نسترن صباغ زاده

کتاب شاهزاده خانوم محکوم

هنگامی که شاهزادهء روس و نامزدش برای خرید لباس وارد مغازه شدند، نامزدِ شاهزاده مقابل آینه ایستاد و از فروشنده که دختری فرانسوی بود، خواست تا در پرو لباس به او کمک و از شاهزاده پرسید " لباس چه طور است؟ "

شاهزاده به آینه نگاه کرد، نگاهش به نگاه دختر فرانسوی در آینه گره خورد، دختر فرانسوی چشمانش را فورا به زمین دوخت اما شاهزاده، همانطور که به چشمان دختر فرانسوی نگاه میکرد، گفت "بسیار زیباست"

WOUND REPAIR

Active TROMBIN cleaves FIBRINOGEN into FIBRIN, which polymerizes into a fibrin network (SCAB) sealing the wound

CAUSES OF TISSUE DAMAGE

Physical

Copromised blood flow

Crushing

Desiccation

Incision

Irradiation

Overcooling

Overheating

Chemical

Agent with unphysiologic PH

Agent with unphysiologic tonicity

Proteases

Vasoconstrictors

Thrombogenic agents

EPITHELIALIZATION

Injured epithelium has a genetically programmed regenerative ability that allows it to reestablish its integrity through proliferation, migration & a process known as contact inhibition

In general, any free edge of epithelium continues to migrate (by proliferation of germinal epithelial cells that advance the free edge forward) until it comes into contact with another free edge of epithelium, where it is signaled to stop growing laterally

Wounds in which only the surface epithelium is injured (e.g. abrasions) heal by proliferation of epithelium across the wound bed

Wounds in which the sub-epithelial tissue is also damaged proliferates across whatever vascularized tissue bed is available & stays under the portion of the superficial blood clot that desiccates (forms a scab) until it reaches another epithelial margin. Once the wound is fully epithelialized, the scab loosens and is dislodged

STAGES of WOUND HEALING

Inflammatory Stage

Fibroplastic Stage

Remodelling Stage

Inflammatory Stage

“Lag Phase” – the period where no significant gain in wound strength occurs.

Principal material holding together during this stage is fibrin.

Wound fills with clotted blood, inflammatory cells and plasma.

Adjacent tissue begins to migrate into wound, and undifferentiated mesenchymal cells begin to transform into fibroblast.

Immediate to 3-5 days

:(Bleeding stops (hemostasis

a. Constriction of blood supply

b. Platelets start to dot

c. Formation of scab

:Inflammation

a. Opening of blood supply

b. Cleansing of wounds

CARDINAL SIGNS OF INFLAMMATION

Redness – rubor

Swelling – tumor

Warmth – color

Pain - dolor

Loss of function

Fibroplastic Stage

Strands of fibrin, from blood coagulation, crisscross wound to form a latticework on which fibroblasts can begin laying down ground substance & tropocollagen

Occurs 5 days to 3 weeks

:Granulation

a. New collagen is laid down

b. New capillaries fill defects

:Contraction

a. Wound edges pull together

: Epithelialization

a. Cells cross over the moist surface

b. Cell travel about 3mm from point of origin

Remodelling Stage

Final stage of wound repair

Continuous indefinitely, from 3 weeks to years

Also known as “WOUND MATURATION STAGE”

Previous randomly laid down collage are destroyed & replaced by new collagen fiber of better orientation to resist tensile forces of the wound

The final process, which begins near the end of fibroplasia & continues during the early portion of remodelling, is wound contraction

During wound contraction, the edges of the wound migrate toward each other

Wound strength never reaches 80-85% of the strength of un-injured tissue

As wound metabolism lessens, vascularity is decreased, which diminishes wound erythema

...ALWAYS REMEMBER

FACTORS THAT IMPAIR WOUND HEALING

Foreign Material

Necrotic Tissue

Ischemia – restriction of blood and oxygen supply

Wound Tension

Foreign Material

"Is anything that the host organism’s immune system views as “non-self

This includes bacteria, dirt, suture material, etc

Bacteria can proliferate and cause an infection in which bacterial proteins that destroys host tissue are released

Non-bacteria foreign material acts as haven for bacteria by sheltering them from host defences & thus promoting infections

Foreign material is often antigenic & can stimulate chronic inflammatory reaction that decreases fibroplasia

Necrotic Tissue

Serves as a barrier to the ingrowth of reparative cells; prolonging the inflammatory stage since the white blood cells fail to remove the necrotic debris

Serves as a protected niche for bacteria

This frequently includes blood that collects in a wound (hematoma), where it can serve as an excellent nutrient source of bacteria

:Example of Necrotic Tissue secondary to extraction*

Ischemia

(Decreased blood supply & oxygen delivery to a wound.(Black or Bluish on color

Result to further tissue necrosis - Lessen delivery of antibodies, white blood cells, and antibiotics to the wound

:Caused by

Tight or incorrectly placed sutures

Improperly designed flap

Excessive external or internal pressure on a wound

Systemic hypotension

Peripheral vascular disease

Anemia

:Example of ischemia of oral tissue*

Wound Tension

Tension from sutures cause tissue strangulation, producing ischemia

If sutures are removed too early, wound under tension may re-open resulting to excessive scar formation and wound contraction

On the other hand, when sutures are left too long, the tract where the sutures ran will epithelize then leave a permanent disfiguring mark

HEALING BY PRIMARY INTENTION

Wound edges without tissue loss are places and stabilized in essentially the same anatomic position prior to injury

Wound repair occurs with minimal scar tissue

A theoretical ideal which is difficult to attain clinically

Generally used term to designate wounds which the edges are closely reapproximated

HEALING BY SECONDARY INTENTION

Implies that a gap between edges of incision or laceration or between bone or nerve ends after repair

Tissue loss prevents close approximation of wounds edges

Requires large amount of wound repair processes

Examples are extraction sockets, deep ulcers or large avulsive injuries

Healing of Extraction Sockets*

After extraction, the remaining empty socket consist of cortical bone (radiographically seen as the lamina dura) covered by torn periodontal ligaments, with a rim of epithelium (gingiva) at the coronal portion

The socket fills with blood, which coagulate and seals the sockets from the oral environment

:First week of healing

Inflammatory stage – White blood cells enter socket to remove contaminating bacterial & to begin break down of any debris left in the socket

