Q .What is craniofacial distraction or distraction osteogenesis?

A. It is a technique that applies gradual and incremental traction force onto surgically separated bony segments to produce additional bone

(Distraction Histiogenesis – distraction of skeleton also causes enlargement of overlying and surrounding soft tissues)



Codivilla – 20th Century – Femur elongation following osteotomy

Abbot – 1927- Femur elongation following osteotomy

Ilizarov – popularized the distraction osteogenesis in long (endochondral) bone of extremities for limb lengthening and closure of bony defects

McCarthy – 1989 – Craniofacial distraction



Terminology – 

Distraction Zone: The location of bony separation

Latency period: Duration of reparative callus formation in distraction zone

Activation period: Duration during which distraction forces are applied to callus (for elongation)

Distraction degenerate: The newly formed bone following activation

Consolidation period: Period for which external fixation is maintained in position to allow newly formed bone to consolidate

Rhythm: The rate of activation

0.25 mm four times a day or   0.5 mm two times a day

i.e. Total 1 mm /day

Vector: Direction along which forces are applied



  1. Bony separation in two segments (osteotomy or corticotomy)
  2. Latency period (5-7 days)
  3. Activation period
  4. Consolidation period (8 weeks)

Process of distraction starts with –

Performing osteotomy or corticotomy.

After which the distraction device will be applied depending on which direction the bone lengthening is desired (vector of distraction).

Following osteotomy a latency period (usually of 5-7 days) is given for callus formation, before activation of the device.

Following latency period, gradual distraction force is applied to separate the segments and thus elongate the intersegmentary callus – this is the activation period.

After, the desired length of bone has been achieved, the activation is stopped and the distraction device in maintained in position to allow consolidation of the newly formed bone- the consolidation period.


Osteotomy – Full thickness bony separation

Corticotomy – Spares the endosteum or marrow space

The most usually done distraction is  – transosteotomy (or transcorticotomy) distraction.

Distraction can be done across a open suture (such as in young patient) – trans-sutural distraction.


Three types of Distraction

  • Unifocal
  • Bifocal
  • Trifocal

Bifocal and Trifocal is across a skeletal defect

Unifocal: Single osteotomy

Distraction forces on either side of osteotomy

Bifocal: Single osteotomy

Transport segment (of bone) spanned across the defect using single distraction device

Trifocal: Two osteotomies used to fill skeletal defect in bidirectional manner


When distracting across a skeletal defect the transport segment has a fibro-cartilagenous

cap which needs to be removed after final “docking” and replaced with bone graft.


Histological Analysis

  • Latency period: Hematoma formation

Migration of inflammatory cells into osseous gaps (PMNs)

  • Activation Period: Presence of tapered cells similar to fibroblasts

New blood vessels (endothelial cells)

New fibrovascular matrix (Type 1 collagen)

At Day 14 –      Osteoid synthesis and mineralization

At day 21 –       Calcification of linearly oriented collagen bundle

Appearance of osteoblasts

Formation of bony spicules

(Linear orientation is parallel to distraction vector)

Four Temporal Zones –

  1. Fibrous central zone – mesenchymal proliferation
  2. Transition zone – osteoid formation
  3. Remodeling zone – osteoclasts
  4. Mature bone zone


Biomolecular analysis

Marked increase in TGF-B1 level

TGF-B1:         Activates VEGF & bFGF

Increase collagen deposition and non-collagen ECM proteins

Leading to mineralization and remodeling of bone

Osteoclast migration, differentiation and bone remodeling



Tensile force applied to developing callus causes elongation of callus.

The mechanical forces are converted to cellular signals – termed as mechanical transduction.

This mechanical transduction is mediated by – Integrin mediated signal transduction


Tensile strain: Defined as amount of elongation as a fraction of original bone length

Eg.     1mm elongation in 1mm osteotomy defect- tensile strain 1/1 = 100%

By day 10 the bone gap will be 10mm

So, tensile strain will be 1/10 = 10%

Maximum tensile strain for bone is 1-2%

So, bone formation does not occur in distraction zone until approx. 4 weeks of activation

i.e. 1/30 = 3%


Mechanical environment in distraction zone depends upon –

  1. Stability of distraction device
  2. Applied distraction force
  3. Inherent physiological loading (muscle action)
  4. Properties of all the local soft tissue


For formation of successful (stable) regenerate –

  1. The distraction device must be stable
  2. Latency period should be adequate (not too short or too long)
  3. Distraction should be gradual
  4. Sufficient time should be given for consolidation


Patient factors that can affect regenerate formation –

Age –

In younger patient – better and faster distraction can be achieved. Latency period in children can be as low as 2-3 day (due to rapid callus formation).

Blood supply – adequate neovascularization should occur to support newly forming bone.

Radiation or chemotherapy – patient receiving RT or CT has poor blood supply and impairs osteogenesis.


[Credits : Dr. Anoop S. (Mch, department of burn and plastic surgery, VMMC & Safdarjung Hospital New Delhi)]

Reconstruction of acquired lip defects


Philtral column

Philtral groove/dimple

Cupids bow

White roll- junction of vermillion and cutaneous surface



Vermillion – the red/pink dry part of lip seen outside


Vermillion is widest in central lip

Philtrum columns are formed by C/L orbicularis oris fibers.

Philtrum columns slightly diverge as then come down.

White roll created by pars marginalis fibers of orbicularis oris.


Upper lip elevators-

  1. Z. major
  2. Z. minor
  3. LLS AN
  4. LLS
  5. LAO

[levator labii superioris anguli nasalis, levator labii superioris anguli, levator  anguli oris]

Retractors and depressor of lower lip-

  1. Platysma
  2. Depressor labii
  3. Depressor anguli oris

Lower lip elevator– Mentalis (makes pout)

Nasolabial crease formed by-

  1. Z. major
  2. LLS
  3. LAO


Orbicularis oris-

Two components-

  1. Pars marginalis
  2. Pars peripherlais

Marginalis anterior to peripherialis [Peripheralis- Posterior]

Marginalis mostly deep to vermillion area

Peripheralis mostly deep to cutaneous portion of lip


Muscular sling that presses lip against gingiva and teeth is formed by-

  1. Orbicularis
  2. Risorius
  3. Buccinator
  4. Pharyngeal constrictor


Blood supply-

Facial artery courses through a plane which between two muscle layers.

Muscles anterior/superficial to artery are-

  1. Risorius,
  2. Z major,
  3. Superficial lamina of orbicularis oris (OO)

Muscles that are deep to the artery are-

  1. Buccinator,
  2. LAO,
  3. Deep lamina of OO

Facial artery branches approx- 1.5cm lateral to oral commissure

Into – superior labial and inferior labial a.

Superior labial- found within 10mm of lip margin

Inferior labial- found within 4-13 mm of lip margin


Labial artery lies within or posterior to orbicularis oris muscle but Never anterior to it.


Nerve supply-


Zygomatic and buccal branch – lip elevators and retractors

Marginal mandibular- lip depressor


V2 –infraorbital & V3 mental branch of trigeminal nerve


Etiology of lip defect –

Most common cause is – Carcinoma lip. MC type of cancer is Squamous cell ca.

96% lip cancer occur in lower lip

96% is SCC type.

96% of patients are male.


Reconstruction – defect wise


Defect by definition does not crosses white roll.

So, reconstruction should – Avoid crossing white roll.

Simplest method—undermining of adjacent oral mucosa with defect closure by advancement.

Wilson & Walker – laterally based bipedical mucosal flap

For Full-thickness defect of vermillion –

-lateral vermillion musculomucosal advancement flap (based on labial artery)

-musculocutaneous flap composed of intraoral mucosa and orbicularis advanced from sulcus in V-Y fashion

Other regional flaps-

Unipedicle vermillion lip switch flap from opposite lip -divided after 10-14 days

Random musculomucosal flap

FAMM flap (facial artery myomucosal flap) – buccinators muscle based on facial artery

Tongue flap (from lateral/lower surface) – two stage procedure cumbersome.


Partial thickness defect-

Primary closure

Advancement flap

Transposition flap

Skin graft not routinely used/required

Except, central philtral defect- full thickness graft used instead of STSG.


Small full thickness defect-

Primary closure-

Lower lip- up to 40% defect

Upper lip- up to 25 % defect


Large full thickness defect-

Two resources to recruit extra tissue to fill the defect – opposite lip & adjacent cheek.

Orbicularis oris- better competent stoma. Microstomia a risk.

Cheek- microstomia less common, functionally and aesthetically inferior outcome


Large central upper lip defect-

Abbe flap (based on inferior labial artery)  –> flap division after 2-3 weeks

Abbe flap with perioral crescent


Large central lower lip defect-

B/L Karapandzic

Modified Bernard (Webster- Bernard)

Nasolabial flap


Karapandzic Bernard
Musculocutaneous rotation advancement flap

Neurovascular flap

First 1cm incision full thickness- after that only skin and muscle divided, mucosa is intact

Burrow’s triangle excised

Lateral advancement flap

First 1cm full thickness incision after that only skin and mucosa intraorally

Burrow’s triangle excised


Interdigitating nasolabial flap

Partial thickness random flap

Full-thickness “Gate-flap”- based on facial a

Full thickness flap denervates upper lip.


Large lateral and commissure defect-


Medially based rotation advancement flap from upper lip to lower lip

Reverse Estlander- from lower lip to upper lip

Gillies-fan flap- rotational advancement flap. A quadrilateral flap

McGregor & Nakajima modified fan flap –

  1. Pivotal flap
  2. Stoma size unchanged
  3. Need for vermillion reconstruction

Abbe-Estlander flap-

Preserves commissure

Need second stage of flap division

Temporary microstomia

U/L Karapandzic

U/L Bernard

U/L Nasolabial flap


Total lip reconstruction-

>80% defect-

B/L Bernard or Nasolabial flap

Submental flap (flap based on submental branch of facial artery)

Radial forearm free flap (RAFF)

Karapandzic – will cause microstomia, so not preferred.

RAFF is the best choice for total lip reconstruction.

Palmaris longus tendon can be harvested along with the flap to be weaved into remaining OO muscle or into modulus.


Lip replantation –


Most commonly – by traumatic amputation by dog bite.

Every attempt should be made for reimplant as the aesthetic and functional outcome is better than free tissue transfer.

Main obstacle in reimplant of lip is – poorly formed labial vein.




Algorithm –

Defect size Defect location Reconstructive option
Up to 25% – upper lip

Up to 40% – lower lip

  Primary closure
25-80 % Upper lateral lip or lower lateral lip Lip switch (Estlander/Abbe) or

Unilateral Karapandzic/ Bernard/ Nasolabial flap

  Central lower lip Bilateral Karapandzic/ Bernard
  Central upper lip Abbe flap +/- perioral crescent
>80%   Bilateral Bernard/ Nasolabial flap or

Free tissue transfer – RAFF

(further reading – Grabb and Smith Plastic surgery 7th Ed. chapter 34)

Radial nerve palsy

Course of radial nerve?

Radial nerve is terminal branch of posterior cord, a continuation of it. It receives supply from C5-T1.

It then descends in front of subscapularis and latissimus dorsi and posterior to axillary artery.

At the level of lower border of teres major it courses posterolaterally and passes through triangular interval (between long head of triceps, teres major and humerus).

It then courses in shallow groove on posterior surface of the humerus – between lateral and medial head of triceps where it gives off branches- muscular and cutaneous.

At level of middle and lower 1/3rd of arm it penetrates lateral intermuscular septum to enter anterior compartment.

It travels between brachialis (medially) and brachioradialis & ECRL (laterally).

At the level of capitulum of humerus it divides into superficial and deep branches.

Deep branch (PIN) passes between two heads of supinator à wraps around lateral aspect of radius to reach back of forearm. [PIN emerges from supinator approx. 8cm distal to elbow joint]

After emerging from supinator it travels between superficial and deep layer of muscles of extensor compartment i.e. it passes/travels over APL & EPB and under the EDC.

It then courses on the dorsal surface of interosseous membrane underneath the EPL and EIP.

At wrist joint it is almost flattened giving sensory fibers to wrist joint and DRUJ.

Superficial branch –

Courses underneath the brachioradialis.

In the proximal third of foreram – it lies on the supinator

In the distal part it travels sequentially over pronator teres àFDS (radial side) à FPL

In the distal forearm – Approx. 7-8cm proximal to the wrist it emerges between BR & ECRL – pierces the deep fascia.

After emerging from BR it winds around radius. Travels over (crosses) the tendons of APL & EPB.

Passes through anatomical snuff box, over the extensor retinaculum and then divides into four or five dorsal digital nerves.


The branches of radial nerve?

Near axilla –

Medial muscular branches – medial and long head of triceps

Cutaneous branches -Posterior cutaneous n of arm (arises in axilla)

In the groove –

Posterior muscular branches – medial and lateral head of triceps

Cutaneous branches – @ the start of groove (originating almost just after first muscular branches) a branch of radial n penetrates lateral head of triceps and overlying fascia and then splits into these two nerves –

Posterior cutaneous n of forearm

Lateral cutaneous n of arm

Lateral muscular branches – branches given after radial nerve, penetrates lateral I/M septum – BR & ECRL

Branches before entering supinator –

  1. ECRB & Supinator

After emerging from supinator –

  1. Short muscular branches – EDC, ECU, EDM

Two long muscular branches –

  1. Medial – EPL & EIP
  2. Lateral – APL & EPB


Sequence of innervation of muscle by radial nerve?

In order of innervation from proximal to distal (helps in guiding the recovery process) –

  1. BR
  2. ECRL
  3. ECRB ↔ supinator
  4. EDC
  5. ECU
  6. EDM
  7. APL
  8. EPL
  9. EPB
  10. EIP

High or low radial nerve injury?

When injury occur above the elbow there is loss of almost all the function of radial n – this is called high radial nerve injury.

When the injury is distal to the elbow, so that only PIN is injured. In this case innervation to BR, ECRL, ECRB (variable) is preserved and hence wrist extension is preserved. When wrist extension is preserved its called Low radial nerve injury.


