Biocompatible Dental Material

The composition and amount of each metal in the alloy determines whether it is classified as a “high noble,” “noble,” or “base” metal. “Noble” metals are defined as gold, platinum and palladium. The most expensive gold alloys are “high noble” and they are defined as hiving at least 60% noble metals and at least 40% gold. An alloy can still be called “noble” if it has at least 25% noble metal content. The cheapest materials fail even that test and are called “base” alloys–they have less than 25% noble metals. It is especially important for patients with metal sensitivities to avoid the base alloys since these usually contain toxic metals such as nickel and chromium;. But even the high noble materials can be incompatible for patients and even toxic; palladium, for example, is toxic.
Titanium Inlay /  Onlay

Titanium is used when a gold alloy is not biocompatible; otherwise, the benefits, cost, and time to perform are the same as for a gold alloy, even though it is not a precious metal. It takes two visits.

Palladium Dental Alloy

Palladium   ( Pd ) is  a  silver-white ductile and malleable  metal that belongs  to the  platinum groups  it is atomic weight  is 106: it is melting point  1557 degrees Celsius. Palladium  is  found in the  platinum mines  of Russia,  Canada, Columbia,   and is used  in  electrical  contacts  as  a  catalyst and  in  Gold, Silver and  Cooper   Alloy. The use of  Palladium in Dentistry  dates  back  to 1986,  and  health  insurances  supported its  use  for what  seen to be  economic  reasons .Only  German Holist Medical  doctors  refer  to Palladium  as  the “ Fool’s Gold”   of dentistry  because  it  may  be mire  dangerous  than Mercury. The  amount of Palladium used  in the  making  on Dental Crowns varies  considerable. The more  durable  Gold  and  Silver  fillings  or  Crowns  may  contain   up to  78.5 %  of  this  Heavy Metal. Like Mercury   Palladium  is bio methylated  in the  digestion  tract  and  once  synthesized  these methylated metals  are   invariable more  toxic  than  their  inorganic  substrates.
This toxicity  is thought  to  be  due  to  the  non  polar  nature  of many  organometallic  compounds  which  allows   them  to  diffuse  rapidly  into  and  though  cell  membranes. Dr.  Elef  Karkalis  M.D.  of Oppenheim Germany  ,  believes  that methylated  Palladium  is more  than  Methylated mercury ,  which  is  known  to  cause  severe  Neurological  disorders,  including  insanity  . MethylMercury  interacts  with  phospholipids, causing  neurotoxicity, MethylMercury   poisoning  has  affected  people  in Japan, Guatemala, Russian  and Iraq, and  the  industrial  dumping   of mercury  into  Lake  St. Clair  touched of  hunt  for  Mercury –contaminated  fish  that invariable  cuased human illness.

Since Palladium  is  easily  Methyltated , it  is  considered to  be equally or possible  more   dangerous  to the  health  than Mercury ,  and  the  extensive use  of  Palladium Dental Crowns may  indeed  be  a  “Fool’s choice “. By   exchanging  “‘GOLD ‘ “  with  other metal  such  as  Nickel,  Chrome , Cobalt , Copper. This  replacement   therapy  may  be more  expensive  health wise  , Dr. Karkalis  is most  concerned  about  the  enzyme  blocking  function  of  Palladium . Dr.  Karkalis  specifies  early  symptoms   of Palladium  over  exposure as”   Chronic  fatigue,  Allergies,  Headaches, Lymph  node swelling, Immune  weakness.  Specifies symptoms  of  advanced  toxicity  as :  Bronchitis, Muscle  and join pain, Memory loss, Digestive  and nervous  disorders, Weight loss, Chronic  sinusitis  and  tinnitus,  excessive  sweating,  Neuralgia, Facial paralysis, Sleeping  disorders, Muscle  weakness.
According  to  German sources  Gold  Dental  Crowns  contain  a maximum  of  18 %   Gold  (  Au )  and   aside  from   containing  Palladium , other  metal  compounds  such  as   Silver, Cooper, Platinum ,   may   be  used.  Metallic  silver  ( Ag ) has   been  reported  as  solid   state  carcinogen   while soluble  compounds  of  silver  increased  DNA  miscopying  in vitro. The  deterioration  of metallic  compounds  such  Mercury, Silver,  Palladium,  Amalgams increases the  oral  intake  of  potentially   TOXIC METAL ,  yet  unlike Mercury Amalgams  which  are know  to  slowly   induce  symptoms  of  Mercury Toxicity , Palladium Dental  Alloy  Crowns   seem  the  induce  toxicity  problems  much   sooner.

Palladium  used  in Dental  Alloy   Gold  Crowns  since  1989. May  more  toxic  than Mercury  Dental  Fillings  . Some  “Gold Alloy “    dental  fillings  like  crowns, fixed  bridge,  inlay, onlay   , Meryland  bridge  ,  contain  up  to   78.5 %  of  Palladium  (  Pd ) . Hair,  urine  and  blood  analysis  detects  long – term chronic  exposure ad  sub-clinical  toxicity. High blood  and  urine  levels are considered signs  of  a  severe chronic  or acute  toxicity.
Trace Mineral International  Inc.

Dental Material Philosophies Conventional

Except in rare situations, currently used dental materials are safe in the mouth. The important criteria are how durable, natural looking, inexpensive, and practical they are for the dentist and dental laboratory to use. Concerns therefore are economics and aesthetics. Because some people have a sensitivity to certain substances, the choice of dental materials may have to be limited. A special blood test may be used to determine sensitivity to corrosion by-products of components.

