Project 1
Part A:
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- Clinical condition - Cystic fibrosis
Is shown in figure-1.
- Organ involved- Lungs.
is shown in figure-2.
- blood supply of lungs
Figure-3.
figure-4.
Most biochemical reactions in the body either generate energy or require energy to progress. Cellular organelles and tissues need oxygen to ensure these reactions proceed with ease.
The lungs are a pair of spongy organs found within the thorax and are involved in the gaseous exchange between atmospheric air and blood. This process is known as the respiratory cycle. At the lungs’ level, inhaled oxygen gets absorbed into the blood, and gaseous by-products are exhaled.
For the exchange of gases to occur effectively, the lungs require a dual vascular supply known as pulmonary and systemic circulations.
The pulmonary circulation is responsible for bringing deoxygenated blood from the body to the lungs for gaseous exchange and then returning oxygenated blood to the heart. This is then pumped back into the systemic circulation, and the cycle continues.
The pulmonary arteries carry deoxygenated blood at low blood pressures from the right ventricle to the lungs, where they form an extensive network of pulmonary capillaries that supply the alveoli. It is at this site that gaseous exchange occurs and oxygen gets absorbed into the blood through the alveoli. This freshly oxygenated blood returns to the left atrium of the heart via four pulmonary veins.
The bronchial circulation is part of the systemic circulation. It is responsible for supplying oxygenated blood at high blood pressures to the tissues that make up the conducting zone of the tracheobronchial tree and visceral pleura.
A paired group of left bronchial branches arise directly from the descending thoracic aorta. In contrast, the right bronchial branch arises indirectly from the descending thoracic aorta via the right-sided posterior intercostal artery, most commonly the third right posterior intercostal artery. Much of the blood supplied by the bronchial arteries returns to the heart via the pulmonary veins.
There needs to be adequate circulation of blood in the lungs for enough oxygen to get to the tissues, and any compromise to the blood supply to the lungs immediately decreases the partial pressure of oxygen in the blood. This scenario is known as hypoxemia. In many cases, it leads to a decrease in tissue oxygenation, a condition known as hypoxia.
- diagnostic techneque.
Prenatal testing.
Prenatal tests for cystic fibrosis are run if CF is known to run in a family, or if an ultrasound during pregnancy reveals that the baby has a bowel obstruction (abnormal meconium or hyperechoic bowel). First, the mother will get a blood test to see if she carries one or two CFTR mutations. If the mother carries a CFTR mutation, the father’s blood will be tested. If both parents are found to carry a CFTR mutation, then amniocentesis will be done to test the baby for CF.
Newborn screening.
Newborn screening for cystic fibrosis became standard in all 50 states in 2010.3 The exact test may vary by state, but basically, a drop of blood is taken from a heel prick and dried on filter paper. The droplet is then tested for the amount of immunoreactive trypsinogen (IRT).
A high level of IRT means that the baby may have partially blocked pancreatic ducts. If a high level of IRT is found, the next test will be a sweat test or a CFTR mutation analysis, which is a type of genetic testing.
Sweat test.
A sweat test measures the amount of salt in someone’s sweat. The official name for a sweat test is quantitative pilocarpine iontophoresis. It is considered the gold standard for diagnosing CF. This test should be conducted at a CF center accredited by the Cystic Fibrosis Foundation.
There are two types of the sweat test: the Gibson-Cooke procedure and the Wescor Macroduct® Sweat Collection System. In both tests, an electrode is placed on the arm below the elbow or on the thigh, with a piece of filter paper or gauze between the electrode and skin. The paper collects sweat which is then weighed and analyzed for chloride concentration. This test is completely painless.
Understanding sweat test results
From birth to 6 months.
| Chloride concentration | Result |
|---|---|
| 0-29 mmol/L | Normal – Cystic fibrosis not likely |
| 30-59 mmol/L | Intermediate/Borderline |
| 60+ mmol/L | Indicates cystic fibrosis |
Children & adults
| Chloride concentration | Result |
|---|---|
| 0-39 mmol/L | Normal – Cystic fibrosis not likely |
| 40-59 mmol/L | Intermediate/Borderline |
| 60+ mmol/L | Indicates cystic fibrosis |
Sweat tests may not be accurate in the first two days after birth. Premature babies may not generate enough sweat for an accurate test for two to three weeks after birth.
For people whose test results are borderline, other factors may be used to diagnose cystic fibrosis, including family history, age, and the fact that certain CFTR mutations are known to create borderline or negative sweat test results. People with borderline results will need follow-up tests.Malnutrition, thyroid issues, and other health conditions can cause a false positive sweat test.
Genetic testing.