Fibroplasia – ingrowth of fibroblasts and capillaries

Epithelium migrates down the socket wall until it reaches a level at which it contacts epithelium from the other side of the socket or when it encounters the bed of granulation tissue under the blood clot

Osteoclasts (Bone destroying cell) accumulate along crestal bone

:Second week of healing

Large amount of granulation tissue fill the socket

Osteoid deposition along the alveolar bone lining the socket

:Third-Fourth week of healing

Cortical bone continues to be resorbed from crest and walls of sockets

New trabecular bone is laid down across the socket

:4-6 Months

The cortical bone lining is fully resorbed, radiographically there is a complete loss of lamina dura

HEALING BY TERTIARY INTENTION

A term surgeon use to refer to wound healing through use of tissue grafts in large wounds

BONE HEALING

Bone heals by primary & secondary intention

If fracture ends are more than 1 mm or so apart, bone heals by secondary intention; wherein large amount of collagen must be laid down to bridge the bony gap

Fibroblasts and osteoblasts produce a lot of fibrous matrix such that healing tissue extends circumferentially beyond the free ends of the bone forming callus

Healing of bone by primary intentions occurs when bone is either incompletely fractured such that fracture ends does not become separated from each other,

Or when a surgeon closely re-approximates & rigidly stabilize fractured ends

In this case, little fibrous is produced & reossification of tissue within fracture area occurs quickly, with minimal callus formation

TWO FACTORS IMPORTANT TO PROPER BONE HEALING

Vascularity

If vascularity or oxygen supplies are sufficiently compromised, cartilage forms instead of bone

If either vascularity or oxygen supplies are poor, fibrous tissue does not chondrify or ossify

Immobility

Placing bone under continuous or repeated cycles of some tension stimulates continued osteoblastic bone formation

Bone is formed perpendicular to lines of tension to help withstand the forces placed on it

Excessive tension or torque placed on a healing fracture site produces mobility & compromises vascularity of the wound, promoting wound infection

IMPLANT OSTEOINTEGRATION

:Wound healing around dental implants; involves two basic factors

Healing of bone to the implant

Healing of alveolar soft tissue to the implant

HEALING OF THE BONE TO THE IMPLANT

This must occur before any soft tissue forms between the bone & the implant surfaces

:Four factors needed to achieve this

Short distance between implant & bone

Viable bone at or very near the surface of the bone along the implant

No movement of implant while bone is attaching to its surface

An implant surface free of contamination by organic or inorganic material. Including bacteria, oil, glove powder, foreign metals and foreign proteins

VIABLE BONY SURFACE ALONG THE IMPLANT

There should be minimized bone damage during site preparation to preserve the viability of the bone near implant surface

Much damage is caused by heat friction during cutting process

It is minimized by using sharp bone-cutting instruments, limiting cutting speeds to minimize frictional heat, & by keeping the bone cool with the irrigation during site preparation

Counter sinking implants & using low profile healing screws decrease chances of unwanted forces to be delivered to the implant

Covering the top of the implant during healing further protects it

?In implant, we use low-speed. Why*

Less torque to minimize damage to the bone & the healing capacity is intact

So that the drill keep on moving and penetrate the bone

FACIAL NEUROPATHY of TRAUMATIC ORIGIN

:The three branches of the trigeminal nerve injured most commonly

Inferior alveolar-mental nerve

Lingual nerve

Infraorbital nerve

types of nerve injuries

Neurapraxia

Axonotmesis

Neurotmesis

Neurapraxia

Least severe form of peripheral nerve injury

Contusion of a nerve in which continuity of the epineurial sheath and the axons is maintained

Blunt trauma or traction (e.g., stretching) of a nerve, inflammation around a nerve, or local ischemia of a nerve

No loss in axonal continuity, spontaneous full recovery of nerve function usually occurs in a few days or weeks

Axonotmesis

When the continuity of the axons but not the epineurial sheath is disrupted

Severe blunt trauma, nerve crushing, or extreme traction of a nerve

Because the epineural sheath is still intact, axonal regeneration can (but does not always) occur with a resolution of nerve dysfunction in 2 to 6 months

Neurotmesis

Most severe type of nerve injury

Complete loss of nerve continuity

Produced by badly displaced fractures, severance by bullets or knives during an assault, or by iatrogenic transection

Prognosis is poor except if the ends of the affected nerve have somehow been left in approximation and properly oriented

(NERVE HEALING (Two phases

Degeneration

a. Segmented demyelination

b. Wallerian degeneration

Regeneration

Segmented Demyelination

Myelin sheath is dissolved in isolated segments

This causes a slowing of conduction velocity and may prevent the transmission of some nerve impulses

:Symptoms

a. Paresthesia -a spontaneous and subjective altered sensation that a patient does not find painful

b. Dysesthesia -a spontaneous and subjective altered sensation that a patient finds uncomfortable

c. Hyperesthesia -excessive sensitivity of a nerve to stimulation

d. Hypoesthesia -decreased sensitivity of a nerve to stimulation

Occur after neurapraxic injuries or with vascular or connective tissue disorders*

Wallerian degeneration

Axons and myelin sheath of the nerve distal to the site of nerve trunk interruption' (away from the central nervous system) undergo disintegration in their entirety

Stops all nerve conduction distal to the proximal axonal stump

Occurs after nerve transection and other destructive processes that affect peripheral nerves

occurring after nerve trauma*

Regeneration

Normally the proximal nerve stump sends out a group of new fibers (the growth cone) that grow down the remnant Schwann cell tube

Growth progresses at a rate of 1 to 1 .5 mm/d and continues until the site innervated by the nerve is reached or growth is blocked by fibrous connective tissue or bone

Begin almost immediately after nerve injury*

Reference:

Lecture of Dr Reece Aldrin Valdez at national university college of dentistry- manila, philippines

تا که بودیم نبودیم کسی، کُشت مارا غم بی همنفسی

تا که رفتیم همه یـــــار شدند، خفته ایم و همه بیــــدار شدند

قدر آئینه بدانیم چو هست، نه در آن وقت که افتاد و شکست

درحیرتم از مرام این مردم پست، این طایفه ی زنده کش مُرده پرست

تا هست به ذلت بکشندش به جفا، تا رفت به عزت ببرندش سر دست

آه میترسم شبی رسوا شوم، بدتر از رسواییم تنها شوم

آه از آن تیر و از آن روی کمند، پیش رویم خنده پشتم پوزخند

شعر: تا که بودیم نبودیم کسی اثر اقبال لاهوری

نقاشی: آفرینش آدم اثر میکل آنژ Michelangelo The Creation of Adam

کتاب هاکلبری فین

زندگی در خانه خیلی خوب است، اما در قایق احساس آزادی و راحتی بیشتری می کنی.