Toxicity

Some dental materials contain toxic substances that, depending on exposure and other factors, may impact total toxic body load. Non-toxic alternatives should be used to decrease exposure to and accumulation of scientifically confirmed environmental toxins. Some dental treatment and materials can be disruptive to the normal flow of energy through the acupuncture meridians. Eastern philosophy believes chronic disruption of energy flow causes dysfunction and resultant health problems on the associated meridian; therefore, the choice of dental materials and treatments is limited.

Electrogalvanism

Dissimilar metals in the mouth, including different formulations of the “same” metal, create microamps of current which could cause oral pain, corrosion of the metal (black mercury amalgam fillings), dry mouth, metallic taste, erythema (red & swollen gums), and possible dysfunction of other organ systems, endocrine glands, etc. on that meridian.

Crown and Bridge Materials

Gold Alloy

A gold alloy is used when maximum strength is desired and appearance is not a factor. There are many formulations of gold, varying from 1% to 99%.

Titanium

Titanium is used when maximum strength is desired, appearance is not a factor, and a gold alloy is not biocompatible. There are different purities of titanium, with grade-1 being the purest. This is used in joint replacement, dental implants, and bone pins. Cost is the same as for gold alloy.

Non-Precious Alloy Nickel  heavy metal  poisoning

Non-precious alloys are used when maximum strength is desired, appearance is not a factor, but cost is most important. Since it does not contain any gold, cost is less. There are two basic formulations, one that contains nickel and one that is nickel-free. The controversial issue is that nickel, beryllium, cobalt, chromium, and palladium may cause immune problems and/or toxicity.

Toxicokinetics

1. Absorption
   
   Health hazards associated with exposure to nickel in the occupational environment have resulted primarily from inhalation. However, in addition to this main exposure route, workers are also indirectly exposed to nickel by ingestion of drinking-water and food, and through skin contact. Tobacco smoking is also an important source of nickel exposure.
   The relative amounts of nickel absorbed by an organism are determined, not only by the quantities inhaled, ingested, or administrated, but also by the physical and chemical characteristics of the nickel compound. Solubility is an important factor in all routes of absorption, following the general relationships nickel carbonyl absorption> soluble nickel compounds absorption> insoluble nickel compounds absorption.
   Nickel carbonyl is the most rapidly and completely absorbed nickel compound (in both animals and human beings).-inhalation exposure: respiratory absorption of nickel is normally the principal route for its entry into the human body under conditions of occupational exposure. It usually involves the inhalation of one of the following substances: dust of relatively insoluble nickel compounds (particulate nickel), aerosol derived from nickel solutions or gaseous forms containing nickel (e.g. nickel carbonyl).Particulate nickel: respiratory absorption of nickel compounds in particulate form is influenced by three processes in the lung: deposition, mucociliary clearance, and alveolar clearance. Moreover, the deposition pattern in the respiratory tract is related to particle size, which determines the degree to which particles are affected by inertial impaction, sedimentation, and diffusion. In humans, about 20-35% of the inhaled less-soluble nickel (nickel oxide, nickel subsulfide) that is retained in the lungs is absorbed into the blood. The remainder is either swallowed, expectorated, or remains in the respiratory tract.Soluble compounds are more readily absorbed from the respiratory tract as indicated by the higher concentrations of urinary nickel found in workers exposed to e.g. nickel chloride or nickel sulfate compared to those exposed to less-soluble nickel compounds.Nickel carbonyl: in the toxicology of nickel, a special position is occupied by nickel carbonyl, a volatile, liquid, liposoluble compound. After nickel carbonyl inhalation, removal of nickel deposited in the lung is the most rapid, compared with the clearance of all other compounds, indicating an extensive absorption and clearance. Nickel carbonyl is the only one of the nickel compounds to cause acute symptoms of poisoning, when inhaled.

   -oral exposure: absorption of nickel from the gastrointestinal tract occurs after ingestion of food, beverages, or drinking-water. A significant quantity of inhaled material is also swallowed following mucociliary clearance from the respiratory tract. Poor personal hygiene and some work practices can contribute to gastrointestinal exposure.
   The rate of nickel absorption from the gastrointestinal tract is dependent on its chemical form and may be influenced by some factors as composition of the diet, or interactions with other elements.
   Soluble nickel compounds (i.e. nickel sulfate) are better absorbed than relatively insoluble ones after ingestion(and/or inhalation). However the contribution of the poorly soluble compounds to the total nickel absorption may be more significant after oral than after inhalation exposure since they are more soluble in the acidic gastric fluids.

   Factors influencing gastrointestinal absorption are: composition of the diet
   Gastrointestinal absorption of nickel is variable and depends on the composition of the diet. In human volunteers who ingested nickel sulfate in the drinking-water or food, at doses of between 12 and 50 µg/kg body weight (one treatment), absorption of nickel averaged 27 (± 17%) of the dose from water compared with 0.7 (± 0.4%) of the same dose from food.
   It was also reported that nickel absorption may be suppressed by binding or chelating substances, competitive inhibitors, or redox reagents; on the other hand, absorption is often enhanced by substances that increase pH, solubility, or oxidation, or by chelating agents that are actively absorbed. Such compounds include: ascorbic acid, citric acid, pectins (from orange juice), which affect trace mineral absorption; tannins (in tea and coffee), which inhibit absorption of iron and zinc; ascorbic acid which suppresses nickel absorption; and complexing agents, such as EDTA, wich depress plasma-nickel levels.

   nickel/iron interaction
   Some authors have suggested that the iron nutritional status may influence nickel absorption

   -dermal exposure: cutaneous absorption of nickel is quantitatively minor, but it may be important in the pathogenesis of contact dermatitis caused by nickel hypersensitivity.
   Because of the ubiquity of nickel-containing objects in industrialised societies, nickel-sensitive patients frequently face considerable problems at the workplace in a
   wide range of jobs.