The sensory distribution of radial nerve?

In the arm – posteriorly and inferior lateral

In the forearm – posterior

In the hand – radial aspect of half of dorsum of hand, proximal portion of dorsum of radial 3 and ½ finger (excluding the tip)


The deficit that you will notice in radial nerve injury?

In motor loss there will be –

  1. Loss of finger extension at MCPJ
  2. Loss of wrist extension
  3. Loss of thumb extension and abduction
  4. Loss of elbow extension if nerve to triceps if also injured

In sensory, there will be loss noted in –

  1. 1st dorsal web space- also known as the autonomous zone of radial sensory nerve.
  2. Lateral 3 & ½ fingers (except distal phalanx)
  3. Posterior aspect of forearm

Surface marking of radial nerve ?

Mark points –

First point – lateral wall of axilla – lower limit

Second point – junction of upper 1/3rd and lower 2/3rd of line joining lateral epicondyle and insertion of deltoid

Third point – in front of elbow joint below level of LE approx 1 cm lateral to insertion of biceps brachii.

1st point to 2nd point – oblique course in radial groove.

2nd point to 3rd point – anterior compartment course.

In forearm –

4th point – junction of upper 2/3rd and lower 1/3rd of line along lateral border of forearm lateral to radial artery.

5th point – anatomical snuff box

3rd point to 4th point – radial nerve is straight

4th point to 5th point – radial nerve curves backwards.


Planning for nerve injury – nerve exploration vs nerve repair vs tendon transfer?

Nerve grows @ 1mm/day with 30 days of latency period.

In case of closed fracture its prudent to wait till the expected(calculated) time of recovery. Nerve exploration to be done if no recovery seen. if more than 3-6 months has passed from expected time of recovery without any recovery.

If more than 16-18 months has elapsed since time of injury then directly planned for tendon transfer.


When do you time the tendon transfer?

There are two approach for tendon transfer-

“Early” tendon transfer – tendon transfer done simultaneously with nerve repair or before the expected time of reinnervation of muscle.

“Conventional” or late tendon transfer – when reinnervation of most proximal paralysed muscles (BR & ECRL) fails to occur by three months after the expected time of reinnervation.

In early tendon transfer there can be –

“Limited” transfer – which is PT –> ECRB only

  1. Provides for internal splintage (eliminates need for external splintage) while the nerve is recovering,
  2. Provides immediate restoration of power grip (by stabilizing the wrist)
  3. If the nerve recovers it works as a helper by adding power of a normal muscle to innervated muscle.

Complete set of transfer (advocated by Brown) –

This is reasonable approach in case where prognosis of nerve repair is poor –

  1. Nerve gap >4cm
  2. There is large wound or extensive scarring or skin loss over the nerve.

Bevin advocated directly proceeding to tendon transfer without attempting nerve repair – benefit of reduced time of disability. This has not been well accepted.


Historical perspective of development of tendon transfer in radial nerve palsy?

First transfer was described by Franke – FCU to EDC.

Followed by Capellen – FCR to EPL

First complete set of transfer was given by Sir Robert Jones (1906)

  1. PT  –> ECRB & ECRL
  2. FCU –> EDC III-V
  3. FCR –> EPL, EIP, EDC II

He subsequently modified it in 1921 (Jones II)

And used FCR to additionally to EPB & APL

  1.  PT –> ECRB & ECRL
  2. FCU –> EDC III-V

Starr was firs to use PL to EPL transfer and left one wrist flexor intact.

Zachary convincingly proved that it’s desirable to leave at least one wrist flexor intact.

In 1949, Scuderi refined PL to rerouted EPL transfer.

These studies resulted in what is called “Standard” set of transfer –

  1. PT to ECRB
  2. FCU to EDC II-V
  3. PL to rerouted EPL

Brand proved that FCU should not be used as it is too strong, too short excursion and is prime ulnar stabilizer of wrist. He then, along with Starr described FCR transfer (which was used instead of FCU) –

  1. PT to ECRB
  2. FCR to EDC II-V
  3. PL to rerouted EPL

Boyes reasoned that FCU is a more important wrist flexor to preserve than FCR because the normal axis of movement of wrist movement is dorso-radial to volar-ulnar (a dart-throwing type of movement).

Boyes also reasoned that wrist flexors (FCU & FCR) (33mm) has inadequate excursion compared to finger extensors (50mm), and it’s better to use FDS which has better excursion (70mm).

Boyes described Superficialis transfer

  1. PT to ECRB & ECRL
  2. FDS IV to EDC
  3. FDS III to EIP & EPL
  4. FCR to APL & EPB.


Aims to achieve by tendon transfer in radial nerve palsy?

Aim is to achieve –

  1. Wrist extension
  2. MCPJ extension
  3. Thumb abduction and extension


The principles of tendon transfer?

  1. One tendon , one transfer
  2. Straight line of pull
  3. Similar amplitude of excursion
  4. Adequate strength (muscle to be transferred should be atleast >85% of its normal strength)
  5. Supple joint
  6. Synergistic muscle
  7. Expendable donor

Example of synergistic muscle – wrist flexor with finger extensor & wrist extensor with finger flexors.


Describe the incision and procedure of FCU set of transfer.

Incision –

First incision – directly over the FCU in distal half of forearm longitudinally. Distal end in J-shaped extension to reach PL.

FCU is transected just proximal to pisiform and freed up as far as possible through that incision.

Second incision – begins 2 cm below the medial epicondyle and angles across the dorsum of proximal forearm directed towards Lister tubercle.

Deep fascia overlying the FCU muscle is incised. Fascial attachments of FCU is completely freed up .

Upper limit of dissection of FCU muscle is 2 inches from its proximal origin where its nerve supply enters.

Third incision – begins on the volar-radial aspect of mid-forearm, passes dorsally around the radial border of forearm in the region of insertion of PT and then angles back on the dorsum.

Tendon of PT is identified in the volar aspect – followed to its insertion on the radius –tendon insertion is freed with a cuff of periosteum around 2-3 cm – muscle tendon unit freed up proximally – PT then transferred around the radius, superficial to BR and ECRL to be inserted to ECRB just distal to musculocutaneous junction .

Through dorsal incision – Kelly’s clamp is passed around the ulnar border to grab FCU and pulled into dorsal wound. (FCU muscle belly may be required to be trimmed if too bulky)

EPL is identified àdivided at its musculotendinous junction à rerouted out of Lister’s canal towards the volar aspect of wrist across anatomical snuffbox à PL transected at the wrist –muscle-tendon unit freed up proximally to allow for straight line of pull.

FCU can alternatively be passed through a window in interosseous membrane.

FCU is sutured to EDC tendons by weaving through all four EDC tendons in end to side fashion at an angle of 45° just proximal to retinaculum.


How will be the tension in tendons adjusted?

1st suture will be PT to ECRB – to be sutured with wrist in 45° extension with PT in maximum tension.

2nd suture is FCU to EDC – to be sutured with wrist in neutral position, with FCU in maximum tension with full extension at MCPJ.

After these two sutures – there should be full flexion of fingers with wrist extended and – full extension of digits with wrist flexed.

Final suture is PL to EPL. Both tendons are sutured under resting tension with wrist in neutral position.

Reconstruction is checked again for full movements – finger flexion with wrist extension & finger extension with wrist flexion.


Post-op care following tendon transfer?

Long term splint for immobilization –

  1. Forearm in – 15-30° pronation
  2. Wrist – 45° extension
  3. MCPJ – slight flexion – 10-15°

Thumb in – maximum abduction and extension

Remove sutures after around 6-7 days

Remove cast at 4 weeks – start physiotherapy.


Potential problems after FCU repair?

Excess radial deviation – removing the only remaining ulnar deviator can lead to radial deviation of hand, especially if ECRL is functioning well (PIN only palsy.). this is also more aggravated if PT to ECRL transfer has been done, less so if PT to ECRB transfer.

Solution –

Avoidance – if preoperatively there is already radial deviation present (PIN only palsy) – avoid FCU transfer.

After transfer – reposition ECRL insertion – i) into ECRB; ii) attach PT to ECRB & ECRL and then detach ECRL; iii) detach from 2nd metacarpal- reroute and inset into 3rd and 4th  metacarpal bone (Tubiana).

Absence of PL –

Solution – i) Use superficialis transfer; ii) include EPL into FCU to EDC transfer ; iii) include EPL, EPB, APL into FCU to EDC transfer; iv) Use BR (if low radial n palsy) to EPL; v) Use FDS III or IV.


Highlights of Superficialis transfer?

Incision –

Long incision on volar side of the radial aspect of mid-forearm.

Expose PT and ECRB

Remove PT with 2-3 cm of periosteum and interwoven into ECRB.

Exposure of FDS (ring and middle) –

Through transverse incision in distal palm or at base of each finger.

Tendon divided proximal to chiasma- freed up and delivered into forearm.

@ Level just proximal to pronator quadratus, two incision made of size 1 x 2 cm in I/O membrane.

“J-shaped” incision in dorsum of distal forearm –

Transverse limb from radial styloid to ulnar styloid. Vertical limb extends proximally along ulna.

Bring out FDS through I/O membrane. FDS of long finger passed radial to profundus mass and FDS of ring finger passed on ulnar side of profundus mass.

FDS III – attached to EIP & EPL

FDS IV – attached to EDC.

Setting of tension – an assistant holds wrist in 20° extension with fingers and thumb held in a fist, until all transfers are done with reasonable tension.

Transverse incision at base of thumb – free FCR tendon –-> pass it dorsally –-> attach to APL (preferably only to APL or with APL & EPB both).


FCR transfer highlights?

Incision –

Straight longitudinal incision in volar forearm on radial side in distal half b/w FCR & PL.

Both tendons identified, transected near their insertion, freed up to middle of the forearm.

Longitudinal incision on dorsum – extending just distal to retinaculum to mid forearm.

FCR passed around radial border of forearm through subcutaneous tunnel.

EDC tendons are identified and divided at musculotendinous junction – withdrawn distally superficial to intact extensor retinaculum to a point over distal radius and sutured to FCR

Adjusting the tension – wrist and MCPJ in neutral position – FCR sutured in maximum tension.

PT to ECRB & PL to rerouted EPL as described for others.


Nerve transfer option for radial nerve injury.

Median nerve to radial nerve

Fascicles of FDS or FCR to PIN & ECRB.

  1. FDS to ECRB
  2. FCR to PIN

Indications –

  1. Very proximal nerve injury – where proximal stump is not available for repair, or even if available regeneration will take a very long time.
  2. Avoiding an area of scarring
  3. Nerve injury presenting in delayed fashion
  4. Partial nerve injury – presenting with well defined motor function deficit.
  5. Level of injury is unclear (idiopathic, radiation induced injury)



Foot and ankle reconstruction

Foot and ankle reconstruction

Foot and ankle reconstruction is possible with –

  1. Simple reconstruction – 90% cases
  2. Complex flap – 10% cases


Vascular anatomy-

Six angiosomes –

  1. Distal anterior tibial artery – anterior ankle. & The dorsalis pedis artery – the dorsum of the foot
  2. Calcaneal branch of PTA – medial and plantar heel
  3. Calcaneal branch of the peroneal artery (PA) – lateral and plantar heel
  4. Anterior perforating branch of PA – anterolateral ankle
  5. Medial plantar artery – plantar instep
  6. Lateral plantar artery – lateral plantar mid- and forefoot

Plantar heel has dual blood supply –> gangrene of heel means a severe vascular compromise.

Because the foot is an end organ, many arterial-arterial anastomoses provide a duplication of inflow (provides a margin of safety) –

Arterial-arterial anastomoses around the foot and ankle-

  1. Between anterior perforating branch of the peroneal artery and anterior tibial artery

via the lateral malleolar artery @ ankle joint

  1. Dorsalis pedis artery with lateral plantar artery

via direct connection @ Lisfranc joint as the DPA dip in 1st interspace

This vascular loop is critical in determining the direction of flow within the anterior or posterior tibial arteries.

  1. Between plantar and dorsala metatarsal arteries – via proximal and distal perforators.

(Proximal perforators are at Lisfranc joint, distal perforators are at digital web space)

  1. Posterior tibial artery and peroneal artery are directly connected

(Deep to the distal Achilles tendon by one to three connecting arteries)


Motor and sensory anatomy –

Sciatic nerve –> Tibial nerve &

Common peroneal nerve   –> deep peroneal nerve &

Superficial peroneal nerve

Tibial nerve –

Innervates muscle of deep and superficial posterior compartment (except gastrocnemius)

Tibial nerve trifurcates deep to flexor retinaculum into –

  1. Calcaneal nerve
  2. Medial plantar nerve
  3. Lateral plantar nerve

All these nerve supplies all intrinsic muscles of the foot (except Extensor digitorum brevis, EDB).

Deep peroneal nerve –

Innervates extensor muscles in the Anterior compartment and then EDB.

Superficial peroneal branch – 

Innervates the everting peroneal muscles of the lateral compartment

And then it pierces the fascia to become subcutaneous and provide sensibility to the lateral lower leg and dorsum of the foot.


Sensory supply –

Superficial peroneal nerve (L4, 5, and S1) –

Anterolateral skin in the upper third of the leg

It becomes subcutaneous approximately 10 to 12 cm above the lateral ankle and travels anterior to the extensor retinaculum to supply the dorsum of the foot and skin of all the toes.

Except the lateral side of the fifth toe (sural nerve) and the first web space (deep peroneal nerve).


Deep peroneal nerve (L4, LS. and S1) –

Exits the anterior compartment deep to the extensor retinaculum.

Supply and ankle and mid-foot joints, sinus tarsi, and the first web space.

The sural nerve (LS and S1) –

Provides sensibility to the posterior and lateral skin of the leg’s distal third and

The skin of the dorsolateral foot and fifth toe.