CFTR mutation analysis is a type of genetic (DNA) testing. This blood test looks to see if the baby has two copies of the mutated CFTR gene, which is the gene that causes cystic fibrosis. The first screening test looks for the 23 most common CF genetic mutations. If this test is inconclusive, another DNA test looks for the next 88 most common variations of CF. However, with 1,700 known CF mutations, genetic testing may still be inconclusive.
- Surgical management.
Cystic fibrosis (CF) is a genetic disease that affects multiple organs. Mutations in the CF transmembrane conductance regulator (CFTR) gene lead to the dysfunction of the CFTR protein, which in turn results in the accumulation of thick and sticky mucus in several areas including the airways. Over time, CF leads to chronic lung disease, and it can potentiate malnutrition and digestive complications.
Managing CF may involve surgical procedures such as the removal of nasal polyps or the placement of a feeding tube to increase caloric intake. Major surgeries such as lung transplant and bowel surgery may be also required.
Lung Transplant in Cystic Fibrosis
Advanced CF lung disease (ACFLD) represents the most common cause of death in patients with CF. Patients with ACFLD have a decreased quality of life, with increased exacerbations and progressive worsening of symptoms. Clinical outcomes after lung transplants in patients with ACFLD have significantly improved, and lung transplants have been shown to provide a better quality of life for these patients. The benefits of lung transplantation may be more pronounced in patients experiencing worse symptoms. Discussing this surgery, as well as other potential treatments, while managing CF is recommended when the patient presents with normal lung function or mildly reduced forced expiratory volume in 1 second (FEV1). Although not all patients will be candidates for a lung transplant, this approach may contribute to better management of the fear and anxiety that patients with CF experience regarding this procedure. A focused discussion on lung transplantation led by the CF care team is recommended when the patient presents with a predicted FEV1 <50%.
Patients with CF have a median survival of 9.9 years after a lung transplant, and about 30% of patients survive for 20 years after transplantation. Additionally, the post-transplant survival in patients with CF is higher than that of other transplanted diagnoses. Patients undergoing a lung transplant should be physically and emotionally prepared, and they will benefit from social support throughout the process and rehabilitation.
Gastrointestinal Surgical Management in Cystic Fibrosis
Different gastrointestinal issues in patients with CF may require surgical intervention. These include meconium ileus in infants, distal intestinal obstructive syndrome (DIOS) in children and adults, and, rarely, rectal prolapse.
Meconium ileus affects about 20% of infants with CF. This intestinal disease may be simple or complex.Simple meconium ileus involves an intraluminal distal bowel obstruction due to abnormal viscid meconium. This condition may be characterized by complications such as meconium peritonitis, pseudocyst formation, or perforation, and it requires surgery. The goal of the surgical procedure is to decompress the bowel and remove the obstruction by clearing the abnormal meconium.
DIOS affects about 15% of CF patients, and it can present as a partial or complete obstruction. These obstructions result from the accumulation of viscid fecal material in the bowel and its combination with the sticky mucus in the intestine. Surgical decompression of DIOS is only performed when medical management is not successful, and it is associated with elevated morbidity and mortality.
Nasal and Sinus Surgery in Cystic Fibrosis
The changes observed in the visco-elastic properties of the abnormal mucus formed in patients with CF contribute to the mechanical obstruction of the nasal and paranasal sinuses. Chronic rhinosinusitis, which may be associated with nasal polyposis, develops in about half of patients with CF. Symptoms of this condition include nasal obstruction, sneezing, and thick nasal discharge. Endoscopic sinus surgery (ESS) can reduce inflammation and improve breathing in these patients.
A recent study reported that ESS can lead to better lung function in patients with moderate to severe CF, as well as in some patients with mild disease. The same study showed that the observed improvement in lung function was maintained 12 months after surgery. A different report also revealed that ESS interventions performed early after lung transplantation can improve the patient’s pulmonary function and decrease exacerbations, while longer waiting times may result in worsening lung function and increased antibiotic use.
- recent advances in cystic fibrosis.
CF pathogenesis
CF is caused by a defect in the CF transmembrane conductance regulator (CFTR) gene, on the long arm of chromosome 7, which leads to absence of normal CFTR protein, a cAMP-activated ion channel. The almost 2000 mutations identified can be grouped into six classes depending on their effect on protein expression/function. Class I mutations are ‘nonsense’ mutations containing premature stop codons preventing the protein from being synthesised. Class II mutations are the most commonly identified and include Phe508del, at least one copy of which is found in around 70% of all patients with CF.2 The protein folds incorrectly, therefore cannot traffic to the apical cell membrane, but undergoes degradation within the lysosomes. In class III mutations, the protein is correctly positioned on the cell surface but fails to open in response to intracellular signals. In class IV mutations, channel opening is normal but conductance is reduced due to pore abnormalities. In class V mutations, there is a splicing abnormality leading to a reduced amount of CFTR protein on the cell surface and class VI mutations lead to protein with a shortened half-life.
