tumors Rehab 521: Pathophysiology Mary Beth Brown, PT, PhD  Overview of bone and soft tissue pathophysiology The musculoskeletal system does not Box 22-1 COMMON function in isolation MUSCULOSKELETAL DISORDERS Fracture Primary disease of the Dislocation musculoskeletal Subluxation system can Contusion Hematoma significantly affect Repetitive overuse, microtrauma other body systems Strain, sprain and vice versa Degenerative disease Some diseases are systemic, meaning that all body systems, including the  Overview of bone and soft tissue pathophysiology Remember this slide from Cell The decisions we module make about treatment of bone and soft tissue For example, what pathology is we do after a based on what we fracture know about 1) cellular adaptations and reversible cell injury in response to stress 2) stages of healing Remember this slide from Cell module Phases of tissue healing Hemostasis and degeneratio n Inflammatio n Proliferation and migration Remodeling and Sun et al. Science, 2014  Overview of bone and soft tissue pathophysiology Remember this slide from Cell 1st, a period of module immobilization to remove longitudinal stress – Allows for phagocytes to For example, what remove necrotic bone we do after a tissue and the initial fracture deposition of the fibrocartilaginous callus As the fracture heals, gradual progression of stress is applied, which is required for correct healing  Overview of bone pathophysiology A variety of conditions can affect bone and require a reparative process – fracture – infection – inflammation (e.g., tuberculosis or sarcoidosis) – metabolic disturbances (e.g., Paget disease, osteoporosis, or osteogenesis imperfecta) – tumors – response to implanted prostheses – bone infarction – systemic diseases that have skeletal manifestations (e.g., sickle cell disease, amyloidosis, or hemochromatosis)  Intro Skeletal-Soft Tissue module Overview of bone and soft tissue pathophysiology Overview of normal bone physiology Bone pathology including: Infectious diseases (osteomyelitis) Fracture Soft tissue and bone tumors Rehab 521: Pathophysiology Mary Beth Brown, PT, PhD QUICK REVIEW OF BONE TISSUE NORMAL PHYSIOLOGY  Bone structure at an organ level Components of bone tissue – Collagen fibers that contain minerals (i.e. calcium, phosphate) Cancellous (trabecular) – Meshwork of trabeculae – Higher rate of bone remodeling – Trabecular orientation altered with mechanical loading, disuse, disease Compact (cortical) – Rigid outer shell – Organized as Haversian systems (also called osteons) Bone cells and their primary function OSTEOBLASTS: these cells form new bone called osteoid (primarily Type-1 collagen) and are found on bone surfaces OSTEOCLASTS: cells that dissolve pre- existing bone and are found on bone surfaces OSTEOCYTES: these cells are embedded in bone and have long branches involved in sensing damage and regions of bone that need repaired Osteocyte network  Process of normal bone remodeling Bone remodeling involves two distinct phases – Bone resorption followed by bone See next slide for description formation (these are coupled) – Only 5 to 20 percent of the skeleton undergoes remodeling at any given time  Process of normal bone remodeling 1. Activation: Resting bone surface converted to a remodeling surface. Osteoclast precursors are recruited to the bone lining cell layer where they differentiate into mature, active osteoclasts 2. Resorption: Osteoclasts remove both mineral and organic components of bone matrix by creating an acidic microenvironment between the cell and bone surface. The resorbing surface has a scalloped, eroded appearance known as a resorption lacunae 3. Reversal: Once osteoclasts have resorbed the mineral and organic matrix, osteoblasts are recruited to the bone surface 4. Formation: Removal of old bone by osteoclasts is followed by the formation of new osteoid (unmineralized collagen matrix) by osteoblasts. During the mineralization process, hydroxyapatite crystals deposit on the collagen matrix and gradually harden which results in the formation of new mineralized bone Really cool bone remodeling video https://youtu.be/0dV1Bwe2v6c (click on Movie 2, https://www.youtube.com/watch?v=78RBp osteoblasts and WSOl08 