Posterior tibial nerve –

Has three branches in the tarsal tunnel –

Calcaneal branch (S1 and S2) – supplies the medial aspect of the heel pad

Lateral plantar nerve (51 and 52) supplies the lateral two thirds of the sole and the fifth and lateral fourth toes

Medial planter nerve (L4 and L5) supplies the medial one third of the sole and the first; second, third, and medial fourth toes.



Wound comorbidities-


Lifetime risk of ulcer in diabetic – 15%

Major cause of diabetic foot wounds – Diabetic peripheral polyneuropathy.

>80% of diabetic foot ulcers arise in the setting of neuropathy.

↑Sorbitol level intra-neurally –> principle mechanism of nerve damage.

Damaged nerve swells –> in tight anatomical compartment this can cause further damage  —- “Double crush syndrome”

This can be partially reversed by nerve release surgery.

↑ Glucose  –> ↑ Advanced glycosylated end products –> causes microvascular injury.

↓insulin and ↓neurotrophic factors –> ↓ed maintenance or repair of nerve.

All these factors lead to peripheral neuropathy.

Other potential causative factor of peripheral neuropathy –

  1. Altered fat metabolism,
  2. Oxidative stress, and
  3. Abnormal levels of vasoactive substances such as nitric oxide

Diabetes and infection –

↑ Glucose –> diminished ability of PMNs to destroy bacteria

Diminished ability to coat bacteria with antibiotics

Diabetics are especially prone to – Streptococcus and Staphylococcus

In patient with diabetic neuropathy – 80-95% of amputation are preceded by non-healing ulcer.

Arterial disease (usually located in infra-popliteal region) significantly increases risk of ulceration and amputation. Arterial disease is present in 50% cases of diabetic foot ulcers.

Although peripheral vascular disease is frequently present, peripheral neuropathy is the primary cause of foot wounds in the diabetic population.


Neuropathic Changes –

Autonomic neuropathy – loss of pseudomotor function –> anhydrosis and hyperkeratosis –> fissuring of skin –> infection.

Charcot deformities (neuroarthropathy) of the joints – 0.1% – 2.5% of diabetic population

MC joints involved – tarsometatarsal joints 30% = metatarsophalangeal joints 30% > intertarsal joints 24%> IP joints in 4%

Possible etiology –

  1. Neurotraumatic – joint collapse from damage that has accumulated because of insensitivity to pain.
  2. Osteopenia triggered by abnormalities in the RANK1/RANK-ligand/osteoprotegerin system.

Pathogenesis –

Ligamentous soft-tissue injury + Synovitis + Effusion  –>

Distention of the joint capsule leads to –> ligament distortion, resulting in joint instability –>

Articular cartilage erosion, with debris being trapped within the synovium.

(These changes occur due to continued use of limb due to lack of pain sensation)

Collapse of the medial longitudinal arch –> Altered biomechanics of gait –>

Heterotopic bone formation and eburnation of load-bearing surfaces

Causes overload specific parts of the foot –>

Increased focal stress –> ulceration, infection, gangrene, and limb loss.


Motor component of neuropathy –

Intrinsic foot muscle becomes atrophied and fibrotic –> leads to MTPJ extension and IPJ flexion –> excessive pressure on metatarsal head and end of toes.


Ischemia –

Atherosclerotic disease is a common cause of non-healing foot ulcers.

Hypercholesterolemia, hypertension, and tobacco use are additional risk factors.

Other causes of ischemia in the foot –

  1. Thromboangiitis obliterans (Buerger disease, generally seen in young smokers),
  2. Vasculitis,
  3. Thromboembolic disease.

Before planning revascularization procedure  – MUST accurately diagnose which angiosome ulcer belongs to.

If the affected angiosome is directly revascularized – wound healing increases by 5O% and the risk of major amputation decreases fourfold.

Site of ulcer Arteriosome to be revascularized
Dorsum of the ankle and foot Anterior tibial artery or dorsalis pedis

(posterior tibial artery- If connection b/w the dorsalis pedis and the lateral plantar artery is intact)

Heel ulcers Posterior tibial artery or

Peroneal artery

Mid- and forefoot plantar wounds Posterior tibial artery

(Dorsalis pedis – If connection b/w the dorsalis pedis and the lateral plantar artery is intact)

If the ideal vessel is not available – >15% chance of failure

Patient with significant peripheral vascular disease presents with gangrene – the timing of revascularization versus debridement is critical –

Stable dry gangrene without cellulitis – revascularization first.

Wet gangrene with or without cellulitis – wound debridement first followed by revascularization urgently.

Following revascularization –> wound coverage attempted only when wound shows signs of healing (appearance of new, healthy granulation tissue and neoepithelialization).

Wound healing starts to occur by 4 – 10 days following bypass and 4 weeks following endovascular procedure.


Connective Tissue Disorders-

CTD causes recalcitrant vasculitis ulcers.

e.g., systemic lupus, rheumatoid arthritis, and scleroderma

Treatment includes – steroids and immunosuppressive agents.

Wound-retarding effects of steroids are mitigated with oral vitamin A (10,000 U/d while the wound is open). Topical vitamin A is also effective.

Almost half of patients with vasculitic ulcers also have coagulopathy leading to a hypercoagulable state.

MC are – antithrombin III, Leiden factor V, protein C, protein S, and homocysteine.

Investigation should include a – coagulation profile.

Treatment of these ulcers is principally medical.

Underlying abnormalities are identified and corrected. Wound healing adjuncts are used to cause healing.


Evaluation and diagnosis of the wound –

Etiology of foot and ankle wounds is often traumatic.

MC systemic comorbidities –

  1. Diabetes,
  2. Peripheral vascular disease,
  3. Venous hypertension
  4. Connective tissue disorders

(Accompanying disease processes include infection, ischemia, neuropathy, venous hypertension, lymphatic obstruction, immunologic abnormality, hypercoagulability, vasospasm, neoplasm, self-induced wound).


Diagnostic Studies-

History –

  1. Etiology,
  2. Duration
  3. Previous treatment of the wound(s),
  4. Comorbid conditions
  5. Current medications,
  6. Allergies
  7. Nutritional status
  8. Assess the patient’s current and anticipated level of activity

If patient likely to used limb and procedure medically tolerable and technically feasible then plan – Limb salvage.

Otherwise – consider amputation.

Physical examination –

General physical examination

Examine wound – length, breadth, depth

Examine tissue involved – epithelium, dermis, subcutaneous tissue, fascia, tendon, joint capsule, and/or bone

(If bone can be felt through wound with metal probe, it is most likely to be involved.)

(Diabetic ulcer >2 cm2 –> 90% chance of underlying osteomyelitis)

Assess vascular status – PTA , DPA. If these are palpable then the blood supply is adequate.

If not palpable –> Doppler should be used.

Doppler findings-

  1. Triphasic flow – indicates excellent blood £low
  2. Biphasic sound – indicates adequate blood flow
  3. Monophasic sound – warrants further investigation

(Monophasic tone does not necessarily reflect inadequate blood flow.)

If the pulses are non-palpable or monophasicà noninvasive arterial Doppler studies are done.

PVRs (pulse volume recordings) at each level is obtained –

PVR amplitude <10 mmHg – indicates Ischemia.

Toe arterial pressure is <30 mm Hg – indicates ischemia

Tissue oxygen pressure levels <40 mm Hg – insufficient local blood flow to heal a wound.

Skin perfusion pressure <50 mm Hg – indicates insufficient blood flow to heal a wound.

If all these noninvasive tests suggest ischemia –> an arterial imaging study is obtained to decide – whether a vascular inflow and/or vascular outflow procedure is required.

The gold standard for revascularization- bypass surgery.

Endovascular techniques are also very effective in treating stenosed or obstructed arteries by dilation, recanalization, or atherectomy with or without stenting. These are also less invasive than bypass surgery.


Sensory examination-

Performed with a 5.07 Semmes-Weinstein filament that represents 10 g of pressure.

If patient cannot feel the filament –> protective sensation is absent

Vibration sensation tested using 128-Hz tuning fork

Pinprick sensation, or

Ankle reflexes

Motor examination –

Looking at the resting position of the foot

Strength and active range of motion of the ankle, foot, and toes.

Bone architecture –

  1. Evaluate if the arch is stable, collapsed, or disjointed.
  2. Look for bony prominences.
  3. X-ray series of foot- AP, Lateral, Oblique.
  4. X-ray appearance of osteomyelitis lags behind the clinical appearance by up to 3 weeks.
  5. Earlier detection of osteomyelitis- best by MRI.
  6. MRI also differentiates between osteomyelitis and Charcot collapse.
  7. Bone scans are of no value in evaluation of osteomyelitis when there is an ulcer present (as increased uptake will be seen due to ulcer).

Evaluate Achilles tendon –

If the ankle cannot be dorsiflexed 10° to 15° beyond neutral –> the Achilles tendon is tight.

If the patient cannot dorsiflex his or her foot with the knee bent or straight –>

Both the gastrocnemius and soleus portions of the tendon are tight.

If the patient can dorsiflex his or her foot only when the knee is bent –>

Then the gastrocnemius portion of the Achilles tendon is tight.


Preparing the Wound for Reconstruction –

Goal of treating any wound is to promote healing in a timely fashion.

First step – establish a clean and healthy wound base.

Acute wound is defined as a recent wound that has yet to progress through the sequential stages of wound healing.

Chronic wound is a wound that is arrested in one of the wound-healing stages (usually the inflammatory stage) and cannot progress further.

Acute wound –

Wound is usually well vascularized.

Simple debridement f/b

Immediate closure or NPWT

Chronic wound (aims to convert it to acute wound)–

  1. Correction of medical abnormalities
  2. Restoration of adequate blood flow,
  3. Antibiotics if infection is present,
  4. Aggressive debridement of the wound
  5. Debridement includes removal of the senescent cells along the edge of the wound (3 to 4 mm of the wound edge)

If the wound responds this therapy –

  • Healthy granulation appears,
  • Edema decreases, and
  • Neoepithelialization appears at the wound edge

Negative-pressure wound therapy (NPWT) is a useful post-debridement dressing for the uninfected, well-vascularized wound – it accelerates the formation of granulation tissue, decreases wound edema and keeps the bacterial countdown.


Measuring the wound area weekly to monitor progress – the rate of normal healing is a – 10%-15% decrease in surface area per week.

At this stage, if the wound healing is not as per expected rate – adjunct to wound healing (such as growth factors, cultured skin, and/or hyperbaric oxygen) can be used.


Surgical debridement-

Must be done thoroughly.

It is mostly under-performed – leaving dead or infected tissue or bone leads to persistent infection.

Biofilm is present in over 90% of chronic wounds. It penetrates every aspect of the wound and can be found up to 4mm deep to its base (as it spreads along the perivascular plane of arterioles feeding the wound bed).

Debridement should be considered complete only when normal bleeding tissue remains.

Colors of the tissue can be used as a guide for debridement

  1. Muscle – red/pink, contracting
  2. Fat – yellow
  3. Bone, tendon, fascia – white

Debridement should be done till such normal appearing tissue are reached.

Debridement can also be aided by painting the base of wound with blue dye and then removing all the painted tissue.

Sequential removal of thin layers of tissue till the normal tissue is reached – is the most effective way of debridement.

Skeletal fixation –

Stabilizing – by splinting or external fixation (monoplanar frame or Ilizarov frame).

llizarov frame provides superior immobilization, allows for bone transport, and minimizes the risk of pin track infection because of the thin wire pins.


Tissue culture – Deep uncontaminated tissue cultures pre- and postdebridement should be obtained during the initial and subsequent debridement to guide antibiotic therapy.


Effective dressings should be done following debridement.

Clean and well vascularized – a moist dressing or NPWT.

Suspected unclean wound – dressing with topical antibiotics and/or biocides

Biologic debriding agents -maggots are useful in patients too ill for anesthesia.

Maggots consume all bacteria (antibiotic resistant also VRE, MRSA), as well as biofilm.


After initial debridement to clean the tissue – its important to keep the wound clean – i.e. prevent biofilm from reestablishing itself, prevent a subsequent buildup of metalloproteases (MMPs destroy the naturally produced growth factors) à this is done by – regular scrubbing or wet-to-dry dressing.


If the wound still doesn’t heals even if bed is healthy and vascularity is good then next step is adding – local wound healing growth factors such as PDGF or cultured skin or inert dermis.

Level-one evidence has demonstrated that systemic hyperbaric oxygen can also be used to convert a non-healing wound into a healthy granulating wound.

When wound shows signs of healing (healthy granulation tissue, neoepithelialization at the skin edge) – then its appropriate to close the wound (not before).



Reconstructive techniques –

Lower Leg and Ankle Flaps-

Lower leg muscles are poor pedicled flaps as most of them are type 4 muscles (segmental minor arterial pedicles).

Muscle of leg Distance up to which defect can be closed
EHL As distal as 2 cm from medial malleolus
Extensor digitorum longus

Peroneus tertius

As distal as 2 cm from medial malleolus
Peroneus brevis As distal as 4 cm from medial malleolus
Flexor digitorum longus As distal as 6 cm from medial malleolus
Soleus muscle (type 2 muscle) anterior lower leg defects as distal as 6.6 cm

above the medial malleolus


Local Muscle flaps are not frequently used in lower leg, ankle and foot –

For defect that are small in size fasciocutaneous flap are better – better coverage without loss of function.

For large defects – free flaps are better.

Fasciocutaneous flaps are useful for reconstruction around the foot and ankle (the donor site always requires skin grafting).


Retrograde peroneal flap –

  1. Useful for ankle, heel, and proximal dorsal foot defects.
  2. Blood flow is retrograde.
  3. Similarly retrograde anterior tibial artery fasciocutaneous flap can be used.
  4. Both peroneal and anterior tibial artery can be isolated as a perforators (saving the main arteries).


Retrograde sural nerve flap –

Neurofasciocutaneous flap

Useful for ankle and heel defects.

Receives retrograde flow from a peroneal perforator 5cm above the lateral malleolus.

Artery first courses above the fascia and then penetrates deep to the fascia at mid-calf.

A common problem with the flap is venous congestion- problem with venous drainage.