Absence of normally functioning CFTR leads to decreased chloride secretion and (due to loss of the normal inhibitory relationship with the epithelial sodium channel (ENaC)) increased sodium absorption across the epithelial surface. The net result of this is depletion of the airway surface liquid (ASL) and impaired mucociliary clearance (MCC). Infection and inflammation start early and become chronic; accumulation of DNA and actin released from incoming neutrophils further increases mucus viscosity and impairs clearance. Proteases and other inflammatory cell products, while possibly being responsible for limiting the infection to the airways, lead to airway wall inflammation, remodelling and, ultimately, irreversible bronchiectasis. Despite currently available treatments, around 90% of patients will die of respiratory failure unless they receive a lung transplant.
Treatment strategies
New treatment strategies target multiple steps in this cascade, including (a) gene therapy, (b) CFTR protein modulation, (c) rehydration of the airway surface and/or mucolytics, (d) anti-inflammatories and (e) anti-infective agents.
CFTR gene therapy
Since the discovery of the CFTR gene, numerous attempts have been made to reverse the basic defect by gene transfer. In vitro experiments demonstrated successful restoration of ion transport with either modified viral vectors or synthetic gene transfer techniques, but achieving similar success in the clinic has been challenging. The majority of clinical trials have been single-dose, proof-of-concept design, often administering the gene therapy to the nasal epithelium for ease of access. Several of these trials have reported success based on transgene expression (mRNA) and electrophysiology (nasal potential difference (PD)), but the results have been variable and expression of short duration. Attempts to dose repeatedly have confirmed that currently used viral vectors lead to immune responses that limit efficacy upon subsequent administration. There are few groups now still working in this field. The UK CF Gene Therapy Consortium is currently conducting a large, phase IIb, repeated dose, randomised, placebo-controlled trial of cationic liposome-mediated CFTR gene therapy. Nebulised doses are being administered at monthly intervals for 1 year, with a primary outcome of change in FEV1. Secondary outcomes include lung clearance index, CT scans, validated quality-of-life questionnaires and sputum/serum inflammatory markers. A subgroup will undergo nasal dosing and nasal PD measurements or will have similar electrophysiological measurements made bronchoscopically. In parallel to this clinical programme, the Consortium is developing a second wave product, a pseudotyped lentivirus, which unlike most viral vectors appears to be repeatedly administrable. The advantages of this approach are high levels of transfection and the potential for long duration of expression, which may allow infrequent dosing. Clearly this approach requires detailed preclinical toxicity testing and optimisation before clinical trials commence, so is some way off.
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- clinical condition- Osteoarthritis
is shown in figure-5.
- organ involved- bone
is shown in figure-6.
- blood supply of bone
is shown in figure-7.
- diagnostic technique.
There is progressive destruction of the articular cartilage in OA patients. Physicians use several methods to diagnose people with this disabling joint disease, and the diagnosis is primarily made according to radiographic findings as well as the presence of certain clinical signs and symptoms. Radiologic evaluation of joint images provides a historical view of the damage that has occurred with OA. There are other alternative methods for diagnosis, such as molecular markers and synovial fluid analysis. These diagnostic techniques can be used not just for diagnosis, but also for prognosis and disease progression monitoring. These various diagnostic methods are important for the development of new disease-modifying treatments (DeGroot, Bank, Tchetverikov, Verzijl, & TeKoppele, 2002).
SYNOVIAL FLUID EVALUATION
- Viscosity – This has been a primary method of diagnosis used by researchers in the field of rheumatology for many years. Viscosity synovial fluid evaluation is done by assessing the physiochemical properties of the synovial fluid in subjects with OA and comparing it to the synovial fluid of subjects without the disease (Esmonde-White, 2009).
- Inorganic Crystals – Because microscopic inorganic crystals are frequently observed in the synovial fluid of people with OA, basic calcium phosphate (BCP) crystals are diagnostic for the condition. BCP crystals are insoluble at physiological pH. Currently, evaluation of OA patients’ synovial fluid is dependent on light microscopy and staining with Alizarin Red-S. Researchers also used O-cresolphtahalein complexone (OCP), a colorimetric reagent, to quantify calcium from the crystals in synovial fluid and found it to be indicative of BCP presence in the fluid. The scientists found that the average calcium content in those with OA was up to 40% higher than in patients with rheumatoid arthritis. Higher levels of calcium were also detected in 3 out of 12 synovial fluid samples in the OA group, correlating a substantial greater number of BCP crystals. This basic method is based on colorimetry and improves OA diagnosis.