2. Distribution
   There are few data on human tissue concentrations of nickel. The levels of nickel in biological fluids, hair, and some other materials increase remarkably in persons with increased occupational or environmental exposure and decline rapidly when exposure is reduced or stopped. Thus, measurements of nickel, particularly in the urine, serum or hair, may serve as indices of exposure. The normal ranges of nickel concentrations in body fluids or tissues (serum, blood, lung, kidney) are not significantly influenced by age, sex, or pregnancy.

 Metabolism

Nickel is taken up by the lungs and via the peroral route, but ionizable nickel compounds do not pass through the intact skin. Once it has entered into the circulation, 75% of plasma nickel is carried by the circulating proteins, e.g. albumin, a2-macroglubulin and nickeloplasmin. As Ni2+ ions have no specific uptake mechanism, they probably enter the cells by way of Ca2+/Mg2+ channels. Water soluble nickel salts are generally not carcinogenic, probably because they cannot enter cells. Water insoluble nickel compounds can produce their carcinogenic response because they are actively phagocytized into the cells. Because of the 24h half-life of Ni2+ leads to an accumulation of nickel in the body during the workweek, biological monitoring for occupational nickel exposure is most efficient at the end of weekly workshift. One should, however, keep in mind that this statement applies only to soluble nickel compounds. Phagocytized nickel compounds may be released slowly, causing high urinary nickel concentrations even weeks or months after exposure has ceased (Savolainen, 1996; Patriarca et al, 1997).
References

1. Patriarca, Lyon and Fell. Nickel metabolism in humans investigated with an oral stable isotope; American journal of clinical nutrition, 1997, 66, 616-21.
2. Savolainen. Biochemical and clinical aspects of nickel toxicity; Reviews on environmental health, 1996, 11, 167-173.
3. Snow. Metal carcinogenesis: mechanistic implications; Pharmacology and therapy, 1992, 53, 31-65.

3. Elimination

The elimination routes for nickel in human beings (and animals) depend, in part, on the chemical form of the compound and the mode of intake.
Urinary excretion is the major route for the elimination of absorbed nickel. Fecal excretion primarily reflects the nickel that is unabsorbed from the diet and passes through the gut.
Other routes of elimination are of minor importance. All body secretions appear to have the ability to excrete nickel; it has been found in saliva, sweat, tears, and milk.
Biliary excretion is minimal in animals, but may be significant in human beings. Hair is also an excretory tissue for nickel.

In nickel workers, an increase in urinary excretion was found from the beginning to the end of the shift, indicating absorption of a fraction that was rapidly eliminated.
An increase in urinary excretion was also found as the workweek progressed, indicating a fraction that was excreted more slowly.
For persons exposed to soluble nickel compounds, nickel concentrations in body fluids are generally elevated after exposure but the relationship with the intensity of exposure is relatively poor. Among electrolysis and refinery workers exposed to soluble nickel compounds (nickel sulfate aerosols), nickel concentrations in the urine were 5.2-22.6 µL for those exposed to concentrations of 0.11-0.31 mg Ni/m3, and 3.2-18 µg/L for those exposed to 0.08-0.2 mg Ni/m3. Nickel is also excreted in the faeces of the workers, but this probably results from mucociliary clearance of nickel from the respiratory system to the gastrointestinal tract or from oral exposure via contaminated surfaces.
Increased concentrations of nickel in urine may also be observed in workers exposed to less-soluble nickel compounds and are indicative of significant nickel
absorption

 2. Target organs

The skin and the respiratory tract are the principal target organs upon occupational exposure.

Skin: nickel and nickel compounds have a strong sensitising potential on the skin, which is manifested by irritation, eczema and allergic contact dermatitis. Oral
intake of low doses of nickel may provoke allergic dermatitis in sensitised individuals.

Respiratory tract: Beside the carcinogenic effects on lung and nasal cavities associated with an exposure to nickel, other respiratory effects have been described:

-epithelial dysplasia (possibly representing precancerous lesions)
-pathological changes of the nasopharynx (nasal septal erosions, perforations, ulcerations)
-hyperplastic/polypoid rhinitis
-hypo-osmia and anosmia
-chronic sinusitis/bronchitis
-decreased pulmonary residual capacity, increased respiratory frequency
-pneumoconiosis
-fibrotic changes
-allergic asthma.

A single case of death from acute respiratory distress syndrome has been reported in a adult following exposure of small size nickel metal particles (<1.4 µm)

Renal effects: biochemical indications of nephrotoxicity in nickel workers have been observed: a significant association was found between nickelemia and increased urinary markers reflecting tubular dysfunction (i.e. b2 – microglobulin).