Venous congestion – can be minimized if the pedicle is harvested with 3 cm of tissue on either side of the pedicle and with the overlying skin intact.

Venous congestion – can be minimized – if the flap is delayed, 4 to 10 days earlier, by ligating the proximal lesser saphenous vein and sural artery.

Inset of flap is critical to avoid kinking of the pedicle.

Splinting is necessary to avoid pressure on the pedicle.

Major donor deficit – the loss of sensibility along the lateral aspect of the foot.

Depression at donor site can be problematic if patient subsequently requires BK amputation.

Donor site deficit can be minimized if the flap is harvested as a perforator flap.


Supramalleolar flap –

  1. Used for lateral malleolar, anterior ankle, and dorsal foot defects.
  2. Harvested either with the overlying skin or as a fascial layer.
  3. Donor site can be closed primarily.
  4. Flap reach is limited, but can be expanded by applying delay approach.


Foot flaps –

Muscles in foot are – type 2.

Useful for coverage of relatively small defects.


Coverage of small mid- and posterior lateral defects of the sole of the foot and lateral distal and plantar calcaneus.

Dominant pedicle is medial to the muscle’s origin at the calcaneus and the muscle has a thin distal muscular bulk.

 AHB –

Larger muscle than ADM

Used to cover medial defects of the mid- and hindfoot, medial distal ankle.

Dominant pedicle – is at the takeoff of the medial plantar artery

Flexor digiti minimi brevis –

Small muscle

Used to cover defects over the proximal fifth metatarsal

lt receives its dominant pedicle at the lateral plantar artery takeoff of the digital artery to the fifth toe.

Flexor hallucis brevis –

Can be raised on a longer pedicle as an island flap on the medial plantar artery – can reach up to proximal ankle.

EDB muscle –

Very little bulk.

Can be used for local defect over sinus tarsi or lateral calcaneum.


Used to cover plantar heel defects.

Medial plantar flap –

Most versatile flap of the foot.

Ideal tissue for coverage of plantar defects.

It can also reach medial ankle defects.

Can be harvested to a size as large as 6 cm x 10 cm.

It is a sensate flap.

Has a wide arc of rotation if harvested till proximal part of medial plantar artery.

Flap can be raised on either of – deep or superficial branch of MPA.

Flap is easier to raise on deep branch, but raising the flap on superficial branch disturbs less of blood supply of foot.

When harvested with retrograde flow – it is based on the deep branch of the medial plantar artery.

Lateral calcaneal flap –

  1. Useful for postetior calcaneal and distal Achilles defects.
  2. Length of the flap can be increased by harvesting it as an L-shaped flap. L-shaped extension below and posterior to lateral malleolus.
  3. It is harvested with sural nerve and saphenous vein.

Dorsalis pedis flap –

  1. Can be either proximally or distally based
  2. Used for coverage of ankle and dorsal foot defects.
  3. Width of flap >4cm require skin grafting for closure
  4. Now rarely used – exposes vulnerable extensor tendons, and vascular structures.

Filet of the toe flap –

Useful for small forefoot web space ulcers and distal forefoot problems

Reach of the flap is always less than expected.

The technique involves removal of the nail bed, phalangeal bones, extensor tendons, flexor tendons, and volar plates while leaving the two digital arteries intact.

A variation is the toe island flap, where a part of the toe pulp is raised directly over the ipsilateral digital neurovascular bundle and then brought over to dose a neighboring defect.


Treatment Options –

Guiding principle – coverage of a wound should be performed as quickly and efficiently as possible.

Once the wound is clean and well vascularized – one of the following technique is used for reconstruction –

  1. Healing by secondary intention
  2. Wound closed primarily
  3. Split- or full-thickness skin graft and or neodermis is applied
  4. Local random flap is transposed or advance
  5. Pedicled or island flap
  6. Microvascular free flap


Biomechanics of foot should be taken care during reconstructive procedure – which may require- bone rearrangement, partial joint removal or fusion, or tendon lengthening or transfer.

Method of soft-tissue reconstruction depends on –

  1. Patient’s medical condition,
  2. Surgeon’s experience,
  3. Size of the wound,
  4. Vascular status of the foot.
  5. Exposed structures (tendon, joint And or bone), and
  6. Access to the wound (i.e., an ilizarov frame limits the access to the foot)

Any procedure chosen aims for – restoration of a biomechanically sound foot (to prevent recurrent breakdown).

No tendon, joint, or bone involved –> Simple coverage (secondary intention, delayed primary closure, or simple skin graft and/or neodermis).

Even some of the complex wound with exposed tendon, bone or joint can be managed by wound care and then simple coverage – With NPWT, granulation tissue forms over tendon, bone, or joints.

It is critical to immobilize the wound over a moving joint and to offload the wound (to prevent shearing forces from disrupting the healing process).

More than 85% of all wounds can be dosed by simple techniques, while less than 15% require flaps.


Delayed primary closure – is planned once edema has subsided. NPWT is helpful in reducing edema.

In some region wound may heal by simpler method but can result in problematic with normal activity – such as over a joint, plantar foot and posterior heel – soft tissue is a better option.


Most foot and ankle wounds – can be closed by skin grafting.

Healthy granulating bed is the necessary prerequisite for STSG.

If the granulation bed contains bacteria/biofilm – it should be removed before placing the skin graft.

Wound can be then pulse lavaged and then skin grafted with 1:1 meshing.

NPWT can be used on low continuous suction as a temporary dressing for the first 3 to 5 days – helps absorb excess fluid and ensure fixation of the skin graft to the underlying bed and minimizes possible skin graft-recipient bed disruption from shear forces.

Ideal graft donor site for a plantar wound is – the glabrous skin from the plantar instep.


Flaps for foot reconstruction should be accurately assessed – vascular pedicle should be dopplerable.

Local flaps are useful for coverage of foot and ankle defect because they only need to be large enough to cover the exposed tendon, bone, or joint while the rest of the wound is skin grafted.


Local flaps and their variation are most commonly used to cover lower leg and foot defect – because pedicled, perforator or free flaps are difficult to plan due to access problem in patient having external fixators.


Pedicled flaps are more difficult to dissect, have higher perioperative complication rate but equally good long-term success as free flaps.

Free flaps in the foot and ankle carry the highest failure rate of free flaps in any anatomic location – most probably because the anastomosis is near zone of trauma.


Postsurgical Care –

No weight bearing for 6 weeks if plantar surface is involved.

Offload specific parts.


Reconstructive options by location of defect –

Forefoot Coverage –

Toe ulcers and gangrene – limited amputation

Ulcer under metatarsal head causes –

  1. Principal abnormal biomechanical force is a tight Achilles tendon.
  2. Bony abnormality (plantar-prominent metatarsal head)
  3. Ulcer present without any abnormality


Patient cannot dorsiflex his or her foot with the knee bent or straight –> both the gastrocnemius and soleus portions of the tendon are tight.

If the patient can dorsiflex his or her foot only when the knee is bent –> only the gastrocnemius portion of the Achilles tendon is tight –> in this case gastrocnemius recession should correct the problem.

In addition the posterior capsule of the ankle joint may be tight.

Treatment require release of Achilles tendon and if it foot still does not dorsiflex then additional posterior capsular release is performed.

Release of the Achilles tendon –> forefoot pressure drops dramatically and if underlying bone is not involved forefoot ulcer within 6 weeks post release.

The lengthening of a tight Achilles tendon has decreased the ulcer recurrence rate in diabetics by half at 2 years.


Patient has normal ankle dorsiflexion, but bony abnormality causing planter ulcer –

Plantar-prominent metatarsal head –> the affected metatarsal head is elevated with osteotomies and internal fixation. The metatarsal head is shifted 2 to 3 mm superiorly –> pressure is relieved –> ulcer to heal by secondary intention.


Ulcer without any bony abnormality –

Small size – heals by secondary intention.

Large ulcer with metatarsal head and shaft involvement –> single metatarsal involved – Ray amputation.

If ulcers are present under several metatarsal –> pan-metatarsal head resection

If  >2 toes with the accompanying metatarsal heads have to be resected –> then a trans-metatarsal amputation.

While doing trans- metatarsal amputation – maintain normal parabola of with the second metatarsal being the longest.

Equinus deformity can result –> to prevent this –> extensor and flexor tendons of 4th & 5th toe is tenodesed with the ankle in the neutral position and/or the Achilles tendon lengthened.

The most proximal forefoot/distal midfoot amputation is – Lisfranc amputation where all the metatarsals are removed. To prevent equinus deformity – anterior tibial tendon is split and lateral aspect inserted on to cuboid bone. Also, achillis tendon is lengthened.

Post-operatively foot is placed in neutral position, until wound heals.


Midfoot coverage –

Defect on medial aspect (non-weight bearing area) – treated with SSG.

Small defects – V -to-Y flap, the bilobed flap, the rhomboid flap, and the transposition flap, pedicled abductor hallucis flap medially or an abductor digiti minimi flap laterally.

Slightly larger defects – large V-to-Y flaps, random, large, medially based rotation flaps, pedicled medial plantar fasciocutaneous flap.

Larger defects – free muscle flaps covered by skin grafts.

Ulcers in midfoot are usually caused by Charcot collapse of the mid foot plantar arch –

If the underlying fragmented bone has healed and is stable (Eichenholz stage 3) à then the excess bone is shaved à the ulcer heals by secondary intention or is covered with a glabrous skin graft or a local flap.

If the midfoot bones are unstable (Eichenholz stage 1 or 2) à then bone is excised using a wedge excision and the arch reconstituted by fusing the proximal metatarsals to the talus and calcaneus.


Hindfoot Coverage –

Among the most difficult of all wounds to treat.

Usually also reflect severe vascular disease.

They are result of the patient being in a prolonged decubitus position.

Partial calcanectomy (preferably vertical) – can create soft tiisue to cover defect.

Collapsed bone or bone spur can cause ulcer – needs to be shaved.

Distally based V-to-Y flap or larger medially based rotation flaps.

Plantar heel defects – pedicled flaps –

  1. Medial plantar fasciocutaneous flap
  2. Flexor digiti minimi muscle flap
  3. Extended lateral calcaneal fasciocutaneous flap
  4. Retrograde sural artery fasciocutaneous flap

Large defect – free muscle flap with SSG.

Underlying bone – if osteomyelitis – bone needs to be debrided.


Hindfoot amputations –

Chopart – leaves an intact talus and calcaneus while removing the mid- and forefoot bones of the foot

Symes – tibia and fibula are cut just above the ankle mortise and the deboned heel pad is anchored to the anterior portion of the distal tibia to prevent posterior migration.

Symes amputation is done if –

  1. There is insufficient tissue to primarily close a Chopart amputation.
  2. There is insufficient arterial blood supply for a free flap, or
  3. If the talus and calcaneus are involved with osteomyelitis.


Dorsum of the Foot –

Most wound treated with – SSG

Small local flaps

EDB muscle flap works well for sinus tarsi defects.

Supramalleolar flap can be used over the lateral proximal dorsal foot.

Larger defect – free fasciocutaneous flap eg. Free radial forearm flap with palmaris tendon to reconstruct extensor tendons.


Ankle Defects –

If wounds granulating – SSG.

NPWT can be used to promote granulation.

Local flaps can be used to cover critical areas (tendon, bone or joint) while rest of area can be skin grfted.

Local flaps – rotation or transposition flaps based on posterior tibial and peroneal arterial perforators.

Pedicled flaps –

  1. Supramalleolar flap,
  2. Retrograde sural artery flap,
  3. Medial plantar flap,
  4. Abductor hallucis muscle flap,
  5. Abductor digiti minimi muscle flap,
  6. EHL, and
  7. EDB muscle flap.

Muscle attachments

Trapezius –

Origin –

  1. Medial third of superior nuchal line
  2. External occipital protuberance
  3. Nuchal ligament
  4. Spinous process of C7 to T12

Insertion –

  1. Lateral third of clavicle
  2. Acromian process
  3. Spine of scapula

Innervation –

  1. Spinal accessory nerve (CN 9)
  2. Cervical nerves C3-C4

Movement –

  1. Descending part – elevates scapula
  2. Transverse part – retracts scapula
  3. Ascending part – depresses scapula
  4. Descending and ascending working together – superior rotation of scapula


Pectoralis major –

Origin –

  1. Clavicular head – anterior surface of medial half of clavicle
  2. Sternocostal head – anterior surface of sternum, superior six costal cartilages
  3. Abdominal part – aponeurosis of external oblique

Insertion –

Crest of greater tubercle of intertubercular sulcus (lateral lip of bicipital groove)

Innervation –

Lateral and medial pectoral nerves

Action –

  1. Adducts and medially rotates humerus
  2. Draws scapula anteriorly and inferiorly
  3. Clavicular head alone – flexes humerus
  4. Sternocostal head alone – extends humerus from flexed position.


Pectoralis minor –

Origin –

3rd to 5th ribs near their costal cartilages

Insertion –

Medial border and superior surface of coracoid process of scapula.

Innervation –

Medial pectoral nerve (C8-T1)

Function –

Stabilizes scapula by drawing it inferiorly and anteriorly against chest wall


Serratus anterior –

Origin –

External surface of lateral part of 1st to 8th-9th ribs

Insertion –

Anterior surface of medial border of scapula

Innervation –

Long thoracic nerve (C5, 6, 7)

Action –

  1. Protracts scapula and holds it against thoracic wall
  2. Rotates scapula


Latissimus dorsi –

Origin –

  1. Spinous process of inferior six thoracic vertebrae (T7-T12)
  2. Thracolumbar fascia
  3. Iliac creast
  4. Inferior 3 or 4 ribs

Insertion –

Intertubercular sulcus (bicipital groove) of humerus

Innervation –

Thoracodorsal nerve (C6-8)

Action –

Extends, adducts and medially rotates humerus

Rectus abdominis –

Origin –

Pubic symphysis and pubic crest

Insertion –

Xiphoid process and 5th -7th costal cartilages

Innervation –

Thoracoabdominal nerves and anterior rami of inferior thoracic nerves

Action –

Flexes trunk and compresses abdominal viscera.