osteoclasts) http://bonebiology.amgen.com/index.html?scene=2  Osteocyte network Mechanical loading applied at the whole bone level is transmitted through the bone tissue to the cellular level and causes movement of the interstitial The osteocytes are fluid distributed throughout surrounding bone tissue and connect to osteocytes in each other and to bone- the lining cells and osteoblasts mineralized on the bone surfaces. matrix. Figure adapted from Rubin REGULATION OF CALCIUM  Three compartments that store calcium in our body Extracellular Matrix – ~99% (1000 g) Calcified bone tissue Warehouse for calcium Calcium in the form of hydroxyapatite crystals – Hydroxyapatite: Ca10(PO4)6(OH)2 Total amount of calcium varies depending on how much bone is being formed, and lost at any given time-point Extracellular Fluid You don’t need to – ~0.1% (1000 mg) memorize these Intracellular numbers, is just for perspective – ~0.9% Net intestinal uptake of Ca2+ is ~175 mg/day You don’t need to ~99% of Ca2+ by know this for exam, kidney is reabsorbed just appreciate that there is a balancing Ca2+ balance urinary act btwn kidneys, excretion matches net bone, and gut, for absorption by intestine calcium forming, resorbing, (~175 mg/day) absorbing, How do we regulate calcium levels? Parathyroid hormone from parathyroid gland Calcitonin from thyroid gland Vit D  Have 4 parathyroid glands, located at posterior thyroid FOUR PARATHYROID Parathyroid GLANDS: LOCATION glands secrete parathyroid hormone (PTH) Normal hormonal function will occur with 2 functional parathyroid Removal glandsof 3 parathyroid glands can result in (hypo)parathyroi dism How does PTH respond to changes in extracellular fluid (ECF) calcium levels? Low blood calcium (hypocalcemia) will trigger secretion of PTH How does the parathyroid gland sense a change in extracellular calcium? – Ca2+-sensing receptor (CaSR) located on cell membrane of a parathyroid gland cell How does an increase in circulating plasma PTH work to INCREASE plasma Ca2+ levels? 1. BONE: Increases bone resorption by targeting osteoclasts, allowing the release of Ca2+ to increase blood levels 2. KIDNEY: Stimulates Ca2+ reabsorption which will decrease urinary excretion 3. INTESTINE: PTH indirectly impacts Ca2+ absorption in the intestine by stimulating the formation of the active form of vitamin D  Have 4 parathyroid glands, located at posterior thyroid FOUR PARATHYROID Parathyroid GLANDS: LOCATION glands secrete parathyroid hormone (PTH) Normal hormonal function will occur with 2 functional parathyroid Removal of 3 glands parathyroid glands can result in A(hypo)parathyroi patient with hypo- dism parathyroidism will have a greater amount of calcium excretion How do we regulate calcium levels? Parathyroid hormone from parathyroid gland Calcitonin from thyroid gland Vit D  Thyroid Gland Remember this slide Largest pure endocrine gland from Endocrine thyroid lecture ? Located inferior to larynx Will be discussed in Extremely vascular BONE/SOFT TISSUE Two hormones produced : module! 1. Calcitonin 2. Thyroid hormone T3 & T4  Calcitonin from thyroid is a counter-regulatory hormone to PTH Released from C cells (also called parafollicular cells) of the thyroid gland when blood Ca2+ levels increase Histological section of Causes decrease in the thyroid tissue level of calcium in the blood to help maintain normal blood calcium levels Osteoclasts are the primary target cells of calcitonin (inhibits them) Deficient or excessive production of calcitonin does not have a profound impact on calcium balance  How is Calcitonin used to treat bone disorders? Osteoclasts are the primary target of calcitonin, by inhibiting the resorptive activity of the osteoclasts to reduce the rate of bone turnover Useful for patients with accelerated bone turnover such as hyperparathyroidism and Paget disease How do we regulate calcium levels? Parathyroid hormone from parathyroid gland Calcitonin from thyroid gland Vit D  Vitamin D (A fat soluble vitamin—but also a hormone) https://pubmed.ncbi.nlm.nih.gov/244 94042/ Sunlight and Vitamin D: A global perspective for health  Vitamin D (A fat soluble vitamin—but also a hormone) 1. SMALL INTESTINE: aids in the intestinal absorption of