Nickel carbonyl is the most acutely toxic nickel compound. Symptoms following nickel carbonyl intoxication occur in two stages, separated by an almost symptom-free interval which usually lasts for several hours. Initially, the major symptoms are nausea, headache, vertigo, upper airway irritation and substernal pain, followed by interstitial pneumonitis with dyspnoea and cyanosis. Prostration, pulmonary oedema, kidney toxicity, adrenal insufficiency and death may occur in severe cases.
Frequent clinical findings include fever with leukocytosis, electrocardiographic abnormalities suggestive of myocarditis and chest X-ray changes.
Hyperglycaemia has also been reported.

3. Teratogenicity:

Only few data are available on the reproduction and developmental effects of nickel in human beings.

-inhalation exposure: an increase in spontaneous abortions and in structural malformations was reported among women who worked in a nickel hydrometallurgy refining plant in the arctic region of Russia. However, the investigators noted that the nickel-exposed women manually lifted heavy nickel anodes and they may have experienced heat stress.

-oral exposure-dermal exposure: no studies were located regarding reproductive or developmental effects in humans.

-transplacental transfer: nickel has been shown to cross the human placenta. Measurable concentrations have been found in various fetal tissues (e.g. liver, kidney, brain, heart, lung, skeletal muscle, and bone) and in the umbilical cord serum, where the average concentration from 12 newborn babies was 3±1.2 µg/L and was identical with that in the mother’s serum, immediately after delivery.
Placental transfer is influenced by gestational age and the availability of nickel in the maternal blood.
The passage of nickel across the human placenta barrier is of relevance because of the presence of female workers in industry. Appreciable amounts of nickel have been found in breast milk.

4. Genotoxicity:

The DNA alterations responsible for the carcinogenic process are generally thought to occur in genes. In view of the positive response obtained in the SCE test, additional experiments should be performed  to test the ability of nickel compounds , such as nickel carbonyl, displaying marked carcinogenic and teratogenic properties, to induce gene mutations in mammalian cells

 5. Carcinogenicity:

Some nickel species are carcinogenic.
Epidemiological studies have demonstrated a strong association between lung and nasal cancers and exposure by inhalation to nickel compounds in nickel refineries, primarily (in) the early stage of nickel refining. The excess risk of cancer seems to be mainly associated with exposure to less-soluble compounds (i.e. nickel sub sulfide, nickel oxide). However, observations conducted in the electrolysis and in the preparation of soluble salts departments suggest that there might also be an association between soluble nickel and respiratory tract cancers.

Excesses of various cancers other than the lung and nasal cavities, such as renal, gastric, or prostatic cancer, have occasionally been reported in nickel workers, but none has been found consistently
In recent years there has been a dramatic increase in the use of nonprecious alloy and porcelain crowns in clinical dentistry. The alloy in these restorations frequently contains a high percentage (greater than 70%) of nickel. Most cases of metal hypersensitivity are related to nickel, and clinical manifestations of the hypersensitivity are the result of a cellular (T lymphocyte) immune response. In this report, we review the cases of two women who demonstrated significant loss of alveolar bone about nickel-rich nonprecious alloy and porcelain crowns. The loss of alveolar bone occurred within 18 months after placement of the restorations. Both individuals displayed a positive patch test to a nickel preparation. These findings suggest that a Type IV hypersensitivity reaction may have accounted for the rapid loss of alveolar bone. Though the majority of individuals treated with nonprecious alloy and porcelain crowns apparently tolerate these restorations quite well, greater care is urged in case selection.
We report a patient with documented IgA nephropathy in whom microscopic hematuria, proteinuria, and hypertension first occurred after placement of nickel alloy base dental crowns. Progressive proteinuria culminating in nephrotic-range proteinuria occurred parallel to increased nickel placement and dramatically resolved following nickel alloy removal. That immunologic alterations occur as a result of nickel exposure has already been suggested by the common occurrence of nickel contact dermatitis, often exacerbated by intraoral nickel placement, increased carcinogenesis in nickel refinery workers, and animal models of nickel-associated carcinogenesis. Our patient may represent an example of nickel-induced sensitization and associated IgA glomerulopathy. Further study of patients with immune-mediated glomerulopathy with attention to dental nickel exposure appears indicated.
As the cost of providing dental care escalates, there has been a substantial increase in the substitution of nonprecious alloys for gold and precious metals found in porcelain-fused-to-metal crowns. These alloys are frequently 69% to 81% nickel. Nickel hypersensitivity is quite common in the general population and periodontal responses have been associated with nickel-containing crowns in nickel-sensitive individuals. In this article, the authors report the case of a nickel-sensitive patient who demonstrated loss of alveolar bone after the placement of crowns with a high nickel content. Nonprecious alloy crowns can not  be well tolerated in most cases,  a history of metal sensitivity should be evaluated.