آیا ما قبلاً یکدیگر را ندیده ایم؟ جایی در یک موسیقی ؟

نقاشی: رقص با موسیقی زمان اثر نیکولاس پوسن Nicolas Poussin A Dance To The Music Of Time

من همه را میبینم اما، تو را نگاه مینم

نقاشی: عاشق تاج گذاری کرد اثر ژان هونوره فراگونارد Honoré Fragonard The lover crowned

هرکه با من همره و پیمانه شد، عاقبت شیدا دل و دیوانه شد
قصه‌ام عشاق را دلخون کند، عاقبت خواننده را مجنون کند
آتش عشق ست و گیرد در کسی، کاو، ز سوز عشق می‌سوزد بسی...

شعر: قصه رنگ پریده اثر نیما یوشیج

نقاشی: جیغ اثر ادوارد مونیک Edvard Munch The Scream

زندگی آوازی است که به جان ها جاری است
زندگی نغمه سازی است که در دست نوازشگر ما است
زندگی خواب خوش کودک احساس من است
زندگی جاده و راهی است به آن سوی خیال
زندگی برف سپیدی است که بر روح تو بنشسته به شب
زندگی بوی خوش نسترن است
زندگی رفتن خاموش به یک تنهایی است
زندگی رفتن و از بودن خود دور شدن است
شعر: زندگی رفتن و راهی شدن است اثر سهراب سپهری

نقاشی: طوفان در دریای جلیل اثر رامبرانت هارمنزون فان راین Rembrandt Harmenszoon van Rijn The Storm on the Sea of Galilee

حیلت رها کن عاشقــا، دیوانه شو، دیوانه شو
و انـدر دل آتش درآ، پــــروانـه شــو، پروانــــــه شو
هــم خــویش را بیگـــانه کن، هم خانه را ویرانه کن
و آنگه بیا با عاشقان، هم خانـه شـو، هم خانه شــو
رو سینــه را چـون سینه ها، هفت آب شو از کینه ها
و آنگـــه شراب عشــق را پیمانـــه شــــو پیمانــه شـو
باید کـــه جملــه جــان شــوی،تا لایق جانان شوی
گـــر ســوی مستــان میــروی، مستانه شـــو، مستانه شو

شعر: دیوان شمس اثر مولوی

نقاشی: دوشیزگان رومی اثر لونا داماس Luna Damas Romanas

زندگی رسم خویشاوندی است
زندگی بال و پری دارد با وسعت مرگ
پرسشی دارد اندازه ی عشق
زندگی چیزی نیست که لب طاقچه ی عادت از یاد من و تو برود
زندگی حس غریبی است که یک مرغ مهاجر دارد
زندگی سوت قطاری است که در خواب پلی می پیچد

شعر: زندگی رسم خوش آیندی است اثر سهراب سپهری

نقاشی: تاب اثر ژان هونوره فراگونارد Honoré Fragonard The Swing

در میان این همه غوغا و شر، عشق یعنی کاهش رنج بشر

عشق یعنی گل به جای خار باش، پل به جای این همه دیوار باش

عشق یعنی تشنه ای خود نیز اگر، واگذاری آب را، بر تشنه تر

عشق یعنی دشت گل کاری شده، در کویری چشمه ای جاری شده

عشق یعنی ترش را شیرین کنی، عشق یعنی نیش را نوشین کنی

هر کجا عشق آید و ساکن شود، هر چه نا ممکن بود ، ممکن شود

شعر: عشق چیست اثر مجتبی کاشانی (سالک)

نقاشی: رقص در مولن دُلا گالت اثر پیر آگوست رنوار Pierre-Auguste Renoir Dance at Le moulin de la Galette

به آسانی مرا از من ربودی، درون کوره ی غم آزمودی

دلت آخر به سرگردانیم سوخت، نگاهم را به زیبایی گشودی

!بسی گفتند: دل از عشق برگیر! که نیرنگ است و افسون است و جادوست

!ولی ما دل به او بستیم و دیدیم: که این زهر است ، اما…نوشداروست

چه غم دارم که این زهر تب آلود، تنم را در جدایی می گدازد

از آن شادم که در هنگامه درد، غمی شیرین دلم را می نوازد

شعر: زهر شیرین از فریدون موشیری

Honoré Fragonard Progress of Love نقاشی: پیشرفت عشق اثر ژان هونوره فراگونارد

چترها را باید بست، زیر باران باید رفت
فکر را، خاطره را، زیر باران باید برد
با همه مردم شهر ، زیر باران باید رفت
دوست را، زیر باران باید دید
عشق را، زیر باران باید جست
زیر باران باید با زن خوابید
زیر باران باید بازی کرد
زیر باران باید چیز نوشت،حرف زد،نیلوفر کاشت
زندگی تر شدن پی در پی
زندگی آب تنی کردن در حوضچه اکنون است.
رخت ها را بکنیم،آب در یک قدمی است،روشنی را بچشیم
شب یک دهکده را وزن کنیم، خواب یک آهو را، گرمی لانه لک لک را ادراک کنیم
شعر: چترها را باید بست اثر سهراب سپهری

نقاشی: پاریس، یک روز بارانی اثر گوستاو کایبوت Gustave Caillebotte Paris Street-Rainy Day

نیست رنگی که بگوید با من: اندکی صبر ، سحر نزدیک است
هردم این بانگ برآرم از دل : وای ، این شب چقدر تاریک است!
خنده ای کو که به دل انگیزم؟ قطره ای کو که به دریا ریزم؟ صخره ای کو که بدان آویزم؟
مثل این است که شب نمناک است
دیگران را هم غم هست به دل
غم من ، لیک، غمی غمناک است

شعر: مرگ رنک اثرسهراب سپهری

نقاشی: منظره‌ای از تولدو اثر اِل گِرکو El Greco View of Toledo

کودکان احساس! جای بازی اینجاست
زندگی خالی نیست
مهربانی هست، سیب هست، ایمان هست
آری تا شقایق هست زندگی باید کرد
در دل من چیزی است مثل یک بیشه نور، مثل خواب دم صبح
و چنان بی تابم که دلم می خواهد
بدوم تا ته دشت، بروم تا سر کوه
دورها آوایی است که مرا می خواند
شاید آن روز که سهراب نوشت : تا شقایق هست زندگی باید کرد
خبری از دل پر درد گل یاس نداشت،باید اینجور نوشت:
هر گلی هم باشی چه شقایق چه گل پیچک و یاس، زندگی اجباریست!