- Raman Spectroscopy – In one recent study, researchers evaluated the synovial fluid of 40 people with clinical OA of the knee, and the severity of the OA was also evaluated by a radiology using Kellgren/Lawrence scores. Ramen spectroscopy was then used to assess the synovial fluid, and the scientists found that Raman bands corresponded to changes in synovial fluid structure in OA patients. This research provided evidence that Raman spectroscopy is suitable for determining the extent of joint damage in patients with knee OA (Esmonde-White et al., 2009).
MOLECULAR MARKERS
According to researcher DeGroot and associates (2002), molecular markers are necessary for diagnosis, they reflect actual disease activity, are sensitive to therapy, and predict the disease outcome. Different molecular markers can be used for preclinical studies of OA pathophysiology and for creation of new treatments. Certain genetic markers have been shown to offer essential information on risk factors for the development and progression of OA.
maging tests
To get pictures of the affected joint, your doctor might recommend:
- X-rays. Cartilage doesn't show up on X-ray images, but cartilage loss is revealed by a narrowing of the space between the bones in your joint. An X-ray can also show bone spurs around a joint.
- Magnetic resonance imaging (MRI). An MRI uses radio waves and a strong magnetic field to produce detailed images of bone and soft tissues, including cartilage. An MRI isn't commonly needed to diagnose osteoarthritis but can help provide more information in complex cases.
maging tests
To get pictures of the affected joint, your doctor might recommend:
- X-rays. Cartilage doesn't show up on X-ray images, but cartilage loss is revealed by a narrowing of the space between the bones in your joint. An X-ray can also show bone spurs around a joint.
- Magnetic resonance imaging (MRI). An MRI uses radio waves and a strong magnetic field to produce detailed images of bone and soft tissues, including cartilage. An MRI isn't commonly needed to diagnose osteoarthritis but can help provide more information in complex cases.
Lab tests
Analyzing your blood or joint fluid can help confirm the diagnosis.
- Blood tests. Although there's no blood test for osteoarthritis, certain tests can help rule out other causes of joint pain, such as rheumatoid arthritis.
- Joint fluid analysis. Your doctor might use a needle to draw fluid from an affected joint. The fluid is then tested for inflammation and to determine whether your pain is caused by gout or an infection rather than osteoarthritis.
Analyzing your blood or joint fluid can help confirm the diagnosis.
- Blood tests. Although there's no blood test for osteoarthritis, certain tests can help rule out other causes of joint pain, such as rheumatoid arthritis.
- Joint fluid analysis. Your doctor might use a needle to draw fluid from an affected joint. The fluid is then tested for inflammation and to determine whether your pain is caused by gout or an infection rather than osteoarthritis.
X-ray image is shown in figure-8.
- Parts of x-ray machine.
is shown in figure-9.
- surgical management.
Hip OA
Conservative treatment
Conservative surgical treatments of hip OA have declined over the last decades after the implementation of total hip replacement (THR). Nonetheless, significant indications remain for young patients. These treatments will surely delay but not always avoid the need for joint replacement in the long-term. The 3 main surgical procedures that can be performed are femoral osteotomy, pelvic osteotomy, and cartilage and labrum procedures under arthroscopy.
Femoral osteotomy
This osteotomy reorients the femoral head, with one of 2 main goals: positioning an adequate portion of the femoral cartilage in front of the acetabulum, such as in rotational osteotomy of the femoral neck for osteonecrosis , and changing the biomechanics of the hip to reduce the load going through the joint, such as in femoral varus osteotomy. The most common osteotomies are valgus and varus femoral osteotomies; others such as flexion, extension or rotation osteotomy or a combination of these are less frequent. The varus femoral osteotomy is usually indicated for hip dysplasia, osteonecrosis, and valgus deformation. It closes the neck-shaft angle when it is superior to 135° . The long-term results for early OA are good, with 75% 10-year survival, defined as the delay before hip replacement. Second-line hip replacement will have the same prognosis as first-line replacement. The procedure is not recommended with isolated serious dysplasia . Valgus femoral osteotomy is mainly performed for femoral neck non-union, slip upper-femoral epiphysis sequelae and congenital varus deformity of the femoral neck.
Pelvic osteotomy
Pelvis osteotomy (including the shelf procedure) is only rarely performed today but can still provide excellent results. The common eligibility criterion is a painful, dysplastic hip in a relatively young patient (usually < 30 years old). Beyond that, we also rely on some other indications such as cartilage degeneration stage and coxometric parameters to decide on the surgical procedure. Shelf operation consists of a bone graft addition on top of the hip where the femoral head is uncovered; although it provides support and balances the load, it does not provide cartilage.