Clinical use of the new base-metal alloys in restorative dentistry involves a risk for both dentist and patient. It is the responsibility of the dentist to determine if a patient is allergic to nickel prior to treatment with a restoration containing a nickel alloy. A patch test is recommended for nickel sensitivity in every patient when such a restoration is planned. In addition, the dentist should include in the work authorization order to the dental laboratory the type of alloy he wants for a particular patient. The dentist should be prepared to check for the presence of nickel in a casting suspected of containing it using the dimethylglyoxime test. The evaluation record for nickel sensitivity should include the patient’s name, age, history of allergies, medication, name of drug, dosage, and reaction. The record should be kept in the patient’s chart.
Cancer of  the  lungs,  nasal  mucosa  and  less   frequently  , of the  larynx account for the most  serious  consequences of   usually  long  term  occupational exposure  to Nickel.
The  first  case  of the  respiratory  tract  cancer  were noted in  1932,  in  Wales,  nickel   refinery. It  has  been  established that  nickel  sulfide  and  nickel  oxide are the most   carcinogenic  agents  of  all the nickel  compounds  encountered. Workers   engaged  in the  nickel  manufacture  and  refinery   appear  to  run  the  highest  risk  of  exposure  to  nickel   compounds. It  emphasized  the likelihood   of  nickel –exposed  workers  to  develop  ling  cancer  as significantly  higher among  smokers than  nonsmokers, particularly asbestos workers.  Nickel  like Beryllium compounds ,  has  been  capable  of  damaging  DNA  and  impairing  its  synthesis  in certain  systems. Available  data  is  considered  inadequate  for  classifying   it as  convincingly  genotoxic. Apart  from  being  carcinogenic,  Nickel  is also  a commonly  know  producer  of local  inflammatory  reaction  of the  skin,   chiefly due  to  sensitization. In  workers  of  a Nickel   refinery, and  even in children   residing  in the  vicinity  of  the plant, there  were found  significantly  elevated  levels  of some  serum  proteins classed  among so  called acute  reactants. Nickel   and  nickel  compounds  are know  to  play  a significant  role in the  etiology  of  eczematous  processes  on the human skin. It is  estimated  that  about  5%-13% of  all cases  of  eczema  are  caused by contact  with   Nickel   or  nickel compound s. Nickel  dermatitis,  sometimes  referred  to as  nickel  itch,  may  both  is  occupationally  ad  non- occupationally   exposed  individual  especially  in  women as  a  result  of direct  contact  with  stainless  steel and  nickel – plated   articles,  such  as coins,  cooking utensils,  watches, costume  jewelry , etc. Leaking  of Nickel  from  these   metals  that  assists in  skin  absorption  resulting  in  allergic    reaction   and  dermatitis, may  be enhanced  by  sweat  and  cosmetics. For  the  action  of   adverse  biological   effects of Beryllium  and  Nickel  of primary  importance is  their  solubility  in water, serum and  from  the   oral   view  point , in the  saliva. So far,  no    cases  of malignant  tumor   at  sites  of dental  prostheses have  been  reported,  but  local  sarcoma  have  developed in humans  and  domestic  animals   at sites  of  metallic  prostheses   made  of Nickel. Chromium   and  Cobalt  alloys.  Nevertheless , among these  netals  Nickel  is the most  potent  Carcinogen.
The  above  mentioned  adverse  health  effects,  namely  immunotoxicity  and  carcinogenicity  of  both  metals  , fully   justify  cautiousness in  their application  in materials  designed for the production  of   Dental  Partial Prosthetics.  They  represent  potential  health  risk  aspects  of  the  usage of  nickel   alloys  for these  purposes   and  because of the  high  sensitization  potential  of  Beryllium  to exclude  Beryllium   al together  from  the preparation  of  metal  alloys  for   prosthetic  and  other material,  namely   from  cements used  to  fix  crowns and  bridge,  Future  increased  application  of these  materials,  especially   Beryllium  alloys  in Oral  practice   would  represent  undesirable  and  simple  avoidable  sources   of potential  health   risk  for the  general population. Instead  of  these Beryllium   alloys  are  alternatives  of  classical  materials,  besides alloys  which  is  from  the point of   view  of  biological   aggressively  safer  material  accordin  to the experience  of surgical  practice.

  HAZARD ASSESSMENT

Nickel dusts and several water-insoluble nickel compounds, especially the oxide and subsulfide, are carcinogenic in animals after inhalation or parenteral administration (Ottolenghi et al., 1975; IARC, 1976; Sunderman, 1984; Horie et al., 1985). Accordingly, increased incidences of pulmonary and nasal cancers in nickel refinery workers have been attributed to the inhalation of nickel compounds (Sunderman, 1977). However, there is no indication from the available evidence that ingestednickel is carcinogenic in humans or in laboratory animals.
While nickel chloride was not mutagenic in several bacterial assay systems (EPA, 1985), nickel did produce chromosomal aberrations in cultured mammalian cells, and sister chromatid exchanges in both cultured mammalian cells and human lymphocytes (Miyaki et al., 1979; Ciccarelli et al., 1981; Saxholm et al., 1981; Newman et al., 1982; Robison and Costa, 1982). The relevance of these findings to the toxicity of nickel compounds in vivo remains to be determined.

The World Health Organization (WHO) has not yet suggested a tolerable intake level for nickel (Private Communication 7, June 26, 1990).
The EPA’s current oral Reference Dose (RfD) for soluble inorganic nickel is 20 g/kg/day. This value was calculated by applying an uncertainty factor of 100 and a modifying factor of 3 to a no observed adverse effect level (NOAEL) of 5 mg/kg/day obtained in a 2-year rat feeding study (Ambrose et al., 1976). Ambrose et al. (1976) studied clinical pathology, ophthalmology, serum biochemistry, body, and organ weight changes, and performed histopathologic evaluations of selected organs (heart, kidney, liver). The EPA’s modifying factor of 3 was applied to the NOAEL, in addition to the uncertainty factor of 100, to compensate for the statistical and other inadequacies in the available reproductive studies (RTI, 1987; Ambrose et al., 1976). A tolerable daily intake of 1,200 g Ni/day for a 60-kg individual can be suggested on the basis of the EPA’s current RfD (20 g/kg/day x 60 kg = 1,200 g/day).