شعر: تا شقایق هست زندگی باید کرد اثر سهراب سپهری

نقاشی: منظره زمستانی با یک پرنده اثر پیتر بروگل Pieter Bruegel Winter Landscape with Skaters and Bird Trap

ابری نیست

بادی نیست

می نشینم لب حوض

گردش ماهی ها، روشنی،من، گل، آب

نردبان از سر دیوار بلند، صبح را روی زمین می آرد

روزنی دارد دیوار زمان، که از آن،چهره من پیداست

می روم بالا تا اوج،من پر از بال و پرم

راه می بینم در ظلمت، من پر از فانوسم

من پر از نورم و شن

و پر از دار و درخت

پرم از راه، از پل، از رود، از موج

پرم از سایه برگی در آب، چه درونم تنهاست!

شعر: روشنی من گل آب اثر سهراب سپهری

نقاشی: گاری علوفه اثر جان کانستبل John Constable Hay Wain

هیچ حیوانی به حیوانی نمی دارد روا
آنچه این نامردان با جان انسان میکنند
صحبت از پژمردن یک برگ نیست
فرض کن مرگ قناری در قفس هم مرگ نیست
فرض کن یک شاخه گل هم در جهان هرگز نرست

فرض کن جنگل بیابان بود از روز نخست
در کویری سوت و کور، در میان مردمی با این مصیبت ها صبور
صحبت از مرگ محبت مرگ عشق، گفتگو از مرگ انسانیت است

شعر: وای جنگل را بیابان میکنند اثر فریدون مشیری

نفاشی: سوم ماه مه فرانسیسکو گویا Francisco Goya The third may

چه کسی میداند؟
که تو در پیله ی تنهایی خود، تنهــــایی؟
چه کسی می داند که تو در حسرت یک روزنه در فردایــی؟
پیله ات را بگشا،تو به اندازه ی پروانه شدن زیبایی!

شعر: آرزوها اثر سهراب سپهری

نقاشی: ژوئن سوزان اثر فردریک لورد Frederic Lord Leighton Flaming June



من اینجا ریشه در خاکم
من اینجا عاشق این خاک اگر آلوده یا پاکم
من اینجا تا نفس باقیست می مانم
من از اینجا چه می خواهم، نمی دانم
امید روشنائی گر چه در این تیره گیهانیست
من اینجا باز در این دشت خشک تشنه می رانم
من اینجا روزی آخر از دل این خاک با دست تهی
گل بر می افشانم
من اینجا روزی آخر از ستیغ کوه چون خورشید
سرود فتح می خوانم

شعر: ریشه در خاک اثر فریدون مشیری

نقاشی: سرگردان بر فراز دریای مه اثر کاسپر دیوید فریدریش Caspar David Friedrich Wanderer above the Sea of Fog

گفت دانایی که: گرگی خیره سر

!هست پنهان در نهاد هر بشر

لاجرم جاری است پیکاری سترگ

روز و شب، مابین این انسان و گرگ

زورِ بازو ، چاره ی این گرگ نیست

صاحب اندیشه داند چاره چیست

هر که گرگش را در اندازد به خاک

رفته رفته می شود انسان پاک

و آنکه از گرگش خورد هردم شکست

گرچه انسان می نماید گرگ هست

و آن که با گرگش مدارا می کند

خلق و خوی گرگ پیدا می کند

!در جوانی جان گرگت را بگیر

وای اگر این گرگ گردد با تو پیر

مردمان،گر یکدگر را می درند

گرگ هاشان رهنما و رهبرند

شعر: گرگ درون اثر فریدون مشیری

Peter Paul Rubens Massacre of the Innocents نقاشی: کشتار بیگناهان اثر پیتر پاول روبنز

قايقي خواهم ساخت، خواهم انداخت به آب

دور خواهم شد از اين خاک غريب

همچنان خواهم راند. همچنان خواهم خواند: دور بايد شد، دور

شب سرودش را خواند، نوبت پنجره‌هاست

همچنان خواهم خواند, همچنان خواهم راند

پشت دریاها شهری است, كه در آن پنجره‌ها رو به تجلی باز است

مردم شهر به یک چينه چنان مي‌نگرند, كه به یک شعله، به یک خواب لطيف

خاک، موسيقی احساس تو را مي‌شنود

و صدای پر مرغان اساطير می‌آيد در باد

پشت درياها شهری است

كه در آن وسعت خورشيد به اندازه ی چشمان سحرخيزان است

شاعران وارث آب و خرد و روشنی اند

پشت درياها شهری است

قايقی بايد ساخت

شعر: پشت دریاها اثر سهراب سپهری

نقاسی: موج نهم اثر ایوان آیوازوفسکی Ivan Aivazovsky Ninth Wave

دی شیخ با چراغ همی‌گشت گرد شهر

کز دیو و دد ملولم و انسانم آرزوست

شعر: دیوان شمس اثر مولوی

نقاشی: تراس کافه در شب اثر ونسان ونگوگ Vincent van Gogh Café Terrace at Night

صدا کن مرا, صدای تو خوب است

صدای تو سبزینه آن گیاه عجیبی است, که در انتهای صمیمیت حزن می روید

در ابعاد این عصر خاموش, من از طعم تصنیف درمتن ادراک یک کوچه تنهاترم

بیا تابرایت بگویم چه اندازه تنهایی من بزرگ است, و تنهایی من شبیخون حجم ترا پیش بینی نمی کرد

و خاصیت عشق این است, کسی نیست

بیا زندگی را بدزدیم آن وقت, میان دو دیدار قسمت کنیم

بیا با هم از حالت سنگ چیزی بفهمیم, بیا زودتر چیزها را ببینیم

بیا آب شو مثل یک واژه در سطر خاموشی ام, بیا ذوب کن در کف دست من جرم نورانی عشق را