- recent advance in Osteoarthritis
Treatments targeting articular cartilage
OA is characterized by the degradation of articular cartilage and bone matrix components. Among the earliest are type II collagen and the proteoglycan aggrecan, leading to the loss of cartilage structure and function. Cartilage matrix degeneration products are well investigated for drug target discovery. Several key anabolic and catabolic pathway enzymes are dysregulated in OA cartilage, providing the opportunity to identify and validate new drug targets. To this end, novel combinations addressing existing known targets may be identified. This also includes combinations of therapeutics that are anti-catabolic and those that target anabolic signaling pathways. If investigated, this might lead to identifying novel efficacious add-ons from combining known drugs and targets. For better classification, there should be discrimination between disease-modifying OA drugs (DMOADs), which target pathways of cartilage catabolism and anabolism, and regenerative strategies based on stem cells and their components.
Anabolic drug: sprifermin
A promising anabolic DMOAD is sprifermin, which is a truncated version of human FGF18 that induces chondrocyte proliferation and cartilage matrix production. The results of a phase Ib study of i.a. injected sprifermin in patients with symptomatic knee OA found a statistically significant dose-dependent reduction in loss of total femorotibial cartilage thickness compared to placebo after 12 months of follow up . Sprifermin is currently being studied in a phase II multicenter randomized dose-finding clinical study (clinicaltrials.gov: NCT01919164). The i.a. administration of 100 μg of sprifermin to participants with symptomatic radiographic knee OA every 6 or 12 months vs. placebo resulted in an improvement in total femorotibial joint cartilage thickness after a follow up period of 2 years. This improvement was statistically significant, but clinical importance was not clear. Application of a lower dose, 30 μg of sprifermin, every 6 or 12 months vs. placebo did not result in a significant difference and it was uncertain whether the response was long lasting.
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- Clinical condition- alzheimer's
is shown in figure-10.
- Organ involved- Brain
is shown in figure-11.
- diagnostic procedure.
Brain imaging
Images of the brain are now used chiefly to pinpoint visible abnormalities related to conditions other than Alzheimer's disease — such as strokes, trauma or tumors — that may cause cognitive change. New imaging applications — currently used primarily in major medical centers or in clinical trials — may enable doctors to detect specific brain changes caused by Alzheimer's.
Imaging of brain structures include the following:
Magnetic resonance imaging (MRI). MRI uses radio waves and a strong magnetic field to produce detailed images of the brain. While they may show brain shrinkage of brain regions associated with Alzheimer's disease, MRI scans also rule out other conditions. An MRI is generally preferred to a CT scan for the evaluation of dementia.
Computerized tomography (CT). A CT scan, a specialized X-ray technology, produces cross-sectional images (slices) of your brain. It's usually used to rule out tumors, strokes and head injuries.
Imaging of disease processes can be performed with positron emission tomography (PET). During a PET scan, a low-level radioactive tracer is injected into the blood to reveal a particular feature in the brain. PET imaging may include the following:
Fluorodeoxyglucose (FDG) PET scans show areas of the brain in which nutrients are poorly metabolized. Identifying patterns of degeneration — areas of low metabolism — can help distinguish between Alzheimer's disease and other types of dementia.
Amyloid PET imaging can measure the burden of amyloid deposits in the brain. This imaging is primarily used in research but may be used if a person has unusual or very early onset of dementia symptoms.
Tau PET imaging, which measures the burden of neurofibrillary tangles in the brain, is generally used in the research setting.
In special circumstances, such as rapidly progressive dementia, dementia with atypical features or early-onset dementia, other tests may be used to measure abnormal beta-amyloid and tau in the cerebrospinal fluid.
- Parts of CT Scan And MRI.
is shown in figure-12 and figure-13.
- surgical management.
Before the surgery, your loved one will have a medical exam and some tests. The doctor will rate their physical status. If the results are OK, they’ll sign a consent form and get a surgical clearance. You may sign the consent form for them if you’re designated to make medical decisions.
Your loved one will be told to not eat or drink anything after midnight on the night before the operation so they’ll be less likely to vomit during or after it.
In the pre-op area, they’ll change out of their clothes into a gown. They’ll be asked to confirm who they are and why they’re there. You may need to do this for them. Then a nurse will record their vital signs. They’ll also place an IV line and give your loved one pre-op medications. You’ll want to stay with your loved one during this entire process, and you may need to remind them several times why they’re there and what’s happening.
In the operating room, your loved one will get anesthesia so they don’t feel pain during the operation. After the surgery, staff will move them to the post-op care unit and watch them closely. When they feel your loved one has recovered from the anesthesia, they’ll move them to a surgical ward elsewhere in the hospital or send them home.
During the post-op period, hospital staff will check the surgery site for signs of infection. The doctors will also want to judge your loved one’s general function and the results of the surgery.
After Surgery
You’ll want to be there when your loved one returns to their room after surgery. If they’re asleep, don’t wake them. Not even for visitors. When they wake up, tell them where they are, what has happened, that you’re there, and that everything will be OK. Assure them that they’ll feel better soon.