Gracilis –

Origin –

Body of pubis and inferior pubic ramus

Insertion –

Superior part of medial surface of tibia

Innervation –

Obturator nerve

Action –

Adducts thigh, flexes leg and rotates leg medially.

Gastrocnemius –

Origin –

  1. Lateral head – lateral aspect of lateral condyle of femur
  2. Medial head – superior to medial condyle

Insertion –

Posterior surface of calcaneus with calcaneal tendon (tendoachillis)

Innervation –

Tibial nerve

Action –

  1. Plantarflex ankle when knee is extended
  2. Raises heel during walking
  3. Flexes leg at knee joint.

Soleus –

Origin –

  1. Posterior aspect of head of fibula
  2. Superior fourth of posterior surface of fibula
  3. Soleal line and medial border of tibia

Insertion –

Posterior surface of calcaneus with calcaneal tendon (tendoachillis)

Innervation –

Tibial nerve

Action –

  1. Plantar flexes ankle (independent of knee position)
  2. Steadies leg on foot

Hemifacial atrophy/ Romberg disease


Progressive hemifacial atrophy (PHA) has no definite pathogenesis – may be a lymphocytic neurovasculitis or a variant of localized scleroderma.

Also called Romberg’s disease.

Most commonly confused with – localized scleroderma (especially in the forehead) as the “en coup de sabre” (ECDS) or saber mark.

Historical perspective –

Dr. Caleb Hillier Parry – first description of the disease.

Dr. Moritz Heinrich Romberg – further described the clinical manifestations of hemifacial atrophy.

Albert Eulenburg, a German neurologist – coined the term “progressive hemifacial atrophy” or PHA

Blair, Sarnat, Greeley and Neumann in the 1950s all described the use of local flaps to augment the soft-tissue deficiency.

Campbell, and later Converse, described the use of onlay iliac bone graft to augment areas of atrophy.

Wallace et al. described the use of an omental free flap for soft-tissue augmentation.

Jurkiewicz described the use of free vascularized tissue for patients with PHA.

Siebert and Longaker used- free parascapular tissue for the treatment of this disorder.


Patient selection and treatment –

Factors to be considered –

  1. Age of the patient
  2. Nature and complexity of the deformity (i.e., which tissue types are affected)
  3. Presence of associated disorders and conditions
  4. Patient’s understanding of the problem and the options for treatment.

Timing of the surgery – best performed after the disease has “burned itself out” (delay up to 2 years following what looks like the end of progression).


Etiopathogenesis –

Exact etiology of PHA is not well understood.

But, has a strong autoimmune and neurogenic component – and a combination of the two been described as a “lymphocytic Neurovasculitis.

Possible etiologies –

  1. Autoimmune process
  2. Neurogenic process
  3. Infection hypothesis
  4. Trauma


Autoimmune process –

PHA is likely a variant of the autoimmune disease localized scleroderma, specifically the subtype of linear scleroderma that affects the face, termed ECDS “en coup de sabre” or sabre mark.

Thought to be different spectra of the same disease.

Similar characteristics – age of onset, female preponderance, neurological involvement, lymphocytic infiltrate on biopsy, and a clinical course of evolution.

Histologic findings –

Findings similar in PHA & ECDS –

A perivascular infiltrate of mononuclear cells, mostly lymphocytes and monocytes in the dermis – surrounding the dermal neurovascular bundles, termed “lymphocytic neurovasculitis”

Degenerative alterations of the vascular endothelia on electron microscopy

Findings different from ECDS –

Dermal collagen fibrils Closely packed Homogenized and fragmented
Elastic fibers Preserved Destruction of elastic fibers
Dermal appendages (hair follicles and sebaceous glands) Hypoplastic Atrophy


Neurogenic process –

Clinical manifestations supporting a neurogenic origin –

  1. Distribution of facial atrophy typically follows a dermatome of the trigeminal nerve. (Unilateral in 95%, rarely crossing the midline)
  2. Dermal lymphocytic infiltrate centered around neurovascular bundles in the dermis
  3. Clinically – CNS involvement are found in approximately 8–20% of patients.
  4. Radiologically – atrophy and calcinosis, multiple or diffuse brain lesions.
  5. CSF analysis – findings consistent with an inflammatory process – presence of oligoclonal bands and elevated IgG levels.


Infection hypothesis –

The most notorious suspect for both PHA and ECDS was Borrelia burgdorferi (not substantiated).

Other agents – Epstein–Barr virus.

These can be mere incidental findings than causative etiology.

Trauma –

Role of trauma inducing PHA is quite controversial.


Epidemiology –

Incidence – not well defined.

Estimated incidence of 5 per 1 000 000 people.

Prevalence of 8 per 100 000 people.

No racial predilection of PHA

Slight female predominance – F: M = 2-3 :1

Median age of onset -is 10 years old (range of 5–15 years)

Most cases of are sporadic, few familial cases have been reported.


Clinical manifestations –

(Cutaneous, subcutaneous, muscle, bone and cartilage)

Initial clinical manifestations include both cutaneous findings and subcutaneous atrophy.

Subcutaneous atrophy typically evolves first on the cheek or temple and later extends to the brow, angle of mouth, and/or neck.

Later in course – atrophy or growth arrest of the underlying bone and cartilage – facial deformity.

Facial muscles – atrophic, but normal function.

The disease typically progresses slowly over several years (2–10 years) and then tends to enter a stable phase.

Cutaneous and subcutaneous involvement –

  1. Hyperpigmentation and hypopigmentation
  2. Dermal atrophy
  3. Subcutaneous atrophy and
  4. Skin thickening/fibrosis
  5. Alopecia of the scalp, eyebrow, and eyelashes

Pigmentary changes –

Hyperpigmentation – “bluish” discoloration – most likely due to increased vascularity during the active or inflammatory phase.

Later on lesion might become hypopigmented.

Discolorations – dermatomal distribution along the trigeminal nerve.

When skin lesion becomes fibrotic (thickened skin) or atrophic and forms a well-demarcated linear depression (groove) in the frontoparietal or hemifacial distribution – considered to be ECDS morphea or linear scleroderma of the head.


Musculoskeletal involvement –

Facial muscle – atrophy and thinning – mostly affecting masseteric muscles, tongue, and palatal muscles.

Function of muscles are usually preserved.

Degree of skeletal hypoplasia is dependent upon the age of onset. Onset younger than 10 yrs – highest risk.

Maxilla and mandible are most often involved – both sagittal and vertical undergrowth.

Bony involvement is also unilateral – profound tilting of the occlusal plane.

When PHA involves the V1 distribution – enophthalmos is common.

Enophthalmos is due to atrophy of the periorbital subcutaneous tissues rather than skeletal hypoplasia.


CNS involvement –

Occur in approximately 8–21% of patients.

Manifestations – Seizures, hemiparesis, migraine headaches, neuropsychiatric disturbances, ischemic stroke, and intellectual deterioration

The most common CNS manifestation is – localization-related seizures.

Brain lesions of PHA appear to be more epileptogenic (than MS and other autoimmune disorder of CNS).

Brain imaging is – often abnormal, 90% cases.

Lesions observed are – T2 hyperintense lesions, intraparenchymal calcifications and brain atrophy.

The brain atrophy “respects” the midline – does not cross the midline.

Not a direct correlation between brain lesion and degree of severity of skin and subcutaneous involvement.

Many patients may be neurologically asymptomatic in spite of visible brain lesions.

Brain biopsies – brain parenchymal inflammation with a perivascular lymphocytic cuffing. (Sclerosis, fibrosis, gliosis of brain parenchyma, meninges, and vasculature have also been reported.)

CSF findings – oligoclonal bands and elevated IgG levels.


Ocular involvement –

The MC findings – uveitis, optic neuritis, and globe retraction.

Other findings – Ocular muscle paralysis, ptosis, Horner syndrome, heterochromia iridis, and dilated fixed pupil.

Slit lamp examination is recommended.


Oral involvement –

Tongue and upper lip of the affected side of the face are often markedly atrophic.

Maxilla and mandible hypoplastic – resulting in malocclusion (unilateral posterior crossbite) and altered dentition.

An abnormally skewed high-arched palate.


Laboratory findings and prognostic indicators –

↑ WBC – 10%

↑ ESR – 20%

Autoantibodies +ve – 40-50% –

Anti-single-stranded DNA (ss-DNA) – a/w disease severity and progressive disease features.

  1. Ant- histone – – a/w disease severity and progressive disease features.
  2. Anti-double-stranded DNA,
  3. Anti-centromere,
  4. Anti-Scl-70 antibodies

Clinical prognostic indicator – age of onset <10yrs – a/w profound skeletal dysplasia.


Differential diagnosis –

  1. Congenital hemifacial atrophy
  2. ECDS subtype of localized scleroderma
  3. Lipodystrophy


Congenital hemifacial atrophy – present since birth. Not progressive.

ECDS is difficult to distinguish and sometime argued to be spectrum of same disease.

Lipodystrophy can occur due to –

Congenital diseases – progeria, Dunnigan syndrome, and Kobberling syndrome.

Endocrine disorders – hyperthyroidism and diabetes

Autoimmune diseases – systemic sclerosis and dermatomyositis

Drug-induced atrophy – protease inhibitors of ART.

Hemifacial microsomia.


Treatment/surgical technique –

Immunosuppression –

Few patients can be considered candidate for immunosuppression –

  1. Patients having any cutaneous features of localized scleroderma
  2. The appearance of a demarcated line, as in ECDS

Drugs – corticosteroids + disease modifying agents such as Methotrexate.

Duration of treatment – usually 3-5 years.

Reconstruction planned when disease is stable “off” the immunosuppression – typically after 1 year.


Nonsurgical intervention –

Alloplastic filling agents –

Advantage – absence of a donor site and their abundant supply.

Disadvantage – Susceptibility to local tissue responses, including capsule formation, seroma development, infection, extrusion, and cost.

Examples – silicone gel, hydroxyapatite beads, and hyaluronic acid.

Structural fat grafting –

Easily harvested, No donor site morbidity, No functional loss.

Atrophy of some portion of fat can occur.

Surgical intervention –

Currently offer the largest amount of tissue with excellent safety.

Can be used in conjunction with fillers to provide the best possible result.

Local pedicle flap –

Provides small amount of tissue.

Most obvious choice of flap – superficial temporal pedicle. It can be used in combination with fat grafting or dermal fat to increase the bulk.

Free flap –

  1. Gracilis & Radial forearm adipofascial flap – for small volume augmentation
  2. Deep inferior epigastric perforator – more soft tissue bulk.
  3. Omentum – lacks internal structure – can lead to soft tissue decent with time.
  4. Superficial inferior epigastric flap
  5. Transverse rectus abdominis muscle flap
  6. Deltopectoral flap
  7. Anterolateral thigh adipofascial flap
  8. Scapular and parascapular flap

Scapular and parascapular adipofascial flap based on the circumflex scapular pedicle are the most useful flaps for restoring facial volume.

Advantages – relatively straightforward harvest, posterior-torso donor scar, and minimal functional deficit.

Disadvantage – positioning in either a prone or lateral decubitus to harvest,

Technique of soft-tissue augmentation –

  1. Mark the defect on face of patient with patient standing.
  2. Make a transparency of the defect using an X-ray film.
  3. Use the transparency to mark the defect on the planned flap.
  4. Procedure begins with creation of the subcutaneous pocket on the face – extent of the dissection must extend beyond the borders of the atrophy.
  5. Suitable recipient vessels are identified for the anastomosis. Achieve hemostasis. Pack the area with counted sponges.
  6. Harvest the flap.
  7. Flap is inset.
  8. Terminal flap ends should be contoured and fixed to the skin with overlying bolsters.
  9. Drains are placed at donor and recipient site.
  10. Hourly monitoring of flap done with audible Doppler for 24 hours, and then 2 hourly for next 24 hours.
  11. Patient is kept NPO for first night, then gradually allowed orally.


Outcomes –

Outcomes from soft-tissue augmentation are usually good.


Secondary procedures –

Revision of flap is almost always required and should be part of the plan of management.

First revision is planned after 6 months following flap placement.


Contents written by – Dr. Kamlesh Kumar (MBBS, AIIMS, New Delhi, MS(Surgery), AIIMS, New Dehi, MCh (Burns, Plastic & Maxillofacial Surgery) VMMC & Safdarjung hospital, New Delhi), 2019.







Wound healing may be best understood as an organism’s global response to injury.

Wound healing represents the response of an organism to a physical disruption of a tissue/organ to re-establish homeostasis of that tissue/organ and stabilize the entire organism’s physiology.

Essentially two processes (for re-establishment of homeostasis)-

  1. Substitution of a different cellular matrix as a patch to immediately re-establish both a physical and physiologic continuity to the injured organ. This is the process of scar formation.
  2. Recapitulation of the developmental processes that initially created the injured organ. By reactivating developmental pathways, the architecture of the original organ is re-created. This is the process of


Balance between-    Scarring ↔Tissue regeneration

Different tissue shows different proportion of these two process. One more than the other.

Eg. Nerve tissue – Scarring >>>Tissue regeneration

Liver and bone-    Scarring <<<Tissue regeneration

Healing is different in different species- eg. Limb amputation in newts results in limb regeneration, whereas in humans, only scarring can occur.

Undesirable or dysfunctional response to injury in a tissue or organ system can occur due to any of the two processes.

It is important to establish which process is responsible for the undesirable effect and which portion of the wound is showing that effect.


Acute wound- wound that is present for less than 3-4weeks

Chronic wound- wound that persists beyond 4-6 weeks. (These wounds also called as non-healing, delayed healing, recalcitrant).


Phases of wound healing-

Three distinct but overlapping phases-

  1. Inflammatory phase (0-4 days)
  2. Proliferative phase (4-21 days)
  3. Remodeling phase (21days – years)

Inflammatory Phase-

Primary purpose- to remove devitalized tissue and prevent invasive infection.