An additional concern not yet addressed in the EPA’s estimate for the RfD for nickel {and the proposed maximum contaminant level (MCL) corresponding to this RfD} is that acute oral nickel ingestion, added to a normal diet, may produce adverse reactions in persons with nickel hypersensitivity. Hypersensitivity to nickel is a common cause of allergic dermatitis in people (Sunderman, 1988). Sensitization due to cutaneous contact with nickel or nickel compounds is observed in 5-13% of various populations exhibiting eczema (NAS, 1975). Furthermore, positive dermal patch tests for nickel were observed in 7-11% of women and 0.2-2% of men from the general population. Nickel hypersensitivity has been attributed to direct cutaneous exposure to stainless steel utensils and other nickel-containing or nickel-plated objects such as coins, watches, jewelry and clothing fasteners (Norseth, 1986; Sunderman, 1988). Nickel hypersensitivity may also cause pulmonary asthma, conjunctivitis, and inflammatory reactions around nickel-containing implants and prostheses (Arvidsson and Bogg, 1959; Sunderman, 1988).

A double-blind study conducted by Gawkroder et al. (1986) showed that a single 5,600 g oral dose of nickel worsened the skin conditions in all 6 of the subjects challenged with this dose, confirming the results of Christensen and Moller (1975). Gawkroder et al. (1986) suggest that oral nickel intake as high as 5,600 g can aggravate the eczematous skin conditions in nickel-hypersensitive persons.
Kaaber et al. (1978) reported that 17 of 28 patients with chronic nickel dermatitis exhibited aggravated eczematous reactions after ingesting a single 2,500 g dose of nickel as nickel sulfate in a tablet. According to Kaaber and his coauthors, the protocol in this study included a “blind challenge with tablets of identical appearance … carried out by giving each patient a placebo tablet and three days later a tablet containing 2,500 g nickel sulfate.” The patients were photographed 3 days after the ingestion of each tablet, and the photographs were then evaluated “blindly”. Thus, this study, like that of Gawkroder et al. (1986), appears to be a double-blind study.

Veien et al. (1983) reported that three patients with positive patch tests to nickel developed flares at the patch test site after a single oral dose of 2,500 g nickel. Accordingly, Kaaber et al. (1979) reported that eczema was aggravated in 11 nickel-hypersensitive patients ingesting a single dose of 2,500 g nickel. In two of these patients, with particularly long-standing (10-17 years) hand dermatitis, a single dose of 600 g or 1,250 g nickel sulfate was sufficient to produce dizziness and nausea as well as exacerbated skin conditions.

Furthermore, Cronin et al. (1980) reported that ingestion of a single dose of 600 g or 2,500 g nickel, administered after an overnight fast, produced a dose-dependent enhancement of hand eczema in female patients known to have been sensitized from nickel contact. Of the five women receiving 600 g nickel, one developed erythema, two presented with worsening of hand eczema, and 3 exhibited flare of the patch test site. Gawkroder et al. (1986) state in their introduction that the reports of Cronin et al. (1980), Kaaber et al., 1979, Veien et al., 1983, and other researchers were not confirmed by two double-blind studies (Jordan and King, 1979; Burrows et al., 1981). However, Gawkroder and his colleagues also mentioned that a subject in one of these double-blind studies (Jordan and King, 1979) consistently reacted to a 500 g oral nickel challenge.

In summary, one double-blind study showed that a single 2,500 g dose of orally administered nickel was sufficient to aggravate the chronic nickel dermatitis in 17 of the 28 patients tested. Other, less reliable studies suggest that as little as 600 g or 1,250 g of ingested nickel may exacerbate the skin conditions in patients with long-standing (10-17 years) nickel hypersensitivity. In one double-blind study (Jordan and King, 1979), one of the 10 nickel hypersensitive patients tested consistently reacted to a 500 g oral nickel challenge. Thus, oral nickel exposure of as little as 500 g may produce adverse reactions in some nickel hypersensitive persons. A tolerable intake for nickel of 50 g/day can be derived by applying an uncertainty factor of 10 to the lowest observed effect level for dermatitis in hypersensitive individuals.

Porcelain

Porcelain is used when appearance and wear resistance is the most important factor. It is much more fragile than metal and may break easily. Porcelain alone is not normally recommended for bridges.

Indirect Composite

Indirect composites are used when appearance is an important factor but when the risk of porcelain fractures and wearing down the other teeth is to be avoided. These are not quite as wear-resistant or esthetic as porcelain but very acceptable for normal situations.

Biocompatible Zirconium Oxide  All Ceramic   Crowns

All Ceramic Restorations

One of the most difficult areas in dentistry today is the restoration of dental structures with biocompatible materials that are strong enough to withstand the forces of chewing (500-1000lbs pressure on molar teeth). Recent technology from Germany now offers a material that has overcome most of the pitfalls of present day products. Patients now have a choice of a material that is esthetic, strong, pure, biocompatible and capable of being used for single and long span dental bridgework. That material is called Zirconium oxide.