calcium and phosphate 2. KIDNEY: to increase the reabsorption of calcium and phosphate 3. BONE: promotes bone mineralization  Vitamin D (A fat soluble vitamin—but also a hormone) Deficiency in Vit D can result in bone disorders and dysregulated calcium balance  Vitamin D (A fat soluble vitamin—but also a hormone) Deficiency in Vit D can result in bone disorders and dysregulated calcium balance Rickets - softening and weakening of bones, usually in children, due to vitamin D deficiency  Intro Skeletal-Soft Tissue module Overview of bone and soft tissue pathophysiology Overview of normal bone physiology Bone pathology including: Infectious diseases (osteomyelitis) Fracture Soft tissue and bone tumors Rehab 521: Pathophysiology Mary Beth Brown, PT, PhD  Overview of bone pathophysiology A variety of conditions can affect bone and require a reparative process – fracture – infection – inflammation (e.g., tuberculosis or sarcoidosis) – metabolic disturbances (e.g., Paget disease, osteoporosis, or osteogenesis imperfecta) – tumors – response to implanted prostheses – bone infarction – systemic diseases that have skeletal manifestations (e.g., sickle cell disease, amyloidosis, or hemochromatosis)  Overview of bone pathophysiology A variety of conditions can affect bone and require a reparative process – fracture – infection – inflammation (e.g., tuberculosis or sarcoidosis) – metabolic disturbances (e.g., Paget disease, osteoporosis, or osteogenesis imperfecta) – tumors – response to implanted prostheses – bone infarction – systemic diseases that have skeletal manifestations (e.g., sickle cell disease, amyloidosis, or hemochromatosis)  Fracture Fracture repair is a healing process by regeneration and remodeling (no scar) Generally a full return of optimal function After an uncomplicated fracture, bone heals in similar overlapping phases previously discussed See figure and description next slide FIGURE 6-26 Fracture healing occurs in overlapping stages/phases A, Immediate vascular response with hematoma formation and inflammatory response B, Granulation tissue and fibrocartilage formation during early reparative phase C, Fibrocartilaginous union (soft callus) is replaced by a fibroosseous union (bony callus) D, Remodeling phase with complete restoration of the medullary canal  Fracture Formation of hematoma – At the moment of fracture, tiny blood vessels through the haversian systems are torn at the fracture site – A brief period of local internal bleeding occurs, resulting in a hematoma around the fracture site: ‘fracture hematoma’ – Bleeding at fracture site delivers fibroblasts, platelets, and osteoprogenitor cells, which secrete numerous growth factors and cytokines These stimulate transformation of the initial hematoma into a more organized granulation tissue  Fracture Inflammatory phase – Inflammatory cells arrive – Vascular response and cellular proliferation – Clinical evidence of this phase includes pain, swelling, and heat – Clotting factors from the blood initiate the formation of a fibrin meshwork. Acts as scaffolding for the ingrowth of fibroblasts and capillary buds around and between bony ends. – By the end of the first week, phagocytes have removed most of hematoma, and neovascularization and initial fibrosis begin  Fracture Reparative phase – Periosteum and endosteum regenerate and begin to differentiate into formation of hyaline cartilage (soft callus) seen on radiographs ~2 wks post – Osteoclasts clear away necrotic bone – Soft callus is replaced by primary bony spicules (hard callus) – Bone growth factors, including bone morphogenetic proteins, fibroblast growth factor, insulin-like growth factors, platelet-derived growth factor, transforming growth factor–β, and vascular endothelial growth factor, are major players here  Fracture Reparative phase – Repair occurs between the fractured cortical and medullary bones when fibrocartilaginous union (soft callus) is replaced by fibroosseous union (hard callus) Called ‘enchondral ossification’ Delayed union and nonunion fractures result from errors in this healing phase – Usually complete between 6 - 12 weeks, is indicated by fracture stability – Fracture line on x-ray begins to disappear  Fracture Remodeling