Functional priorities`-

  1. Attainment of hemostasis
  2. Removal of devitalized tissues
  3. Prevention of colonization and invasive infection by microbial pathogens

Attainment of hemostasis-

Coagulation cascade activated- ultimately leading to formation of fibrin mesh (fibrinogen –> fibrin –> fibrin mesh). This fibrin mesh is called the provisional matrix.

Formation of platelet plug- during formation of formation of platelet plug, platelets also degranulate releasing growth factors – PDGF, TGF-β.

Other two functions are done by neutrophils and macrophages.

Inflammatory cells are attracted by-

Activation of the complement cascade

TGF-β released by degranulating platelets

Bacterial degradation products such as lipopolysaccharide.


These are the first inflammatory cells to be recruited.

Prominent type for first 2 days.


  1. Remove dead tissue by phagocytosis
  2. Prevent infection by oxygen-dependent and oxygen-independent killing mechanisms.
  3. Release a variety of proteases to degrade remaining ECM (to prepare the wound for healing)

Neutrophils play a role in decreasing infection but, their absence does not appear to prevent the overall progress of wound healing.

Instead, there prolonged presence has been proposed to be a primary factor in the conversion of acute wounds into non-healing chronic wounds.



  1. Follows after neutrophils. Appear 48 to 72 hours post-injury.
  2. MCP-1 attracts these monocyte/macrophage to the site of injury.
  3. By day 3, they are the predominant cell type.
  4. Macrophages phagocytize debris and bacteria.
  5. Produces growth factors necessary for the production of the ECM by fibroblasts and the production of new blood vessels in the healing wound.
  6. Unlike the neutrophil, the absence of monocyte/macrophages has severe consequences for healing wounds.


Last cell to enter the wound. [Last- Lymphocytes]

Enters between days 5 and 7 post-wounding. Its role in wound healing is not well defined.


Proliferative Phase-

Occur from days 4 to 21 following injury.

Re-epithelialization probably begin almost immediately following injury.

Injury –> Regression of the desmosomal connections between keratinocytes and basement membrane –> formation of actin filaments in the cytoplasm of keratinocytes –>  keratinocytes actively migrate into the wound –> Keratinocytes proceed between the desiccated eschar and the provisional fibrin matrix beneath (this movement is via interactions with ECM proteins (such as fibronectin, vitronectin, and type I collagen) via specific integrin mediators)

Provisional fibrin matrix is gradually replaced by granulation tissue.

Granulation tissue is largely composed of three cell types- [EFM-G]

  1. Endothelial cells
  2. Fibroblasts
  3. Macrophages

Granulation tissue begins to appear by about day 4 post-injury.

Fibroblasts are the workhorses during this time –> they produce the ECM that fills the healing scar and provides a scaffold for keratinocyte migration.


Macrophages produces –> PDGF and TGF-β1 –> stimulates fibroblast –> they proliferate, migrate and produces ECM. PDGF and TGF-β1 –> Stimulates endothelial cells –> produces new blood vessels.


Provisional matrix is replaced by type 3 collagen during proliferative phase.

Type 3 collagen will then be replaced by type 1 collagen during remodeling phase.

Endothelial cells- produce new blood vessels.

Hypoxia –> induces hypoxia inducible factor-1 (HIF-1) –> ↑ Proangiogenic factors released by macrophage (VEGF, FGF-2, angiopoietin 1, and thrombospondin.)    –> angioneogenesis.


Remodeling phase –

Longest phase of wound healing

Day 21 – 1 year (years)

Begins with the programmed regression of blood vessels and granulation tissue.

Two process that define remodeling phase are – Wound contraction & Collagen remodeling.

Wound contraction occurs by – myofibroblast.

Myofibroblasts are – fibroblasts with intracellular actin microfilaments capable of force generation and matrix contraction.

Myofibroblasts contract the wound through specific integrin-mediated cell-matrix interactions with the dermal environment.

Collagen remodeling – replacement of type III by type I

Collagen remodeling is a slow remodeling phase which is largely mediated by a class of enzymes known as – matrix metalloproteinases

At 3 weeks wound strength is – 20% [wound strength – 21% @ 21 DAY]

Finally, wound strength is around – 70%- 80% @ 1 year.

Abnormal response-

  1. Inadequate regeneration –
    1. CNS injury
    2. Bone non-union
    3. Corneal ulcer
  2. Inadequate scar formation –
    1. Diabetic foot ulcer
    2. Pressure sore
    3. Venous stasis ulcer
  3. Excessive regeneration –
    1. Hyperkeratosis
  4. Excessive scar –
    1. Keloid
    2. Hypertrophic scar



Are less common – <6% of population

Have genetic component

Overgrowth of dense fibrous tissue beyond the borders of the original wound

Large thick collagen fibers composed of numerous fibrils closely packed together

Hypertrophic scars are also characterized by the formation of dense collagen fibers following injury but, in contrast to keloids, do not extend beyond the original wound margins.

Etiology and pathophysiology – unknown

Treatment Modalities –

  1. Steroid injections,
  2. Pressure therapy with silicone sheeting, and
  3. External beam irradiation

Recurrence rates – 75%.

Ear Reconstruction

Anatomy –

Vascular supply –

Superficial temporal

Posterior auricular

Sensory supply –

Greater auricular – lower half

Lesser occipital – upper part posterior

Auricotemporal – upper part anterior

Vagus – conchal part

History –

1st description – Sushruta Samhita

Tagliacozzi – 1597, retroauricular flap for ear deformity

Dieffenbach – 1845, advancement flap for ear’s middle third

Gillies – 1920 – carved costal cartilage for microtia repair (kept cartilage under mastoid skin and then separated with cervical flap)

Pierce – modified Gillies – used SSG to form new sulcus and tubed flap for helix

Gillies – used maternal ear cartilage àresorbed

Radford Tanzer – 1959 – autologous rib cartilage and carving in blocks

Cronin – 1966, silicon ear frameworks – high incidence of extrusion

Young and Peer – framework fabrication

Burt Brent – 1970, four-stage repair

Nagata – 1990, two stage repair

Tanzer – father of modern auricular reconstruction.

Embryology –

Middle ear and external ear – derived from – 1st (Mandibular) & 2nd (Hyoid) branchial arches.

Auricle derived from – Six “Hillocks” of tissue.

Anterior hillock –

Upper – helix

Middle – crus of helix

Lower – tragus

Posterior hillock –

Upper – antihelix

Middle – antitragus

Lower – lobule & lower part of helix

Microtia –

Incidence – 1: 6000 live birth (ref. Grabb’s)

Etiology –

Hereditary factors –

Multifactorial inheritance –

Risk in 1st degree relatives – 3-8%

Risk in 3rd sibling with 2 siblings having microtia – 15%

Syndromes A/W microtia –

  1. Treacher Collins
  2. Craniofacial microsomia
  3. Townes-Brocks syndrome

Specific factors –

In utero tissue ischemia  <–obliterated Stapedial artery or Hemorrhage in local tissue

Other factors –

Rubella infection in mother

Ingestion during 1st trimester of pregnancy – Thalidomide, Isotretinoin,  Clomiphene citrate, Retinoic acid

Diagnosis –

Classification –

Roger classification –

  1. Microtia
  2. Lop ear – folding or deficiency of the superior helix and scapha
  3. “Cup” or constricted ear – with a deep concha and deficiency of superior helix and antihelical crura
  4. Prominent or protruding ear

Tanzer classification (classification according to signal correction approach)- [ACMS-P]

  1. Anotia
  2. Complete hypoplasia (Microtia)
    1. With atresia of EAM ( external auditory meatus)
    2. Without atresia of EAM
  3. Hypoplasia of Middle third of auricle
  4. Hypoplasia of Superior third of auricle
    1. Constricted (Cup or Lop ear)
    2. Cryptotia
    3. Hypoplasia of entire superior third
  5. Prominent ear

Nagata classification –

  1. Lobule type – ER (Ear Remnant) + ML (Malpositioned Lobule)
  2. Concha type – ER + ML + concha + Tragus & antitragus with intertragal notch
  3. Small concha type – ER + ML + small indentation
  4. Anotia – ER only
  5. Atypical


Associated deformity –

  1. Branchial arch deformities –
    1. Obvious bony or soft tissue defect
    2. Facial nerve weakness
  2. Macrostomia – 2.5%
  3. Cleft lip and/or palate – 4.3%
  4. Urogenital defect – 4.0
  5. Cardiovascular malformation

Clinical characteristics –

MC type is – Vertically oriented sausage shaped nubbin

[M: F = 2:1],        [Right: Left: B/L = 6:3:1],       [U/L: B/L = 9:1]

1/3rd to ½ patients have gross characteristics of hemifacial microsomia

Timing of surgery –

Psychological and physical consideration

Psychological – ideal before child enters school

Physical – there should be enough rib growth for fabrication of framework

Brent – @ 6yrs of age

Nagata – @ 10 yrs of age & Chest circumference >60cm @ Xiphoid level


Steps of surgery –

Brent – Four-stage [FLET]

  1. Framework placement
  2. Lobule transposition (correction)
  3. Elevation of reconstructed auricle & creation of retroauricular sulcus
  4. Tragus creation and concha deepening

Nagata – Two-stage [FLT]

  1. FLT (Brent steps 1+2+4)
  2. Elevation of reconstructed auricle & creation of retroauricular sulcus (Brent 3)


@ Age 4 – ear is 85% of adult size

@ Age 6 – ear is within 6-7 mm of its full vertical height

Reconstructed ear may grow with child.


Middle ear problem –

Hearing impairment related to – abnormal auditory canal, tympanic membrane & middle ear.

Microtia patient have hearing threshold of 40-60 dB on affected ear. (Normal – 0-20 dB)

Most patient of microtia have atresia of external auditory canal and tympanic membrane with variable deformity of middle ear ossicles.

Hearing restoration – to be done in bilateral cases (NOT in unilateral cases).

BAHA (bone anchored hearing aid) is given.Hearing aid should be given early – within weeks of birth.

U/L BAHA is sufficient for B/L microtia with bilateral hearing loss.

BAHA can be used in U/L microtia with U/L conductive hearing loss à both audiological and subjective benefits.

Hearing impairment is – Conductive loss – due to malformed middle & external ear.

(Internal ear is derived from distinct separate ectodermal origin and hence is mostly spared)

Internal ear abnormity is seen in – 10% of microtia patients.



Canaloplasty –

In microtia –> approx half of patient have surgically correctable middle ear anatomy –> this is important in bilateral microtia (Surgery may eliminate dependence on hearing aids).

Canaloplasty NOT done in unilateral microtia.

[A before C] – Auricle reconstruction to be done Before Canaloplasty.

Auricle reconstruction after canaloplasty has compromised result due to scar (present after canaloplasty).

Cholestoma formation can cause/worsen hearing loss in adulthood.


Reconstruction –

Patient assessment –

Look for dysmorphic features.  20-60% have associated anomaly.

Microtia is a feature of –

  1. Hemifacial microsomia
  2. Treacher- Collins syndrome
  3. Nager syndrome
  4. Townes-Brocks syndrome

Facial asymmetry –

In such cases it’s better to correct bony asymmetry before ear reconstruction.


Skin envelope –

Soft, elastic skin should be available.

Limited availability can hamper ear reconstruction à will make auricle definition poor.

Check for scar around ear – can cause stretching of the supple skin envelope.

Scar along the course of STA (superficial temporal a) –> may suggest a severed STA –>  it is the pedicle for TP flap (temporoparietal)  –> A salvage flap for ear reconstruction.

Assess vestige skin –

Assess location, shape & volume of vestigial skin.

If vestige skin is located far away from auricular rectangle (RA), it need to be transposed within AR – otherwise not.

Volume/size of vestige skin –

Relatively large – a deep concha can be formed.

Small – conchal cavity will be shallow

Assess Hairline –

Low hairline – may require hair removal. If low hairline exceeds beyond upper 1/3rd of auricular framework.

Trapezium – space behind side burn –

Missing sideburn may be the initial sign of hemifacial microsomia.

The auricle is located 20mm behind sideburn.

Placing auricle in trapezium shaped space results in anterior inclination of new auricle.

Auricle rectangle (AR) –

Auricle rectangle is identified within which framework will be placed.

Identify relationship of AR with vestige skin.

Auricular template –

Tracing of normal ear.

Flipped on abnormal side and traced.


Position of tracing –

Axis – almost parallel to nasal profile

Distance – equi-distance from lateral canthus – measure distance from lateral canthus to helical root on normal side – replicate this on affected side.


Obtaining the rib cartilage –

Obtain en-bloc from contralateral side – utilizes natural rib configuration.

Helical rim from – first free floating cartilage

Framework from synchondrosis of rib 6 & 7.

Extraperichondrial dissection is preferred.

Preserve even a minimal rim of upper margin of 6th rib cartilage à maintains shape of chest.

Framework fabrication –

Aim is to exaggerate the helical rim and the details of the antihelical complex.

Basic ear silhouette is carved from cartilage block

Framework fabrication is essential in older patient, but not so much in children.

Deliberate warping is a favorable direction à allows flexion necessary to create a helix.

Framework implantation –

Cutaneous pocket created

Incision – small incision along the backside of the auricular vestige.

Native remnant cartilage is excised and discarded.

Framework is inserted.

(This framework placement displaces this skin centrifugally in advantageous postero-superior direction so as to displace the hairline just behind the rim – this principle of anterior incision and centrifugal skin relaxation – given by Tanzer).

Place a closed suction drain (this helps maintain shape).


Immediate post-op care –

Dressing – non-compressive, convulated

Remove drain – 5th day

Post-op –

Return to school – 2 weeks

Running and sports – 5 weeks

2nd stage – rotation of lobule –

Done by Z-plasty transposition of a narrow, inferiorly based triangular flap.


Tragal construction and conchal definition –

Placing a thin elliptical-shaped chondrocutaneous composite graft beneath a J-shaped incision in the conchal region.

The main limb of “J” is proposed tragal margin.

The crook of “J” represents intertragal notch.