You’ll also want to build a close relationship with the nurses. Let them know that you’re there to help, and ask if there’s anything they want from you. It will make caring for your loved one easier if you explain how well they usually function and what their normal mental state is. Tell the staff about anything that helps to calm them when they’re upset, in case a situation arises when you’re not there.
Keep an eye on your loved one’s mental and physical state. If something bothers you, let the staff know. Tell them what you think is different. Know the typical side effects and complications of the surgery your loved one had so you can watch out for signs of trouble.
Talk to the medical team about how to take care of your loved one when they go home. Find out what danger signs you should look for.
If you can’t be there, arrange for a family member or friend to be there. Explain the things they need to watch out for. Give the staff your phone number in case a problem comes up. If you’re the family member who’s most involved in decisions and care, check in regularly when you’re away. Let everyone who stays with your loved one know when it’s OK to call you.
Part B>
- the type of bone the skull belongs to Flat bones
Is shown in figure-14.
The skull begins to form prior to week 12 of embryogenesis. A cartilaginous mould begins to grow and is slowly replaced by bone in a process called intramembranous ossification.
This process occurs at different rates in two different regions of the skull:
- Calvarium (roof): the frontal, occipital and parietal bones tend to grow slightly earlier
- Base: the sphenoid, ethmoid, occipital and temporal bones tend to grow slightly later
By week 37, the cartilaginous frame for the skull is almost entirely replaced by bone, and only two relatively small cartilaginous structures remain:
- Anterior fontanelle: the soft region on the front of the infant’s head
- Posterior fontanelle: the soft region on the back of the infant’s head
The fontanelles undergo complete ossification within 9 – 18 months from birth.
Clinical relevance: Fontanelle abnormalities
An enlarged anterior fontanelle can be due to endocrine pathologies like congenital hypothyroidism.
A bulging anterior or posterior fontanelle may suggest raised intracranial pressure, which may occur in hydrocephalus.
A sunken anterior or posterior fontanelle may suggest dehydration.
Bones of the calvarium
The calvarium, also known as the roof or skull cap, consists of three bones:
- Frontal bones
- Parietal bones
- Occipital bones
These bones protect the brain superiorly, but also provide an anchor for important muscles of facial expression and eye movement. The parts of these bones that lie inferior to the brain are considered to be a part of the skull base (mentioned below).
Of particular importance is the strength of these bones relative to how thin they are. These bones of the skull cap contain two thin layers of cortical bone separated by diploë, which is synonymous with the spongy bone seen in long bones.
Diploë provides structural integrity and transmits forces along the length of the bones of the skull cap.
Frontal bone
The frontal bones start as two paired bones. During childhood and adolescence, these two bones fuse into one.
The fusion of these frontal bones forms a metopic suture, which may be visible in some skull specimens.
There are three important parts of the frontal bone to know:
- Orbital plate of the frontal bone: forms the roof of the orbital cavity and separates the frontal lobe of the brain from the eye
- Glabella: the brow ridge that serves as an attachment point for the frontalis muscle and superior portion of the orbicularis oculi
- Supraorbital notch: nerves supplying the forehead to emerge through this aperture
- the microscopic anatomy of bone Osteons.
Is shown in figure-15.
As noted earlier, there are two types of bone: compact bone and spongy bone. When viewed microscopically, compact bone is formed of a number of subunits called osteons. An osteon (os)-te-on) is composed of a central canal containing blood vessels and nerves, surrounded by the lamellae (singular, lamella), concentric layers of bone matrix.
Bone cells, the osteocytes (osAe-o-sitz), are arranged in concentric rings between the lamellae and occupy tiny spaces in the bone matrix called lacunae.
Blood vessels and nerves enter a bone through a nutrient foramen (fo-ra’-men; plural, foramina), a channel entering or passing through a bone. The blood vessels form branches that pass through perforating canals and enter the central canals to supply nutrients to the osteocytes. Canaliculi the tiny tunnels radiating from the lacunae, interconnect osteocytes with each other and the blood supply.
The trabeculae of spongy bone lack osteons, so osteo- cytes receive nutrients by diffusion of materials through canaliculi from blood vessels in the bone marrow surrounding the trabeculae.
The structure of the other bone types is like that of the epiphyses of long bones. Their external structure is a thin layer of compact bone covered with periosteum; the internal structure is spongy bone covered with endosteum. In most of these bones, red bone marrow fills in the spaces between the trabeculae.
- The blood supply of bone. Nutrient arteries
is shown in figure-16.