phase – Begins with union (no movement at fracture site) – Persists until bone is returned to normal, including restoration of the medullary canal – May take months to years – Immature, disorganized woven bone is replaced with mature organized lamellar bone*, adding stability to fracture site – The excessive bony callus is resorbed, bone remodels in response to the mechanical stresses placed on it  immat mature ure *Mature bone has organized concentric lamellae (also referred to as osteons) ‘lamellar bone’  Fracture The time for overall bone healing varies depending on – the bone, fracture site, and type* – treatment required (e.g., immobilization vs. surgical repair, bone grafting) – degree of soft tissue injury – treatment complications – other factors mentioned previously (e.g., age, vascular supply, smoking, nutritional status, or immunocompetency)  Fracture *Types In a transverse fracture, the fracture line is at a right angle to the long axis of the bone; this fracture is usually produced by shearing force. An oblique or spiral fracture occurs following a twisting or torsional force; fragments displace easily in the oblique fracture, whereas nonunion rarely occurs in a spiral fracture because of the wide area of surface contact. A fracture is comminuted if the bone is broken into more than two fragments and segmental if a fragment of the free bone is present between the main fragments. The separation of a wedge-shaped piece of bone is called a butterfly fracture. See Box 27-15 for other types of fractures and their definitions.  Fracture Remodeling phase – Begins with union (no movement at fracture site) – Persists until bone is returned to normal, including restoration of the medullary canal – May take months to years – Immature, disorganized woven bone is replaced with mature organized lamellar bone*, adding stability to fracture site – The excessive bony callus is resorbed, bone remodels in response to the mechanical stresses placed on it  Fracture Remodeling phase – Is also a normal, lifelong process even in the absence of fracture in the normal adult skeleton, approximately 10% - 30% of bone is replaced or remodeled to replace microfractures from stress and maintain mineral balance – Osteocytes detect local mechanical loading and send signals to the surface Recall earlier osteoblasts to direct bone slide about remodeling via this osteoblast/osteoclast activity  Fracture Remodeling phase – Is also a normal, lifelong process even in the absence of fracture in the normal adult skeleton, approximately 10% - 30% of bone is replaced or remodeled to replace microfractures from stress and maintain mineral balance – Osteocytes detect local mechanical loading and send signals to the surface osteoblasts to direct bone remodeling via osteoblast/osteoclast activity  Bone pathologies: Infectious diseases Osteomyelitis – Infection in bone- areas affected most often include the spine, pelvis, and arms or legs – The pathogen (usually bacterial) enters through an open wound or the GI tract, spreads quickly through circulation – In adults, usually secondary to an open injury to bone and surrounding soft tissue – Acute osteomyelitis is relatively uncommon but very serious, occurs more in children Vascular loop in growing bone- initial infection site  Bone pathologies: Infectious diseases Osteomyelitis pathophysiology FIGURE 25-1 The vascular loop in growing bone is a common initial site of bacterial seeding  Bone pathologies: Infectious diseases Osteomyelitis pathophysiology See explanation in notes section FIGURE 25-2 Osteomyelitis  Bone pathologies: Infectious diseases Osteomyelitis S & S – Initially, pain may not be a factor because of the lack of pain fibers in cancellous bone – When the infection extends into the periosteum, increased joint pain; diminished function; and systemic signs, such as fever, swelling, and malaise may rapidly develop – Pain often described as deep and constant, increasing with weight bearing when in the lower extremity – Spinal osteomyelitis - back pain  Bone pathologies: Infectious diseases Osteomyelitis treatment – Immediate treatment is required – Antibiotics – Surgery if infection has spread to the joints Articular cartilage can be