Composite graft harvested from – Anterolateral conchal surface of opposite ear.

FTG harvested and floor of tragal region resurfaced (tragal region is excavated before placing FTG)


Tragus – created as integral strut of the main framework.

Brent – small piece of rib cartilage – first fastened to the frame à then curved around and affixed by its distal tip to frame’s crus helix.

Nagata – uses extra cartilage piece to its main framework.

Modification Kirkham method –

Anteriorly based conchal flap doubled on itself.


Detaching the posterior auricular region (framework elevation) –

  • SSG – to create retroauricular sulcus
  • Placing a wedge of rib cartilage behind the elevted ear –> greater projection of auricle achieved. Cartilage placed need to be covered with – by temporoparietal flap (Nagata) or Turnover “bookflap” of occipital fascia from behind the ear (Firmin, Weerda, Brent)


Managing the hairline –

Low hairline is MC and troublesome problems in ear reconstruction.

Options of removing hair –

1). Electrolysis, 2). Laser, 3). Replacement of follicular skin with a graft – for larger area



  1. Skin flap preparation –

Lobule splitting technique for lobule type microtia.

Nagata described in 1994 – lobule is split into two –

-Anterior lobule flap – transposed backwards to cover the anterior lobule of the framework

-Posterior lobule flap – transposed anteriorly to cover the posterior aspect of the tragugs and concha cavity.


Skin incision for small concha type microtia –

Skin incision made along small indentation –> indentation turned inside out (this will be used to cover framework)

Skin incision for concha-type microtia –

1994 – Z-plasty type incision with posterior V-shape design.

V shaped design changed to W-shaped.


  1. Removing vestige auricular cartilage –

Lobule type – all of vestige cartilage is removed.

Concha type – remnant concha is preserved as a cuff.


  1. Skin pocket dissection

2 mm thick skin flap (do not use epinephrine)

Extent of skin dissection – 1 cm beyond the hair line.


  1. Harvesting costal cartilage –

Brent harvest cartilage with perichondrium

Firmin keeps anterior portion of the perichondrium to the cartilage, leaving rest of the perichondrium at donor site.

Nagata – leaves entire perichondrium at donor site.


  1. Auricular framework creation –


Bolster suture –

Nagata uses bolster dressing for post-operative dressings

Brent uses suction.


Second stage – Auricular elevation –

Normal auricle – separated by supporting cartilage. Gives better elevation.

Raising TPF (temperoparietal fascia) flap –

Covers the cartilage block.

Augments blood supply of auricle posteriorly (which might have been lost during separation)

Alternate flap option –

1). Deep temporal fascia flap, 2). Free vascularized fascia flap


Complication –

Rate – 0 – 72.9%, Avg – 16.2 %

Most serious complication – cartilage infection. To prevent this address skin necrosis immediately.

Secondary reconstruction –

Difficult but not impossible.

Excise all scarred tissue and damaged skin envelope à replace it with well vascularized supple and thin skin envelope with well-planned framework à TPF (temperoparietal fascia) is the workhorse flap for this purpose.



Constricted ear –

Described first by Tanzer – 1975. A/k/a – “cup” or “lop” ear

Helix and scapha fossa are hooded and crura of antihelix flattened.

Inadequate helical rim circumference.

Group 1 & 2A –

Mild deformity of helix (a/k/a – “Lop” ear)

Helical cartilage with minimum skin defect.

Musgrave technique – Expands the helix. –> Multiple cuts made in curled cartilage –> fan upwards and backwards –> fixed to curved strut made of concha cartilage.

Group 2B –

Has both skin and cartilage defects – in upper third of auricle

Grotting flap – modified by Park – is used for helical skin defect – by creating both skin flap and fascial flap with the same pedicle (fascial flap provide additional coverage to skin flap which is limited in width (10-13mm)).

For helical cartilage – 8th rib cartilage is harvested.

Group 3 –

Most severe cupping. Treated as microtia – concha type microtia.


Cryptotia –

Upper pole of the ear cartilage is buried under the scalp.

Superior auricotemporal sulcus is absent.

High incidence in Japan – 1:400.

Goal of surgery – creating a retroauricular sulcus.

Methods –

1). SSG, 2). Z-plasty, 3). V-Y advancement, 4). Rotation flap

Stahl ear –

Described by Binder, 1989 (named after Dr Stahl)

Characterized by third crus extending towards helical rim.

Three types –

  1. Obtuse angle bifurcation (superior crus missing)
  2. Trifurcation
  3. Broad superior crus & broad third crus

Treatment –

Early infancy – ear remodeling.

Surgical treatment – cartilage /skin excision or cartilage alteration.


Ear remodeling –

First described by Matsuo. 

Early initiation has better result – presence of maternal estrogen makes cartilage more elastic.

Lop ear and Stahl ear – responds to ear molding only if started in neonatal period.

Cryptotia and protruding ear – responds well until approx 6m of age.

Results poor if molding started after 3m of age.

Helix-antihelix adhesion responds poorly – contraindication for ear molding.


Traumatic ear amputation –

Cartilage can be stored (under abdomen, scalp) –> but stored cartilage does not provides good definition –> best reconstructed with rib cartilage.


Burnt ear –

Burn injury – there is non-availability of good skin.

TPF flap powerful tool for coverage of framework.


Partial ear reconstruction –

Pure helical rim defect – Antia-Buch helical rim advancement.

Major middle- third auricular defect – Converse tunnel procedure.


Prominent ear –

MC anomaly of head & neck area.

Incidence – 5% of general population.

M:F = 1:1

Normal ear – separated by less than 2 cm from and forms an angle of <25° with side of the head.

Cause of protrusion of ear –

  1. Underdevelopment or effacement of the antihelix
  2. Over-development of the deep concha
  3. Combination of 1 & 2

Timing of surgery – around 5-7 yrs of age.

Surgical techniques –

McDowell normal distance from skull to the helix.

From mastoid –

Upper third – 10-12mm

Middle third – 16-18mm

Lobule – 20-22mm

Antihelical fold alteration –

  1. Scapha-conchal suture –

Mustarde – permanent Mattress suture through cartilage without any cartilage incision (useful in soft cartilage of children). Suture from scapha to triangular fossa or concha.

  1. Anterior cartilage alteration –

Chongchet – scored the anterior scapha cartilage with multiple cartilage cut to roll it back and from an antihelix (done under direct vision).

Strenstrom – Scored antihelcial region through posterior stab incision near the cauda helicis. Principle of Gibson – cartilage bend away from abraded side.

  1. Restore helical fold by excision –

Luckett – excising a crescent of anterior skin and cartilage – conchal excision and primary closure.

Converse/wood-Smith technique – two parallel incision – parallel to desired antihelical fold –> then tubing sutures places to create defined fold.

  1. Conchal alteration –

Dieffenbach – first otoplastic attempt, 1845 –> excising skin from auricocephalic sulcus and then suturing conchal cartilage to the mastoid periosteum.

Suturing – angle b/w concha & mastoid reduced by placing sutures b/w the concha and mastoid fascia – Furnas.

[Fascia- Furnas]  [Mattress – Mustarde]


Correction of earlobe prominence-

Gosian technique –

Small amount of skin excised from medial (posterior) surface and then closed à with a bite to undersurface of concha.

Webster technique – repositioning helical tail (by suturing to concha) can reposition ear lobe (but not reliably).


Ear reconstruction – specific regional defects –

External auditory canal stenosis –

  1. FTG over acrylic mold (for several months)
  2. Multiple Z-plasty
  3. Local flap

Helical rim defect –

Up to 1.5 cm (<2cm) – Antia-Buch helical rim advancement (chondrocutaneous flap) / with V-Y advancement of helical crus (additional advancement achieved).

Thin tube of retroauricular skin – its “waltzed” into place.

Upper 1/3rd defects –

  1. Local skin flaps
  2. Helical advancement (HA)
  3. C/L conchal graft covered with a retroauricular flap (Adanis) (CG with RA)
  4. Chondrocutaneous composite flap
  5. Rib cartilage graft covered with retroauricular skin or temporoparietal flap/skin graft (RC with RA)
  6. Banner flap


Middle 1/3rd defect –

  1. Primary closure with excision of accessory triangle
  2. HA
  3. CG with RA
  4. RC with RA
  5. Diffenbach technique

Cartilage graft can be inserted through Converse tunnel procedure

Lower- third defect (Ear lobe) –

  1. Soft tissue flaps –
    1. Converse two flap technique
    2. Reverse contoured flap
    3. Zenteno-Alanis flap
  2. Cartilage graft


Pardue’s flap – for closure of split ear with maintaining tract lined with skin (for use of ear rings immediately)


Macrotia – reduction otoplasty (Crescent of scapha removed with excision of redundant helical skin)

Shell ear – wedge excision of helical rim and suturing

Question mark ear (supralobular deficiency) – deficiency treated by cartilage graft (conchal graft or rib graft)

Stahl ear (extra third crus) – excision of extra crus.

Cryptotia (buried upper pole of ear) – creation of retroauricular sulcus (SSG, Z-plasty, V-Y, Local flap)

Constricted ear (different degree of helical rim deficiency causing overhanging rim) – overhanging skin/cartilage excised & reconstructed with cartilage graft.


Differences in different techniques of ear reconstruction –


Brent Nagata Firmin
Age  of surgery 6 yrs 10 yrs 10 yrs
Steps of surgery 4 stage 2 stage 2 stage
Pieces of cartilage used 2







Conchal unit






Tragus and antitragus

Projection piece

Spare piece (to construct posterior wall of concha)

Suture used Non-absorbable (Prolene) Wire Wire
Cartilage harvest Resect entire perichondrium with cartilage Leaves entire perichondrium at donor site Leaves the posterior perichondrium at donor site
Post op dressing Uses suction to maintain shape Uses bolster dressing to maintain shape


TMJ ankylosis


Humphry- 1st to do mandibular condylectomy for TMJ ankylosis , 1864

Esmarch- pseudo-arthrosis, 1855

Murphy-1914, interpositioning of flap of fat and temporal fascia to maintain pseudoarthrosis.

Pickerill- 1942, cartilage graft for TMJ reconstruction

Stuteville- established- condyle as growth center of mandible.

Ankylosis def.- stiffness of joint as a result of disease process with fibrous or bon fusion across the joint.

TMJ ankylosis- condylar head fuses with glenoid fossa


Type of joint- Diarthodial, Ginglymus (hinge), synovial joint

Movement- rotational and translatory

Articulation- mandibular condyle with squamous portion of temporal bone (glenoid fossa)

Blood supply of mandible- inferior alveolar artery and muscle and gingival attachments.

Glenoid fossa –

Anterior articular surface formed by inferior aspect of temporal squama.

Surface – smooth, oval & deeply hollowed out.

Roof of glenoid fossa forms the partition of middle cranial fossa and TMJ.

Fossa is lined by fibrocartilage.

Posterior wall of glenoid fossa – formed by squamo-tympanic fissure – separates it from tympanic plate.

Glenoid fossa is the cranial component of TMJ.

Its limit –

Anteriorly – articular eminence or tubercle.

Posteriorly – a small conical postglenoid tubercle.

(Articular eminence – a small prominence on ZA

Postglenoid tubercle – separates articular surface of fossa laterally from the tympanic plate – tympanic plate separates TMJ from bony part of EAM.)

TMJ articular surface-

Lined with fibrocartilage (avascular fibrous tissue with cartilage)

(TMJ is a synovial joint, but has fibrocartilage lining, while other synovial joint has hyaline cartilage as lining)

Articular disk or meniscus-

It separates TMJ into two spaces-

Upper joint- 1ml volume– extends from glenoid fossa to articular eminence.

Lower joint- 0.5ml volume– begins above the insertion of the lateral pterygoid and then spreads out over the condyle.

Articular disk has two bands for attachments-

Anterior band – is thick and narrow- attaches –

Superiorly –to articular eminence and superior belly of lateral pterygoid

Inferiorly – to condyle (though synovial membrane) along attachment of lateral pterygoid.

Posterior band- it is wide and thick – a Bilamellar structure- highly innervated and vascular.

Upper layer- attaches to – tympanic plates of temporal bone

Lower layer- attaches to – posterior meniscus to neck of condyle.

A third intermediate zone is also described – its thinnest part – gives meniscus flexibility and ability to alter shape under pressure.

Histologically – Disc is meshwork of firmly woven avascular fibrous connective tissue. It is non-innervated.

Disc –

Promotes lubrication

Energy absorption

Joint range of motion

Main shock absorber

Has very little potential for repair after insult

Movements in joint-[HITS]

Hinge movement- Inferior joint space

Translational movement- Superior joint space


Shape- elliptical/oval (broad laterally and narrow medially)

Size- 20mm- medial to lateral (13-25mm)

10mm- AP diameter (6-16mm)

Two condyles of a patient can be asymmetrical.

Surface is mostly convex superiorly (58%) – but can be flat, pointed, angular, round, bulbous.

Articular surface is covered with dense fibrous connective tissue.

This is thickest – anteriorly and superior surface.

The hyaline cartilage is the head of condyle is the growth center of the condylar process.

TMJ capsule –

Thin, Funnel-shaped, Blends with periosteum of mandibular neck

Attachment –

Superiorly –

Anteriorly – to anterior border of articular eminence.

Posteriorly – to lip of squamotympanic fissure & anterior surface of postglenoid process.

To the circumference of the cranial articulating surface

Inferiorly –

To neck of condyle both lateral and medial side.

Capsule is fibrous having a synovial lining on inside.

(Fibrous capsule- attaches to – Zygomatic arch -above & Condyle- below)

Capsule is reinforced- medially and laterally by temporomandibular ligaments.

Ligaments –

Lateral or temporomandibular ligament –

Extends downwards and backwards – from articular eminence to external and posterior side of condylar neck.

Its posterior fibers unites with capsular fibers.

Made of collagenous fibers – have poor ability to stretch à hence maintains integrity and limits movement of TMJ à called ‘check-rein’ ligament

Prevents – Anterior excursion of jaw & Posterior dislocation.