The blood supply to bone is delivered to the endosteal cavity by nutrient arteries, then flows through marrow sinusoids before exiting via numerous small vessels that ramify through the cortex. The marrow cavity affords a range of vascular niches that are thought to regulate the growth and differentiation of hematopoietic and stromal cells, in part via gradients of oxygen tension. The quality of vascular supply to bone tends to decline with age and may be compromised in common pathological settings, including diabetes, anaemias, chronic airway diseases and immobility, as well as by tumours. Reductions in vascular supply are associated with bone loss. This may be due in part to the direct effects of hypoxia, which blocks osteoblast function and bone formation but causes reciprocal increases in osteoclastogenesis and bone resorption. Common regulatory factors such as parathyroid hormone or nitrates, both of which are potent vasodilators, might exert their osteogenic effects on bone via the vasculature.
- bone remodeling and new bone formation- Ossification
is shown in figure-17.
Bone Ossification
Bone is the rigid tissue that is a part of the skeleton system in vertebrates. They help in the production of the red and white blood cells, provides structure, it stores minerals, enables mobility, and provides support to the body. It has complex internal and external structures, now let us see how bones are formed. Bone tissue is also known as osseous tissue, thus the process of formation of the bone is called Bone ossification. Now let us define ossification and the steps involved in it.
The process of remodeling the bone is called ossification; it is also known as osteogenesis. It is the process of remodeling the bone by laying the particles of the new bone material in the cells called osteoblasts. There are several hypotheses that propose the evolution of the bone as a structural element. According to one of the hypotheses, bones are evolved in order to store the minerals. In the cartilage, the specialized calcium minerals were stored from this classified cartilage the bone forms. There are two processes of bone formation, they are Intramembranous ossification and endochondral ossification.
Bone Formation
1.Intramembranous Ossification: In this process, the formation of the compact and spongy bone takes place directly from the sheets made of the undifferentiated mesenchymal connective tissue. By this process the bones that are located in the face such as flat bones, the collar bones or clavicle, and cranial bones.
There are 4 Stages of Bone Formation and Growth in Intramembranous ossification:
- When the mesenchymal cells that are present in the embryonic skeleton gather together then the process begins in order to differentiate into specialized cells. Some of these cells become osteogenic cells and some of them differentiate as capillaries. The osteogenic cells are further converted into osteoblasts. The early osteoblasts in a cluster of cells called the ossification centre.
- The osteoblasts secrete osteoid, it is an uncalcified matrix that consists of collagen precursors and other types of organic molecules. Within a few days, mineral salts are deposited on the matrix and it gets hardened by entrapping the osteoblasts. When these are entrapped the osteoblasts get converted into osteocytes. The osteogenic cells that are present in the surrounding of the connective tissue get differentiated to form new osteoblasts at the edge of the growing bone tissue.
- Osteoid clusters get united around the capillaries in order to form a trabecular matrix whereas the osteoblasts that are present on the surface of the newly formed spongy bone that becomes the cellular layer of the periosteum.
- This periosteum then secretes the superficial of the compact bone to spongy bone. Nearby the blood vessels the spongy bone crowds that eventually condenses to form new red bone marrow. Under the action of osteoclasts, the new bone gets remodeled.
- Formation of the ossification centre
- Formation of osteocytes
- Trabecular matrix and periosteum form
- Development of compact bone
2.Endochondral Ossification: In this process, bone develops by replacing cartilage. Cartilage does not become bone. Instead, cartilage serves as a template to be completely replaced by new bone. Endochondral ossification takes much longer than intramembranous ossification. Bones that are present at the base of the skull and long bones form through the process of endochondral ossification.
In a long bone, a number of the mesenchymal cells differentiate into chondroblasts or cartilage cells at about 6 to eight weeks after conception, which forms the hyaline cartilaginous skeletal precursor of the bones. This cartilage is a flexible, semi-solid matrix that is produced by cartilage cells and consists of chondroitin sulfate, collagen fibres, hyaluronic acid, and water. They're also called chondrocytes as the matrix surrounds and isolates the chondroblasts. Unlike most connective tissues, cartilage is avascular which means that it has no blood vessels that are supplying the nutrients and removes the metabolic wastes. All of those functions are carried on by the process of diffusion through the matrix from vessels within the surrounding perichondrium, a membrane that covers the cartilage.
As more and more matrix is produced, the cartilaginous model grows in size. Blood vessels that are present in the perichondrium bring the osteoblasts to the edges of the structure and these arriving osteoblasts deposit bone in a ring around the diaphysis this process is called a bone collar. The bony edges of the developing structure prevent the nutrients from diffusing into the middle of the cartilage. This leads to the death of chondrocytes and disintegration within the centre of the structure.
Without cartilage inhibiting vessel invasion, blood vessels penetrate the resulting spaces, not only enlarging the cavities but also carrying osteogenic cells with them, many of which can become osteoblasts. These enlarging spaces eventually combine to become the medullary cavity. Bone is then deposited within the structure that is creating the first ossification centre.