Zirconium oxide has the following superior characteristics that make it the most ideal material available:

* Excellent biological compatibility: absolutely bio-inert.
* Outstanding physical and mechanical qualities:
* Hardness (Vickers) 1200 HV
* Compressive Strength 2000 MPa
* Bending Strength 1000 MPa
* Modulus of Elasticity 210 GPa
* Tensile Strength 7 Mpavm
* Wear characteristics (Ring on disc) <0.002 mm 3/h
* Absolute corrosion resistance: Ringer’s solution 370C <0.01mg/ m2x24h
* Very small particle size: <0.6ym
* No glass phase for particle binding
* Extremely high density
* Porosity: 0%
* Purity (Zr/Hf/Y): 99.9%
* Translucence of the framework material makes excellent cosmetic results possible
* Equivalent fit to precision gold castings: edge opening 20-50 ym. Precludes the need to use adhesive cements.
* Zirconium oxide is manufactured and optimized industrially so that the material qualities remain unchanged through the complete pro duction chain.
* Optimal material for crowns: tasteless, radiopaque, no pulp irrita tion because there is no need to use adhesive cements and minimal invasive preparation by dentist.

Zirconium oxide forms the core of each crown and provides the cross-link that bridges the gap of missing teeth. The precision fit of the Zirconium core is derived from computer guided Swiss lathes that cut the form out of a solid Zirconium oxide block. The cutting instructions are obtained from a laser beam that reads 120 points per millimeter from the anatomy of a model of the prepared teeth. Once formed, new synthetic porcelain (99.9% pure) is baked on to the Zirconium core and then shaped like a tooth. Because of the extreme accuracy of the crown fit, the crowns can be cemented with biocompatible dental luting material. This avoids the use of an invasive procedure of etching the tooth with acid and injuring the pulp or nerve of the tooth. This latter procedure often times results in the pulp dying and necessitating root canal therapy.
Advantages of ET zirconium high performance ceramic compared with other full ceramics.

Zirconium oxide ceramic primarily stands out due to its high crack resistance. Crack resistance is the resistance with which the material counteracts the spreading of cracks. If a material is stressed, it usually comes to excessively high tension within a defect area (pores, surface deficiencies, cavities) or it cracks. While with metals under high tension in the area of cracks, plastic deformation appears and the top of the tension can be reduced by rounding the cracks; in ceramics due to missing plastic deformation possibility the cracks continue to grow. The unusual feature of zirconium oxide ceramic in comparison with other ceramics is that at the appearance of a high-tension area a transformation of the crystal structure can take place. This process is also accompanied by a volume expansion. By this volume increase it builds wedges in the crack and therefore it reduces the continuation of the crack. While the critical tensile strength (KIC) e.g. ofDicor, Vita Mark II and Empress is in the area of 1-2.5 Mpam-1/2, zirconium oxide shows values in the range of 10 Mpam-1/2. Even In-Ceram (glass infiltrated Al203 ceramic) and Procera aluminum oxide (pure Al203 ceramic) show values less then 5 Mpam-1/2.

In connection with the tensile strength there also stands the characteristic of bending strengths. While conventional glass ceramics show results of 100-200 Mpa and aluminum oxide ceramics lie in the area of 400-600 Mpa, zirconium oxide reaches a bending strength of over 1000 Mpa.
Because of the high tensile strengths exhibited in test results, it is now possible to fabricate posterior bridges with zirconium oxide. Further decisive advantages of zirconium oxide are its high resistance to corrosion; stability to hydrolysis and its high biocompatibility in comparison with other ceramics makes this material ideal for restorative dentistry.
In medicine, zirconium oxide is being used more and more as the material of choice especially for hip prosthesis. For years there has existed substantial clinical tests and examinations which confirm the high quality of zirconium oxide.

All Ceramic Restorations

new Procera® Crown Zirconia 0.4

The ever-popular Procera® Crown Zirconia is now even thinner yet still has exceptional strength

• Thinner coping enables more flexible esthetic opportunities
• Combines zirconia extreme flexural strength, 1200 MPa, with a beautiful esthetic result

Procera® Crown Zirconia

• Fracture rate less than 0.5%
• Proven strength and all-ceramic beauty
• Highly biocompatible material
• No specialized clinical preparation or cementation procedures
• Zirconia for the highest load situations

Biocompatible  Denture  Materials

Denture Materials

Today dentists are prescribing flexible material for removable partial dentures (RPDs) because it makes a better, stronger appliance faster. Flexible material reduces chair time, eliminates invasive procedures and the cumbersome materials associated with rigid partials. In short, there is no longer any need for metal.

Metal-based RPD design is complex because it has to adapt rigid materials to a flexible environment. This leaves room for error particularly under conditions where ideal designs and clinical preparations are challenged.

In contrast, the material in flexible partials is perfectly suited to the variety of natural conditions in the mouth. It simplifies the design and enables the RPD itself to balance the simultaneous requirements of retention, support and stability.

Flexibility removes many of the unwanted aspects of metal partials. There are fewer steps in the treatment process because preparation of natural teeth is unnecessary. Without the metal frame, the fabrication and try-in processes have also been simplified. In addition, the choice of a Valplast® or Lucitone FRS partial avoids the placement of metal in your patient’s mouth, which allows you to satisfy the patient’s interest in metal-free dentistry.

When you prescribe a genuine Valplast or Lucitone FRS partial, you give your patient far more than just a dental appliance. Valplast or Lucitone FRS takes a comprehensive approach to both the science and the business of flexible partials. Since the beginning, it has been our mission to elevate removable partial dentures to a higher-level of function, simplicity and patient satisfaction. We provide the industry’s most proven flexible RPD material backed by the most extensive knowledge, experience, training and advanced equipment.