damaged in hours Goal of surgery is to drain exudate (pus) Often extensive debridement of bone and surrounding soft tissue is required  Intro Skeletal-Soft Tissue module Overview of bone and soft tissue pathophysiology Overview of normal bone physiology Bone pathology including: Infectious diseases (osteomyelitis) Fracture Soft tissue and bone tumors Rehab 521: Pathophysiology Mary Beth Brown, PT, PhD  Overview of tumors (AKA neoplasms) Primary tumors occurring in bone and soft tissue Metastatic tumors to bone (from metastasis of cancers elsewhere)  Overview of tumors (AKA neoplasms) Neoplasia: abnormal proliferation of cells Neoplasm: abnormal tissue mass (tumor) – Benign Typically not invasive and are slow growing Do not typically metastasize – Malignant Can spread to other sites (local and distant), organs, and are less common  Overview of tumors (AKA neoplasms) BENIGN MALIGNANT Cartilage Cartilage  Enchondroma  Chondrosarcoma  Chondroblastoma Bone  Osteochondroma  Osteosarcoma Bone Bone Marrow  Osteoma  Multiple Myeloma  Bone island  Ewing’s Sarcoma  Osteoblastoma AS A PT: you may be the one to recognize and recommend early detection How is Bone Destroyed by Tumor Cells? Presence of neoplastic (tumor) cells stimulates stimulates osteoclastic osteoblastic activity activity Can result in osteolysis Can result in osteosclerosis (bone destruction) (abnormal bone formation)  Normal vs abnormal skeletal tissue responses Remember, the NORMAL process of bone remodeling is coupled – Formation and resorption are in balance ABNORMAL – A. Osteolysis (osteolytic) Too much bone resorption (destruction) – B. Osteosclerosis (osteosclerotic) Too much bone formation  Overview of tumors (AKA neoplasms) Primary tumors occurring in bone and soft tissue Metastatic tumors to bone (from metastasis of cancers elsewhere) How are primary musculoskeletal tumors classified? Benign OR Malignant Primary Musculoskeletal Tumors (Localized Region) Soft Tissue OR Bone  Clinical Manifestations Primary Tumors PAIN—this is usually why they end up being seen RED FLAG: Changes in pain Infrequent… Constant… ↑ w/weight bearing… Awaken from sleep …… Sudden intense pain  Clinical Manifestations Primary Tumors PAIN—where is the pain? – Pain is typically caused from any mechanical changes (pressure/tension) acting on the periosteal or endocortical surfaces Periosteum  Endosteum  Clinical Manifestations Primary Tumors Pathological Fractures: – Occur as a result of an increase in osteoclastic (AKA osteolytic) damage to the bone tissue – If a fracture occurs, sudden intense pain – Mid-shaft fractures can occur, depends on where the tumor forms on the cortex, and how much of the cortex is involved  Clinical Manifestations Primary Tumors Other: – Swelling – Mass, lump – Inflammation – Increased serum calcium – Changes in serum bone markers (of formation and resorption) – Metastases (tumors elsewhere)  Clinical Manifestations Primary Tumors Why is serum calcium up? Especially common in patients with cancer – Due to parathyroid hormone- related peptide – Abbreviated ‘PTHrP’ – Acts on PTH receptors Remember that calcium – ↑s bone resorption levels represent a careful balance between bone, (osteoclast activity) gut, and kidney calcium – ↑s renal tubule handling activities… reabsorption of calcium tumors, especially (more Ca++ goes into malignant ones, can blood) upset this balance Recall earlier slide about how an increase in circulating plasma PTH works to INCREASE plasma 2+  Clinical Manifestations Primary Tumors Classification of Primary Tumors: Osteolytic (bone loss overpowers bone formation) Osteoblastic (bone formation overpowers bone loss)  Osteolytic presentation Osteopenia in region of bone tumor Focal bone destruction (osteolytic), increased bone resorption is the primary response – There is a secondary response of increased bone formation at tumor site in response to the increased osteoclast activity You don’t need to memorize these Increased serum calcium factors  Osteoblastic presentation Balance is more toward osteoblast activity, so increased bone formation Bone tissue is sclerotic Calcium may become trapped in bone resulting in a higher than normal increase You don’t need to in serum PTH