While these deep changes are occurring, chondrocytes and cartilage still grow at the ends of the structure, which increases the structure’s length at an equivalent time bone is replacing cartilage in the diaphyses. This continued growth is the reason for the remodeling inside the medullary cavity and the overall lengthening of the structure. Cartilage remains at the epiphyses and the joint surface as articular cartilage when the fetal skeleton is formed completely.
After birth, this same sequence of events occurs within the epiphyseal regions, and each of these centres of activity is referred to as a secondary ossification centre. Throughout childhood and adolescence, there remains a skinny plate of cartilage between the diaphysis and epiphysis referred to as the expansion or epiphyseal plate. Eventually, these cartilages are going to be removed and replaced by bone to become the epiphyseal line.
- the anatomical basis of bone implant.
is shown in figure-18, figure-19, figure-20.
Bone strength is directly related to its density, and the low-density bone of this region is often five to ten times weaker compared with bone found in the anterior mandible. 5 The various bone densities directly influence the bone-implant contact (BIC) percent, which accounts for the transmission of forces to the bone. The posterior maxilla most commonly exhibits D4 bone (Misch classification), which has the greatest biomechanical elastic modulus difference when compared with titanium under.
This anatomical variation might jeopardize the result of the total hip arthroplasty when the surgeon uses a cementless femoral shaft. Indeed, if the secondary fixation of an implant stays under the dependency of many parameters, one has to obtain before anything else a very good primary stability, obtained by the morphological appropriateness of the bone-implant. The authors propose to define the cementless indications, as regards total hip arthroplasty, defining two radio-anatomical parameters: the Cortico-Medullary Index and the Femoral Flare Index.
Linear and angular measurements were obtained from the maxillae and zygomata of 40 dry skulls. Based on mean and standard deviation values, the installation angle of the additional implant in the four zygoma technique was between 25 degrees and 47 degrees , and that of the conventional zygomatic implant was between 39 degrees and 62 degrees . The distance between the alveolar crest in the canine region and the lateral margin of the orbital socket was 53.42 mm, and between the alveolar crest in the premolar region and the area closest to the lateral margin of the orbital socket was 42.47 mm. When the angle of installation of the additional implant is less than 25 degrees and that of the conventional zygomatic implant is less than 39 degrees , perforation of the maxilla, zygoma, or the infratemporal fossa must be avoided. When the angle of installation of an additional implant is greater than 47 degrees and that of the conventional zygomatic implant is greater than 62 degrees , perforation of the orbital floor must be avoided. The length of an additional implant was greater than the length of a conventional zygomatic implant, and should be measured prior to drilling, because the greatest value found for this distance was 61.94 mm, while the maximum length of the zygomatic implants currently available on the market is 52.5 mm.
- Indications and contraindications for the implantation
1. Chronic diseases in the stage of decompensation.
2. Disorders of coagulation and hemostasis.
3. HIV seropositive and any other infection.
INDICATIONS
1.Single defects dentition, when implantation would avoid dissection adjacent to the defect of the teeth.
2. Included defects of dentition, when using the implant can be avoided
dissection limiting defect teeth and removable prosthesis.
3. Limit the defects of dentition in which implants allows for
removable prosthesis.
4. Full edentia when using the implant can be made removable prosthesis or to provide a more reliable fixation of complete removable dentures.
5. Mental illness.
CONTRAINDICATIONS
There are a number of diseases in which implantation, as well as any other planned surgery is contraindicated. They accepted include:
1. Chronic diseases in the stage of decompensation.
2. Disorders of coagulation and hemostasis.
3. HIV seropositive and any other infection.
4. Mental illness.
• There are also diseases, physiological and functional status, with
which only at a certain period of time execution of any operation may harm the health of the patient, or in this period the state of the organism will not achieve the positive results of surgical intervention.
These include:
1. Acute inflammatory diseases and acute viral infections.
2. Chronic infectious diseases (tuberculosis, actinomycosis, etc.).
3. Exacerbation of chronic diseases.
4. The high degree of risk of bacteremia (patients with prosthetic heart valves and had suffered bacterial endocarditis, rheumatic fever).
5. Recent infarct or stroke.
6. Pregnancy and lactation.
7. Treatment with drugs that have an adverse tissue regeneration (hormonal and chemotherapy, receiving immunosuppressive agents, etc.).
As a contraindication for dental implantation should be considered osteopathy, diseases that adversely affect bone formation, diseases of the central nervous system disorders, which leads to violations of bone metabolism, diseases in which significantly reduced resistance to infections, as well as certain diseases and conditions organs and tissues of the maxillofacial region that did not help achieve the desired result of implantation.