Valplast Partials

Valplast is a flexible denture base resin that has been used in dentistry since 1954 and is ideal for partial dentures and unilateral restorations. The resin is a biocompatible nylon thermoplastic with unique physical and aesthetic properties that provides unlimited design versatility and eliminates the concern about acrylic allergies. It allows your patient’s natural tissue tone to appear through the material, matching the basic shade categories (medium, light pink, and meharry). Patient’s report that it feels more comfortable because of the thinness and light weight. It is also guaranteed for life against breakage when fabricated and handled according to the manufacturer’s specified procedures.

Valplast Nesbit and Flipper

The Valplast Nesbit is ideal for posterior single tooth replacement and the Valplast Flipper is ideal for anterior single tooth replacement. The design of the new flexible plastic framework takes the danger out of an accidental swallowing of the appliance. In the event that someone did swallow one, it is unlikely that any damage could be done to the lining of the digestive system.

 Bonding

Below is a white composite filling. This is the most common filling material used to replace mercury fillings. A direct composite is made up of plastic resin, reinforced with filler particles of silicone dioxide (glass) or zirconium.

Since all direct fillings (composites) and most indirect restorations (inlays, onlays, and crowns) being placed today use a process called bonding, it’s good to have a basic knowledge of how this process works. While there are a myriad of variations in this process, here are the basic steps:
Step 1–Prepare the tooth surface using a mild acid solution. This creates a “honeycomb” in the top layer of tooth.
Step 2–Paint a liquid resin-bonding agent on the tooth. It flows and “locks” into the honeycomb created in Step 1 (technically forming a hybrid layer that is part-tooth and part dental-resin). This layer is “cured” (hardened using a photo-chemical reaction) with a visible light source.
Step 3–Place luting cement if an indirect restoration (e.g., crown) is being used. Essentially, this material is a more liquid form of white filling material. It bonds to both the tooth and the pre-fabricated ceramic restoration and fills the gaps between them. The surface of the first layer of cured bonding agent is highly reactive and is easily bonded to with today’s composite filling materials.

Advantages of Bonding

There are a number of advantages to using bonding. Besides allowing the placement of non-metal restorations, less removal of healthy tooth structure is required. The dentist needs to remove only the unhealthy tooth structure and a precisely fitted piece can be bonded into place to replace it. In the case of fillings, bonded restorations have other physical advantages over amalgam. Even the ADA, in its Journal of the American Dental Association (JADA) , recently acknowledged, “Resin-based composites eventually will replace amalgam as a direct restorative material because they possess many characteristics not inherent in amalgam. Some of the more important of these properties are esthetics, micro-mechanical bonding to tooth structure, smaller cavity preparations and better sealing potential.” (JADA, Vol. 132, August 2001, p. 1100).

New Advances

Breakthroughs in the development of dental materials and techniques are occurring on a regular basis. We have yet to find one single material that is compatible for everyone. Debate continues about how to best restore a patient’s mouth to optimal health and no perfect solution has yet presented itself. The best we can do is to to keep an open mind and keep searching for answers. Only by thorough testing can it be determined which is most compatible for any one person.

Testing for Dental Compatible Material

All dental materials should be tested for compatibility prior to their use in order to insure maximum safety and good health. You cannot assume that your body will handle all material for you. It is important to include dental material testing in your decision making process.

Blood Compatible Reactivity Testing

Using  serum  from a patient’s   blood  sample,  antibodies  formed  against     the  chemical  groups  that  result  from  dental  product  breakdown  are  detectable  . Once   the  patient  is  sensitized  from  any  source  and is producing  antibodies, use of any  product  that   contains or may  give off  these  substances   should  be  avoided. This procedure makes it possible  to select  those  materials  that   are  least  likely  to cause a  reactivity  problem. This   special  testing   service  which  can  help  to  reduce  you  risk from adverse  reactions  with  dental  materials. This  procedure  can be  performed   from  a simple   blood  specimen.  Also   provided  that    it is  used as part  of a  risk   assessment program  to  assist  the  doctor  in  selecting  those  materials  which  may be  safest  to use with  the patient.

Biocompatibility/Clifford Testing

If you are concerned about the biocompatibility of the materials used to restore your teeth, we recommend the Clifford Materials Reactivity Test. This test only requires a blood sample, and from that little sample, it can be determined, among the myriad of materials available, which ones are most suitable for you!

Clifford Materials Reactivity Testing (CMRT) is a laboratory screening process used to help identify existing sensitivity problems to various chemical groups and families of compounds in an individual patient. This process is currently being implemented in the CMRT Dental Test. After a patient’s test has been completed, the patient’s reactivity test results are compiled in a report. The test currently reports on over 7100 trade-named products and 89 chemical groups and families.

The Clifford Materials Reactivity Testing can be useful for any patient who is preparing for restorative or reconstructive bio-materials placement and who would like to have some additional peace of mind that the materials proposed for use are not likely to induce adverse bio-reactivity. Additionally, there are several groups of patients who might derive special benefits from the added safety of materials reactivity pre-assessment testing.

Some of these groups include:

• Any patient who has experienced difficulty with prior materials placement
• Patients with severe immune-compromised status
• Patients with identified autoimmune diseases or conditions
• Endocrine, hepatic or renal compromised patients
• Patients with universal reactor/environmental illness status
• Patients with severe allergic problems
• Patiens with known sensitivity to jewelry, watchbands, clothing fasteners
• Patients with identified galvanic or bruxing issues
• Patients who receive daily does of numerous medications
• Patients facing high-cost, complex restoration projects
• Patients previously treated by multiple unrelated healthcare professionals

Read more at: biodentistrydrvizcarra.com