memorize these factors How are primary musculoskeletal tumors classified? Benign OR Malignant Primary Musculoskeletal Tumors (Localized Region) Soft Tissue OR Bone Primary benign tumors 1. Bone Island 2. Osteoid Osteoma 3. Osteoblastoma (Giant Osteoid Osteoma) Hint, none of these names have the dreaded ‘sarcoma’ as a part of them! 1. Bone Island (also known an enostosis)  1. Bone Island MRI Small, sclerotic region of bone tissue Typically oval in shape and asymptomatic Plain Radiograph 1. Bone Island  1. Bone Island Benign Typically found incidentally on imaging studies Treatment – None – Follow up 3-6 months Typically no complications Important: for patients with breast- or prostate cancer a bone island can be mistaken for an osteoblastic metastasis  2. Osteoid Osteoma Benign vascular osteoblastic lesion typically found in the bone cortex Typically do not expand Location: primarily long bones near ends of diaphysis and spine  2. Osteoid Osteoma Intra-articular lesion Nidus (osteoid tissue) surrounded by sclerotic bone tissue Radiograph CT Scan  2. Osteoid Osteoma Sclerotic region surrounding nidus – Sclerosis is “reactive” part of the lesion This is a secondary response to the formation of the osteoid tissue – Effected area typically not larger than 1 cm – Nidus (central osteoid region) is not calcified so it appears radiolucent on X-ray – May cause dull ache—worse pain at night Joint effusion can occur when located near joint  2. Osteoid Osteoma Benign-osteoblastic tumor Typically resolve without treatment – Pain management with NSAIDS – If patient is not able to tolerate pain they tumor can be removed – May take several years to resolve on its own Majority of cases are seen in younger adults (early 20’s), males 2. Osteoid Osteoma 3. Osteoblastoma  3. Osteoblastoma Reactive bone lesion that has the ability to expand “to blast off” Location: diaphysis, spine, sacrum, flat bones Bone lesions are typically osteolytic with a sclerotic border More rare  3. Osteoblastoma Note the sclerotic border surrounding osteolytic AP View of Tibia Lateral View of Tibia region  3. Osteoblastoma Pain is usually present, with tenderness over lesion Distinguished from osteoid osteoma based on size – Can spread to surrounding soft tissue (“to blast off”) – Can lead to osteosarcoma (malignant) Requires excision to remove lesion – Reconstructive procedures such as grafting, internal fixation with rods/pins may be required depending on size of lesion and location  3. Osteoblastoma The spine can be affected resulting in: – Painful functional scoliosis – Muscle spasms – Limited range of motion Most often affects the posterior elements How are primary musculoskeletal tumors classified? Benign OR Malignant Primary Musculoskeletal Tumors (Localized Region) Soft Tissue OR Bone Primary malignant tumors 1. Osteosarcoma 2. Ewing’s sarcoma  Typically spread via blood vessels rather than via lymphatics – Primary tumors originating in the bone typically go to the lungs or liver Primary malignant tumors Osteosarcoma Ewing’s SARCOMA 1. Osteosarcoma  1. Osteosarcoma Malignant tumor with destructive lesions and abundant sclerosis – Can be primary or secondary Noted by extensive sclerosis in the bone tissue Location: most common in long bones, pelvis  1. Osteosarcoma Left: note osteolytic destruction of cortical bone of the pelvis Above: note extensive sclerosis clearly identified by X-ray  1. Osteosarcoma May result in reactive bone formation Erosion of under cortex periosteum extending into metaphyseal region Ossification of soft tissue  1. Osteosarcoma Clinical presentation – Photograph of large mass of the distal femur (most common location) – Obvious mass is not always evident, can be minimal swelling during initial stages  1. Osteosarcoma Symptoms in young children – Limping – Persistent pain that could be mistaken as growing pains – Lump will begin to appear – Fracture may occur – Important: if you are working with a pediatric patient experiencing constant pain that does not dissipate with rest refer to a physician This is particularly important if knee pain is present 1. Osteosarcoma  1. Osteosarcoma Limb-sparing technique 1. Osteosarcoma  2. Ewing’s Sarcoma Malignant non- osteogenic primary