مرا گرم کن

شعر: صدا كن مرا. صداي تو خوب است اثر سهراب سپهری

نقاشی : شب پرستاره اثر ونسان ونگوگ Vincent van Gogh Starry Night

من اينجا بس دلم تنگ‌ست
و هر سازی که می‌بينم بدآهنگ‌ست.
بيا ره‌توشه برداريم،
قدم در راه بی‌برگشت بگذاريم،
ببينيم آسمانِ "هر کجا" آيا همين رنگ‌ست؟

شعر: من اینجا بس دلم تنگ است اثر مهدی اخوان ثالث

نقاشی: خش خش باران اثر لئونید آفرمو Leonid Afremov Rain’s Rustle

Endodontics Notes

*Cardial sign of inflammation & their causes:

Dolor = pain

Calor = heat

Tumor = swelling

Rabor = redness

Functionalsia = loss of function

*First is vasodilation followed by vasoconstriction (anterior constriction); the sequence:

↑ blood flow

↑ vascular permeability

Enema / Exaduation

Escape of Leukocytes of sites of injury

necrosis

*Types of inflammation:

1. Chronic : long - Macrophages

2. Acute : suddenly - Neutophils

*Causes of pulpal inflammation:

1.Bacterial (most common cause)

2.Physical

3.Chemical

4.Idiopathic

1. Bacterial (mostly streptococcus mutans)

At Coronal (crown) & Radical (root) cause caries which leads to :

Fracture (complete or incomplete)

Non-fracture trauma (weakness due to pathologic)

once there is caries or fracture on crown which provide an opening or passage for bacteria to reach the apex & by disturbuting of infection cause widdening of periodomtal space & breakage of lamina dure & formation of sinus tract & in advance result toinflammation at lymph nodes:

Parotid gland = stensen's duct

Sublingual gland = Bartholin's duct

Submandibular gland = Wharton's duct

At Anomalous tract :

Tubercle or protuberance from the involved surface thats shows extra bump or cusp.

originates from the central groove or lingual ridge.

Dens invaginatus : incisor, most common is max lateral.

Dens envaginatus : Premolars & molars, most common is mandibular premolars.

At Radiation

Retrogenic infection through:

Periodontal inflammtion & calcular deposite cause 1.periodontal disease(gum recession) 2.periodontal pocket 3.periodontal abscess

Blood cause hematogenic (pertaining to the formation of blood or blood cells).

Saliva cause periodontal cancer by radiotion therapy.

bacteria has 2 way to reach apex: 1.pulp 2.periodontal ligument

2. Physical

Acute:

Sudden Fracture by 1.coronal 2. radiation

Vascular stasis during correction of orthodontic problem by forces that apply to the tooth.

Luxation (labial/buccal or lingual movement) & Avulsion (tooth suddenly lock out of socket)

Chronic:

Adolescent

Female Bruxism that leads to 1.Abrasion 2.Malocclusion 3.TMJ problem 4.Truma to periodontium 5.Pulp exposure

Attrition (physiological) /Abrasion (mechanical)

Erosion (chemical)

3. Chemical

Filiing material

cement:

IRM (Internative & Restorative material; Disadvantages is Expensive)

GIC (Flouride release that stop formation of caries)

Zinc Oxide Eugenol (Temporary cement that Promote tertiary dentin)

Polycarboxylate (True adhesion to tooth structure as a base or lutting cement when the cavity preparation is close to the pulp;The powder is zinc oxide & liquid is polyacrylic acid or a copolymer of that acid; Disadvantages are low tensile strength & no fluoride release & intraoral solubility)

Zinc phosphate (Never use in vital teeth because it contain acid & can irrigant the pulp)

Plastic:

Polymeric resins (use in restoring & replacing tooth structure or missing teeth that can be bonded with other resins or directly to tooth structure or to other restorative materials such as amalgam; Polymer is the liquid & Monomer is powder. Examples: Self cure resin & Heat cure resin)

Composite resin resotorative fillings (Because of the resin mimics has the appearance of natural teeth that also known as “white fillings” or “tooth-colored fillings")

Etching agent:

Removes smear layer & wet of the enamel to promote adhesion. 35% phosphoric acid for 15 seconds & wash well the tooth with water & dry after use

Cavity liners:

Cavity warnish for Amg

Bonding agent for composite

curing times is 20 sec

Alcohol/ether:

Cavity base that provides protection

Calcium hydeoxide (Dycal)

GIC type I (Luting cement for cementation of crown & bridges), type II (Restorative)

Disinfectant

AgNo3 (silver nitrate)

Phenol (using during pulpotomy)

NaFl (sodium fluorescein)

4. Iatrogenic

Cause by dentist druring:

Cavity prepration by Expose the pulp.

Restoration by wrong pack (No space between filling material).

Intentional extripation (ریشه کنی و نابئدی عمدی) by Exposing pulp tissue.

Orthodontic movement by forces that apply to the tooth.

Periodontal curettage by Severe mobility of tooth

Electrosurgery by Laser burns

Periapical curettage

Osteotomy by Cutting the bone.

Intubation by strike the teeth as it's rapidly and forcefully passed through the mouth and cause chipped teeth.

*Idiopathic - None cause:

Aging

Internal resorption

External reorption

Hypophosphatasia

Effect bone formation & disturbe mineralization

Sickle cell anemia

Hematogenic disease that decrease RBC so ↑ risk of infection.

*Pathogenesis:

1st ↓dentin permeability that leads to dentin sclerosis (hardening of dentin)

2nd formation of new dentin (secondary dentin)

3rd inflammatory & immune reaction (hyperemia) that leads to pulpitis then necrosis.

*Disease of the pulp :

1. Hyperemia

Physiologic term for inflammation.

↑ blood flow of pulp tissue.

Different with pulpitis.

Significance is 1st sign of pulp in stress.

Because of presence of causes (bacteria, trauma,...) that leads to Hypercemia (vasodilation followed by vasoconstriction) which finally result to Pulpitis.

2. Pulpitis

inflammation of pulp can be:

Acute/Chronic

Partial(some part of pulp expose) / Total (all part of pulp expose)

Infected (pus/abscess) / Sterile (no pus)

*Types of Pulpitis:

Inflammatory (Reversible & Irreversible)

Pulp Degeneration (calcific & Atrophic & Fibrous & Pulpartifacts & Tumors)

Necrosis

Inflammatory

Reversible

Mild to moderate inflammation of pulp because of noxious stimuli.

Px complain of pain that produced by thermal (hot & cold) stimuli.

Capable to retaining to uninflamed state by removal of stimuli.

Pain of brief duration produced by thermal stimuli.

Pain subside as soon as stimuli removed.

Sharp pain for few second or moment. (dentinal tubules is exposed)

Symptomes by cold food or cold air.

No accur spontaneously, its reactive.

No continue to accour when cause removed.

Thernal response are momentary, quick, sharp, hypersensitive response, subsides as soon as stimulus removed.

Percussion & Palpation is Negative.

in X-ray :

Caries not reach the pulp. (only in enamel or dentin)

No radiolucency at apex.

No widdening of periodontal space

Lamina dura is intact - continious & radiopaque (lamina dura is thin bone occupize periodontal space but if there is break ,No contact)

Tx of reversible:

Early detectable & removal of cause.

Retreatment of cure.

prepare wet cavity & proper utilization chemical drug & restorative procedure.

Never desicate dentin during restorative procedure.

Outcome of treated reversible:

Favorable if irritant is removed early enough; if not detectable & treate on time, will continue & develop into irreversible.

Irreversible

Persistant inflammatory condition of pulp cause by Noxious stimulus.

Can be Symptomatic (pain) or Asymptomatic (no pain)

Can be Acute or Chronic.

Can be with Pus (infected) or No pus (sterile)

Progression of reversible pulpitis.

Pain caused by hot/cold stimulus.

Pain man accour spontaneously.

Pain persist for several min to hour.

Lingering after removal of thermal stimuli (Can ot go back to normal)

Hemorrhage & pain during probing.

In X-ray:

Deep cavity extending to pulp or decay under filling.

Caries exposed pulp or envolved surface of pulp.

Tx irreversible:

Emeregency tx is pulpectomy & placing material such as Formocresol (has too much formalin cause bone resoption)

Root canal tx

Extracted if its not restorable

Outcome of treated irreversible:

Favorable after proper endodontic procedure is done with proper restoration of tooth; if not detectable & treate on time, will continue & develop into necrosis.

Types of irreversible:

1. Acute

Short duration

Abnormally response tp cold/heat

Caries:

Smooth surface (labial, buccal, lingual, proximal)

Pit & Fissure&occlusal (lingual pit of max 1st molar, Buccal pit of mand molar, incisors)

Radiographic:

Deep caries with apparent pulpal exposure, extensive restoration

Theckening of periodontal space (advance stage)

Symptomatic:

Moderate-severe spomtaneous(accour naturally)

Inter mittent(on&off) or continous, sharp, dull

Radiating(not local,can go to neck) or Reffered(can not determined location), difficult to localize.

Intense pulsating type which becomes intermittent & throbbing

Contious for long period & worse when heat is applied

Pain relieved by application of heat/cold

Affect by postiral change(at night, sleep); Sleep with elevated head(seatin position)

Types of acute:

Suparative pulpitis presence of pus

Serous Pulpitis Extensive carise with No pulp expusure; Mild pain & increase sensivity during hot/cold test, sprecially hot test & negative to percussion

2. Chronic:

Asympotomatic

With pulp exposure

Hyperplastic pulpitis

Internal resorption

Types of chronic:

Chronic Close pulpitis No gross cavity & slowing advamcing caries

Chronic open pulpitis Big caries involvement

1. Ulcerative

expose the pulp & may favorable if symptomes relieved

2. Hyperplastic

Other name is pulp polyp

Chronic proliferative pulpitis, productive inflammation(hyperplasia) of pulp to extensive caries exposure of young pulp.

Characterized by development of granulation tissure that covered with epithelium; in otherword Granuloma with stratified squamous epithelium lined with polymorphous cell.

Clinical appearance is Fleshy reddish pulp that filled pulp chamber.

Resulting from long standing low grade irritation of pulp.

In young px & adult, no more above 50 y.o

Pain is not common unless disterbuted, painfull during presence of food & sensitive to hot/cold.

Tx is cut the pulp with spoonshape & excavation then RCT.

Outcome is favorable after endo tx or resto & can be unfavorable if left withouy tx.

X-ray of pulp polyp shows big radiolucency with direct access to pulp chamber.

*Pulp inflammation overview

1. pulp hyperemia

If does not treat will lead to Reveressible

2. Reversible pulpitis

If does not treat will lead to Irreveressible

3. Irreversible pulpitis

3.1. Actue Irreversible pulpitis

3.1.a. Acute Suparative pulpitis

3.1.b. Acute Serous pulpitis

3.2. Chronic Iireversible Pulpitis

3.2.a. Chronic Close pulpitis

3.2.a.b. Chronic Open Pulpitis

3.2.a.b.a. Chronic ulcerative Open Pulpitis

3.2.a.b.b. Chronic huperplastic Open Pulpitis

If does not treat will lead to Necrosis

4. Necrosis

4.1. Liquifactive necrotic pulp

4.2. Coagulative necrotic pulp

4.2.a. Caseation Coagulative necrotic pulp

Necrosis

Common condition affecting tooth which pulp killed by Acute or Chronic inflammation.

History of pain that disappear.

Pulp extripation on tooth extraction is necessary.

Pulp Death that cause reduction of pain of tooth because all the tooth's nerves are in pulp, by death of pulp the px can feel the pain any more

Death of pulp can be partial or total.

sequel of inflammation of pulp following a traumatic injury:

1. Pulp is destroyed before inflammatory reaction takes place.

2. Ischemic infarction causing Dry-gangreous necrotic pulp whicj is blackage or bluish discoloration is most common cause by trauma.

3. Liquifactive, proleolytic enzyme convert pulp tissue into softtened mass that results liquid amorphous debris.

3. Coagulative necrotic, soluble portion of tissue is precipitated or converted into solid material.

4. Caseation is form of Coagulative necrotic, tissue converted to chessy mass consisting chiefly of Coagulated protein, fat, water.