tumor that can arise in bone or soft tissue – Tumor is comprised of cells from neural origin Location: pelvis and lower extremities  2. Ewing’s Sarcoma Hemorrhagic necrosis – Results from tumor growing faster than blood supply Tumor is soft Onion skin: lesion perforates cortex and lifts periosteum X-ray shows osteolytic damage and reactive bone on bone surface 2. Ewing’s Sarcoma 2. Ewing’s Sarcoma  2. Ewing’s Sarcoma Genetic disorder – Tumor may have started in fetal or embryonic tissue that has developed into nerve tissue – Tissue has islands of small, round cells of neural origin 2. Ewing’s Sarcoma  2. Ewing’s Sarcoma Pain is the most common presenting symptom With progression of lesion, pain and swelling increase Goal is to treat local lesions and potential metastasis that may occur – Local regions may be treated with high-dose radiation – Chemotherapy – Limb-sparing surgery – Amputation  Overview of tumors (AKA neoplasms) Primary tumors occurring in bone and soft tissue Metastatic tumors to bone (from metastasis of cancers elsewhere)  Metastatic Tumors to Bone Skeleton is one of the most common organ for tumor metastasis! – Breast, prostate and lung cancer commonly go to bone – ~350,000 people/yr die from bone mets in the US – Skeletal regions with good blood supply typically most affected e.g. breast cancer  Metastatic Tumors to Bone Example: Metastatic thyroid carcinoma Patient had hip pain for 2 years Biopsy of lesion in the femoral neck showed metastatic thyroid carcinoma  Metastatic Tumors to Bone Cord compression can occur, causes nerve damage, loss of movement, muscle weakness Bone metastasis can cause bones to fracture  Overview of tumors (AKA neoplasms) BENIGN MALIGNANT Cartilage Cartilage  Enchondroma  Chondrosarcoma  Chondroblastoma Bone  Osteochondroma  Osteosarcoma Bone Bone Marrow  Osteoma  Multiple Myeloma  Bone island  Ewing’s Sarcoma  Osteoblastoma AS A PT: you may be the one to recognize and recommend early detection “So this all started when I went deep sea fishing around April in 2015, I get really “I think this story is really important motion sick so being out on the ocean I threw up many times on that trip. After that, to share with future PTs as this went I noticed some pain on my right side. without diagnosis for a long time for Everyone thought I had just pulled a muscle from throwing up so many times that day, me.” but this pain didn't go away. I noticed it throughout the summer as I would swim and do other activities but just brushed it off because at that point it wasn't stopping me from anything I wanted to do. Then August rolled around and it was time for volleyball tryouts for school. I thought this would be a good time to go to the doctors cause the pain was still present and I knew volleyball would exacerbate the problem. So I went in and got an x-ray which I linked below. There was no radiologist in that clinic at the time so this got misdiagnosed as a broken rib that had never healed from when I threw up on that deep sea fishing trip. Then I started playing volleyball and the pain got so much worse. Having to use my abdominal muscles a lot more from hitting and serving the ball I was in too much pain to play. Oftentimes I would have to ask the coach to get subbed out to take a break cause my broken rib was hurting. During this time I went to see a physical therapist who would tape my ribs to make them more stable so I could continue playing. I also decided to get a second opinion because the pain was getting so much worse. I went to Childrens as I was 16 “Hopefully this story can help future at the time and they had me get a CT scan PTs learn to screen for red flags that to see the tissue more. We decided to get  Overview of bone pathophysiology A variety of conditions can affect bone and require a reparative process – fracture – infection – inflammation (e.g., tuberculosis or sarcoidosis) – metabolic disturbances (e.g., Paget disease, osteoporosis, or osteogenesis imperfecta) – tumors – response to implanted prostheses – bone infarction – systemic diseases that have skeletal manifestations (e.g., sickle cell disease, amyloidosis, or hemochromatosis) Stay tuned, we will talk about many of the rest of these next lectures!