End product of pulp decomposition is Hydrogen sulfide, Ammunis, Fleshy substance, Indican, Ptomaines, water, carbon dioxide.

Intermediate products contribute to unpleasant odor emanting from root of canal.

*Periapical Abscess

Result of decay & infection extending into pulp of tooth.

Break in periodontal ligument provide passage of bacteria toward the apex.

pain is severe, persistant, throbbing.

Tooth is tender to touch if not treted pus.

Tx:

Incision-dranaige of pus & Antibiotic therapy (Amoxicillin 500mg, Dispence # of antibiotic with type of anitbiotic either capsule or tablet, instruction take one capsule 3 times aday)

Root canal therapy

Extraction

*Periapical Granuloma:

Other name is Acute Periodontitis.

One of the most common sequel of pulpitis

Localized mass of chronic granulation tissue formed due to infection.

Hyperemia, Edeme, Inflammation of apical periodontal ligument.

X-ray:

Thickening of periodontal space

Root canal at apex is circumscribed.

*Osteomyelitis:

Inflammation of bone & bone marrow

Result of Odontogenic infection that develops to the Jaw.

Reference:

Lecture of Dr annalie De Lemos at national university college of dentistry-manila philippines

Anesthesis summery

A.Trigeminal nerve (Cranial nerve V) devision:

1.Ophthalmic (V1)

2.Maxillary (V2)

3.Mandibular (V3)

*sensory: To skin of the face, Nose & nasal cavity, Forehead, Temple, Teeth, Tongue, Palate .( involve V1,V2,V3)

*motor: To muscle of mastication & Anterior belly of digastric & Masseter.(only V3)

1. Ophthalmic (V1 ):

2. Maxillary (V2 ):

*Nasopalatine: Lower posterior nasal septum, Mucous membrane of anterior hard palate.

*Greater palatine: Mocous membrane of posterior hard palate.

*Lesser palatine: Soft palate of tonsils

*Superior Alveolar Nerves:

Anterior Superior Alveolar Nerves (ASAN): Anterior teeth & Maxillary sinus

Middle Superior Alveolar Nerves (MSAN): Premolars & MB root of 1st molar & maxillary sinus

Posterior Superior Alveolar Nerves (PSAN): DB and palatal root of 1st molar , 2nd molar , 3rd molar , Maxillary sinus

3. Mandibular (V3) :

*Lingual nerve: Anterior two third of the tongue, Lingual gland, Submandibular gland, Sublingual gland.

*Buccal nerve: Cheek, Buccal gingiva of lower molars

* Inferior Alveolar nerve (IAN): goes into the mandibular foramen

Dental nerve: Lower molars & Premolars

Mental nerve: Skin of lower lip & Chin (exits the mental foramen)

Incisive nerve: Lower Incisor & Canines

*Temporal nerve

*Lateral pterygoid nerve

*Medial pterygoid nerve

B.contraindicated:

*when there is infection or inflammation in the area of the injection site.

*when there is presence of pus because pus is Acidic and anesthesia is Base so its does not work & aside from that is too much painful, so aspirate &treat the pust before anesthesia.

*when the health of px is compromised.

C. Maximum Recomendation Dose:

*Maximum amount of carpules that can be use in a person at a time is 10 carpules.

*Using different types of carpules a person at a time can cause Anaphylactic shock.

*Choose the Anesthetic Drug base on px health condition; For example Never use Lidocaine for Asthma px causeit can increasing heart rate ,use Aritrocainre Or Never use Lidocaine for hyperthroid px cause it leads to anfractuous, use articaine.

D. Dosage Calculation:

*Formulla: Maximum Recomendation Dose ✖ Body Weight= Total ÷ Amount of lidocaine in 1 carpule

*Example: 20 kgr child can tolerate how many carpule of 2% lidocaine with vasoconstrictor?

For "Amount of lidocaine in 1 carpule" read the written information on the carpules that you bought (depends on the carpule brands)

Usually in 1 carpule 1.8 mL of 2% lidocaine is used.

2% lidocaine is equal to 20 mg/ml

So Amount of lidocaine in 1 carpule = 20 mg/mL ✖ 1.8 mL= 36 mg/carpule

Maximum Recomendation Dose ✖ Body Weight= Total ÷ Amount of lidocaine in 1 carpule

4.4 mg/kg ✖ 20 kg = 88 mg ÷ 36 mg/carpule = 2.4 carpules

It means to say for 20 kg child, you can use two & half carpules.

E. Local Anesthetic Drug Information:

*Most common used: 2% Lidocaine with vasoconsrictor 1:100 000 Epinephrine

*Epinephrine as vasoconstrictor increase pulse rate

*Before using the cartridge, sterile with 70% alcohol & wash with body temprature water.

*Place the carpule at Hot water for 5min for better control of the pain produced during the administration of dental anesthesia injection; because Heat can cause the lidocaine to be absorbed into your body faster .

F. Topical anesthesitic:

Identify the landmarks by palpation & dry the area

Apply topical anesthetic Gel 20% Benzocaine. The Onset is 20 sec & recommended applying for 1-2 min & effecting time is 5-15 min.

Once the color of tissue change to white means " Blanching" that shows tissue numbness.

G. Needle:

As increasing # gauge we have decreasing of needle diameter

The most common gauges are 25, 27, and 30 gauge.

27 gauge, the smallest gauge -largest diameter) is highly suggested Because the diameter is small so it will not be painful for patient & easy aspiration but has enogh strength to penetrate the tissue without deflection.

Long needle is about 32 mm (1.5 inches) and the short needle is about 20 mm (1.0 inch).

Bevel of the needle shoud face the cortical bone.

H. Aspiration & Deposite:

*Syringe should contain No air.

*Always make sure that you are heat the bone then, withdraw the needle 1mm

*Aspirate for 20 sec must be negativeTo make you sure that you will deposite in the nerve not in the blood vessels & if after aspiration you see the blood it means its positive & you must correct your needle position base on landmarkes

*After Aspiration, Deposite slowly in 60 sec ;To avoid pain and ulceration.

*Once you insert the needle ask the px to Inhale.

*Once you deposite the carpule ask the px to Exhale.

*Always Slowly remove the needle & palpate the area to help disturbution of anesthesia.

*Wait for 2-3 min to act.

H. Techniques:

1. Inferior alveolar nerve block (IANB)

*Other name: Vazirani

*Numbness : Half of the mandible

*Once you need numbness of both side of mandible: Bilateral IANB

*Landmarkes & procedure:

*Use Long needle 27 gauge

*Never use short needle for IAN BLOCK cause needle will break

Needle should be at level of occlusal plane & between Lower 1st & 2nd PM .

For pediatric px needle should be above occlusal plane.

Slowly insert Half of the needle & heat the bone .

Change your neddle direction, Follow the central fossa of teeth & insert whole of the needle & Deposite the rest of the carpule.

*Example: Px came to your clinic for endo tx of tooth # 16. After Ian block & starting procedure, px is complaning of pain

1st complain : Proceed to Interligamentray anesthesia(Complement anesthesia for IAN) ; Bend the short 27 gauge needle by scoop technique & insert the needle 30 degree to interligument.

Anesthesia solution effects in interligament by passing PDL cell sheets(صفحات غربالی)

2nd complain: Intrapulpal anesthesia (secondary anesthesia); Bend the short 27 gauge needle by scoop technique & insert the needle 90 degree directly to the pulp.

*After IAN Block we proceed to Infiltration techmique for Reducing bleeding

2. Infiltration technique:

*Numbness: Soft tissue around the tooth & Dental plexus nerves

*Landmarkes & procedure:

On Labial or Buccal ,looks for Muccobual fold & Apex of root of the offending tooth.

On palatal, look for Gingival maring & Midline of the plate.

On Lingual, look for muco-lingual fold.

On Labial or Buccal, insert the needle 2mm away from the muccobucal fold at 45 degree till you heat the bone.

On palatal , insert the needle at 90 degree between Gingival maring & Midline of the plate.To achive this, the needle should derived from opposite side.

On Lingual, insert the needle above the muco-lingual fold to avoid dissemination of the solution into the floor of the mouth.

Deposite half of carpule on each side for 60 sec.

*Use 27 gauge short needle

3. Buccal nerve block

*Insert the needle parralel to occlusal plane, Distal to second molar.

*Use 27 gauge short needle with length of 20 mm (1.0 inch) .

*Deposit about 1 ml of solution around the inferior alveolar nerve.

4. Mental nerve block:

*Landmarkes:

Retract the cheek and lip & locate the junction of mandibular 1st &2nd premolars & down 1 cm inferior to the gum line (just medial to the midline pupil)

*Insert the needle Distal to second premolar.

*Use 27 gauge short needle.

*Deposit one third to one half of the cartridge.

*The difference between the mental nerve block & the incisive nerve block is that the incisive nerve block requires pressure to the mental foramen.

5. Incisive nerve block:

*This technique is painful and not used routinely especially for the pediatric patient

*Landmarkes & procedure:

Palatal mucosa just lateral to the incisive papilla (located in the midline behind the central incisors).

*Use 27 gauge short needle.

Insert the needle approaching incisive papilla at a 45 degree.

Place the cotton applicator directly onto the incisive papilla & Apply sufficient pressure so there is blanching.

Place the bevel of the needle against the blanched soft tissue at the injection site.

Apply enough pressure to slightly bow the needle.

Deposit a small amount of anesthetic; Straighten the needle and penetrate the tissue with the needle & Continue to apply pressure with the cotton applicator while injecting until bone is contacted (about 5mm).

Deposit no more than a ¼ cartridge.

6. Greater palatine nerve block

* It is less traumatic than the nasopalatine nerve block because the palatal tissue in the area of the injection site is not as anchored to the underlying bone

*Landmarkes & procedure:

Maxillary first molar (or second primary molar in the primary dentition)

First Place a cotton swab at the junction of the hard palate and the maxillary alveolar process.

Apply pressure with the cotton swab while moving posteriorly.

The cotton swab on will fall into the depression created by the greater palatine foramen.

Move the cotton swabr posteriorly so it is directly over the greater palatine foramen and apply sufficient pressure to blanch the tissue for 30 seconds

Direct the syringe into the mouth from the opposite side of the mouth from the injection site at a 90 degree

Deposit a small volume of anesthetic( Straighten the needle and allow the needle to penetrate the mucosa, while depositing)

Slowly advance the needle approximately 8mm until palatine bone is contacted.

Deposite ¼ cartridge of anesthetic solution over 30 seconds.

Reference:

https://www.dentalcare.com/en-us

Lecture of Dr jimmy Aldecua & Dr Rea Corpuz at national university college of dentistry- manila, philippines

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نگاهم به نوشته ای افتاد "پدر به تو کمک خواهد کرد"
چشمهایم را بستم، کلمه ی پدر در من ماند، اول آشکارا به شکل یک نوشته، سه حرفش پشت پلکهای بسته ام ایستادند ومحو شدند.
کلمه ی پدر در من فرورفت و به نظر میرسید همینطور پایین تر میرفت، هیچ جا متوقف نشد و ناگهان دوباره در درونم بالا آمد و قلبم را در نور دید، در رگهایم انباشته شد و مثل خون جریان یافت و به طرز وحشتناکی احساس دلتنگی کردم اما دوباره نسبت به همه ی این چیزها بی تفاوت شدم.

کتاب موش ها و آدم ها

لِنی، مردی درشت هیکل و کودنی بود واز نوازش چیزهای نرم لذت میبرد ولی به خاطر ظاهرش فقط موش و سگ، برای نوازش نصیبش میشد.
با دستانِ زمختش سر آنها را به آرامی نوازش میکرد،کم کم دستش رامحکمتر میکشید و میگفت چقدر لطیف! حیوان ازدرد تقلا میکرد ولی لِنی با دستانش سعی در ساکت کردنش داشت،وقتی دستش را برمیداشت که حیوان بی حرکت بود.
لِنی از ازاینکه دیگران ممکن است اورا دعوا کنند، عصبانی میشد و جنازه را با عصبانیت به طرفی پرت میکرد و داد میزد چرا مُردی؟

کتاب عقد و داستان های دیگر

چه کسی زندگی را تعریف کرده است؟

داستانی که نویسنده ای مینویسد ولی خوانده نمیشود یا ترانه ای که نوازنده ی خام دستی میزند ولی به دل نمی نشیند.

کتاب بوف کور

و من فهمیدم تا ممکن است باید خاموش شد،تا ممکن است باید افکارخودم را برای خودم نگه دارم.