Accessory ligament –

Makes no contribution to joint activity.

These are –



Sphenomandibular ligament –

Arising from sphenoid spine and pterygoid fissure

Runs downward and medial to the TMJ

Gets inserted on lingula of mandible.

Its remnant of Meckel’s cartilage

It’s an important landmark – internal maxillary artery and auricotemporal nerve lies b/w it and mandibular neck.

Stylomandibular ligament –

Dense thick band of deep cervical fascia.

Runs from styloid process to mandibular angle.

Blood supply of TMJ-

Superficial temporal vessels and massetric artery branches through sigmoid notch of mandible.

Nerve supply of TMJ –

CN V3 branches –

Largest branch – auricotemporal n – supplies the posterior, medial, lateral part of the joint

Masseteric nerve

Branch of posterior deep temporal nerve – supplies anterior part of joint.

Mean distances-

Outer aspect of zygomatic arch (ZA) to middle meningeal artery –  31mm

MMA to height of glenoid fossa (HGF) –  2.4mm

ZA to carotid artery      –       37.5 mm

ZA to IJV           –                         38.3 mm

Outer aspect of ZA to CN V3      –   35mm

HGF to CN V3               –        9.2mm


Excessive bleeding during TMJ resection – MC related to IMA (internal maxillary artery)

Anterior tympanic artery is intimately related to retroauricular region- supplies posterior part of TMJ.

Retrodiscal venous plexus (pterygoid venous plexus) – venous space in retromandibular space.

Mandible movements and muscles:

Protusion or elevation-



Medial pterygoid

Lateral pterygoid- superior portion in elevation

Depressor or retractor-


Anterior belly of diagastric – main




Lateral pterygoid – inferior portion in depression

Masseter – elevation and protrusion

Medial pterygoid – protrusion and elevation. U/L movement – mediotrusion

Tempolaris –

Anterior fibers – elevation

Middle fibers – elevation and retrusion

Posterior fibers – retrusion

Lateral pterygoid-

Inferior portion- attaches to neck of condyle à produces movement of the joint – mouth opening and protrusion

Superior portion- attaches to fibrous capsule and meniscus of TMJà stabilizes meniscus during movement of mandible.

At rest condyle articulates with intermediate zone of disc.

Mouth opening – condyle disc complex translates down the articular eminence and then disc rotates posteriorly on condyle.

Superior retrodiscal tissue – limits the forward sliding of disc.

Mouth opening is initiated by – superior head of lateral pterygoid.

Mouth closure – each head glides back and hinges on its disc.

The initial 20-25° of mouth opening is pure Hinge movement. Beyond this condyle translates forwards and rest of the movement occur.

[Depression – Diagastric][Protrusion – Pterygoids][Elevator – Temple & mass – Tempolaris and Masseter][Superior lateral pterygoid- originates from Sphenoid greater wing]

TMJ and its characteristic features –

  1. Articular cartilage – covered by avascular fibrocartilage (not hyaline).
  2. Right and left movements are coupled through mandible
  3. Mandible is stabilized by three functionally linked articulation – 2 TMJs and the dentition. Problem in any of the three will affect mandible movement.
  4. Multiple muscle involved in movement – requires delicate neuromuscular balance
  5. TMJ is the only joint that has rigid endpoint of closure (as a consequence of teeth contacting).
  6. The joint function as a regional adaptive growth center for the growth and development of the mandible and middle third of face (in response to changes in the “functional matrix” of surrounding mastectomy muscle and other sift tissue).

TMJ ankylosis-







Topazian classification:

Type 1 Fibrous adhesion in or around the joint

Restricted condyle gliding

Type 2 Formation of bony bridges between the condyle and glenoid fossa
Type 3 Condylar neck is ankylosed to the fossa completely

CP Sawhney classification-

Type 1 Fibrous adhesions all around the joint making any movement impossible

Condylar head- flattened or deformed lies closely approximated to the articular surface.

Type 2 Bony fusion of the head to the outer edge of the articular surface either anteriorly or posteriorly but only to a small area

Condylar head- misshaped or flattened but was still distinguishable

Deeper to it the articular surface and the articular disk were undamaged

Type 3 Bony block seen to bridge across the ramus of mandible and the zygomatic arch.

Condylar head displaced and atrophic lying free or fused

Upper articular surface and articular disk of the deeper aspect intact

Type 4 Bony block wide and deep and extends between ramus and upper articular surface, completely replacing the architecture of joint

Type 4 is the MC type.

El- Haki & Metwalli, 2002

A1- fibrous ankylosis with or without bony fusion

A2 – Bony fusion <50%

A3 – Bony fusion >50%

A4 – complete fusion


Consolidation and fibro-osseous restructuring of a hemarthosis.

Hemarthosis itself may have many cause.


Trauma results in ankylosis- 29-100% cases.

Condylar neck fracture is the MC cause.

Factors leading to ankylosis-

  1. Age-Younger age group

Higher osteogenic potential

Rapid repair

Articular capsule not well developed- easier condylar displacement out of fossa- damage to disk

Anatomically different condyle in children—condyle neck is wide and condylar head has blunt anatomyàmore chances of comminuted fracture. More frequent medial displacement of condylar head – more chance of glenoid fossa fracture.

Prolonged period of self- immobilization

  1. Severity of trauma
  2. Site of fracture
  3. Intracapsular fracture à greater risk of ankylosis
  4. Condyle in children poorly tolerates crishing injury directed along its long axis—resulting in burst fracture- severe hemarthosis with multiple osteogenic fragments
  5. Duration of immobilization
  6. Articular disk

Torn or displaced meniscus – provide direct contact b/w a comminuted fracture and glenoid fossa- key factor in developing ankylosis.


Septic arthritis- organisms- Neisseria Gonococcus, staphylococcus, streptococcus, hemophilus.

Predisposing factors (for infection):

Blunt trauma, Previous joint disease, Burn wound to region, Systemic/autoimmune disease- RA, Reiter’s, alcohol abuse, hypogammaglobulinemia, Drugs- steroids, immunosuppressant, STDs



Contiguous – from middle ear

Direct- arthroscopy, arthrocentesis, injection in the area, acupuncture

Previous TMJ surgery-

Discoplasty, Dissectomy, High condylar shave procedure, Failed alloplastic material

Orthognathic surgery:

Fibrous ankylosis- following prolonged MMF

Extra-articular ankylosis:

Jacob’s disease- osteochondroma of the coronoid process à subsequent fusion to the base of the zygoma

Ankylosis can occur in non-articular site.

Other causes-

Forceps delivery- a trauma to TMJ.

Congenital –

Fusion of maxilla-mandible (extra-articular)


Clinical features:

Trismus- is the functional characteristics. The cause of trismus can be many.


  1. Direct on mandible
  2. Indirect (secondary effect)

Maxilla (No place to grow because of hypoplastic mandible)

Soft tissue-

Shortened pterygo-masseteric sling

Shortened ligament attaching mandible to skull base

Hypertrophy of – tempolaris, coronoid process, suprahyoid muscle

Narrowing of oropharyngeal airways

Narrowing of space between mandibular angles

Facial features

Facial deformity is severe if ankylosis occurs before 15yrs of age.

Unilateral ankylosis-

  1. Deviation of chin and mandible towards affected side
  2. U/L vertical deficiency (of ramus) on affected side
  3. Roundness and fullness of face on affected side,
  4. Flatness and elongation of face on opposite side.
  5. Concave mandible that ends up in well-defined “antegonial notch”
  6. Class II angle malocclusion on affected side + U/L posterior cross bite on affected side.
  7. Absent condylar movement on affected side
  8. Occlusion cant with deviation of maxilla and mandibular midline towards affected side.

Bilateral ankylosis-

  1. Retrognathic/micrognathic mandible (which is symmetrical)
  2. Neck chin angle (cervicomental angle) – reduced or almost completely absent.
  3. Bilateral well-defined antegonial notch
  4. Class II malocclusion
  5. Anterior open bite with protrusive upper incisors
  6. Oral opening ↓↓ (<5mm)
  7. Multiple dental caries
  8. Severe malocclusion crowding and impacted tooth
  9. Convex facial profile
  10. Short hypo-mental distance with tight suprahyoid musculature
  11. “Bird-face” deformity (Ande-Gump deformity)- Vogelgesicht
  12. Markedly elongated coronoid process

Obstructive sleep apnea can occur- due to oropharyngeal airways narrowing

Narrowing can occur in-

Cephalocaudal direction- due to shortening of mandibular rami

Transverse – reduced space b/w angle of mandible

Antero-posterior diameter- hypoplastic (↓ed) body.

Key difference b/w intra-articular vs extra-articular

Intra-articular- translational movement – ↓ed or absent

Extra-articular- translational movement- not as limited.

Rotational movement- affected in both


  1. History – of trauma or infection
  2. Clinical findings
  3. Radiology

Orthopentagraph (OPG)-

Easy, quick, shows adjacent areas.

Blind area of OPG – angle (blinded by cervical shadow) & symphysis (pharyngeal shadow)

Presence of antegonial notch

Antegonial notch- develops- secondary to contraction of depressor muscle and their action against elevator muscles

Prominent and elongated cornoid process

Shallow sigmoid notch

Cephalometric studies– lateral and antero-paoterior. Required for aesthetic correction.

CT scan-

Very helpful. 3-4 mm cuts are obtained. Evaluates- medial extent of bone mass, Density of bone mass, Thickness of temporal bone

Typical appearance of ankylotic joint is – “mushroom- shaped”

CT scan can also- differentiate any extra-articular contribution to ankylosis.

Minimum 3 slides needed to diagnose

3D-CT –

Allows measurements. Allows subtraction CT

Cone beam CT- CBCT-

Small area of CT. Low radiation dose. Smaller equipment. Small cuts are used 1-2mm.

Provides multiplanar and reformational and 3D images


Fibrous ankylosis- reduced joint space and hazy

Bony ankylosis-

  1. Complete obliteration of joint space
  2. Distorted TMJ anatomy
  3. Deformed condylar head
  4. Complete bony consolidation
  5. Elongation of coronoid process

Sequel of untreated ankylosis-

  1. Facial growth and development affected
  2. Speech impairment
  3. Nutritional impairment
  4. Poor oral hygiene – multiple caries and impacted tooth
  5. Malocclusion
  6. Respiratory distress

Aims and objective of surgery

  1. Restore mouth opening
  2. Restore joint function
  3. Allow for condylar growth
  4. Correct facial profile
  5. Relieve upper airway obstruction
  6. Prevent recurrence

Surgical strategies depend upon-

  1. Age of onset of ankylosis
  2. Extent of ankylosis
  3. U/L or B/L involvement
  4. Associated facial deformity

Surgical technique-

Various technique has been used- but, basically three strategies-

  1. )Condylectomy, 2). Gap arthroplasty, 3). Interpositional arthroplasty.

Surgical approach



Incision- Behind the external ear in the crease near superior aspect of external pinna and extended to tip of mastoid.

Advantage-good cosmesis

Disadvantage- several

Small exposure- poor access and poor exposure, Stenosis of EAM (external auditory meatus), Infection of external auditory canal, Chondritis, Paraethesia, Deformity of pinna

Endaural approach (Lamport)

Incision- short facial incision with extension into EAM

Begins just above zygomatic arch, extends downwards and backwards into intercartilaginous cleft b/w helix and tragus and then extends inwards along the roof of EAM for approx. 1cm.

Advantage- cosmesis

Disadvantage- Limited access, Meatal stenosis, Chondritis

Submandibular (Risdon’s)-

Incision- 1 cm below and parallel to lower border of mandible going slightly behind

Disadvantage-poor access to condylar head

Used for-approach to neck of condyle and ramus

Post-ramal (Hind) approach-

Indicated for surgery involving condylar neck and ramus

Incision- 1cm behind ramus, extends 1 cm below ear lobe to angle of mandible

Advantage- cosmesis, Excellent visibility and accessibility


Incise parotidomasseteric fascia –>Avoid injuring to facial vein and facial n.

Expose posterior border of ramus –>Incise pterygomasseteric sling (PMS) at the angle

Reflect masseter and parotid glands –> Condylar neck is now exposed.

After procedure PMS is re-approximated.

Preauricular (Dingman’s) approach –

Most basic and standard approach to TMJ
Described by Dingman in 1951

Incision – at the junction of the facial skin with the helix of the ear.

Incision from – helix to the upper border of the tragus.

Modifications of preauricular incision –

  1. Blair and Ivy – “Inverted hockey stick” incision ove the zygomatic arch.
  2. Thema – angulated vertical incision.
  3. Al-Kayat & Bramley, 1979 –

Preauricular approach with temporal extension over zygomatic arch considering the main branches of vessels and veins in vicinity.

Facial and main trunk – 1.5cm -2.8 cm below the lower border of EAM.

Temporal branch – 0.8cm – 3.5cm anterior to anterior border of EAM.

Popwich and Crane modification of Al-Kayat & Bramley –

Incision is longer and wider than conventional.

Skin incision is “question mark”. Begins about pinnas length away from ear.

Curves, backwards and downwards well posterior to main branch of temporal vessel. Till it meets upper attachment of ear.

Rest of incision is same.

Advantage –

Decreased facial nerve palsy.

Provision of donor site for temporal fascia

Decreased hemorrhage (avascular plane of dissection)

Improved visibility and easier identification of facial planes.

Reduction and post-op edema and discomfort.

Good cosmesis.

Reduction in operative time.

Avoidance of auricotemporal nerve aneasthesia or paraethesia.

Coronal approach –

Hemicoronoal (U/L incision)

Bicoronal (B/L incision)

Incisions particularly useful for TMJ ankylosis surgery –

1). Dingman’s and its modification, 2). Risdon, 3). Combined approach – Dingman + Risdon, preauricular + coronal (Poswillo, 1974)

Internationally accepted protocols –

Kaban, Perrot, Fischer, 1990

  1. Early surgical intervention
  2. Aggressive resection of bony or fibrous ankylotic segment – gap of at least 1-1.5cm should be created
  3. Ipsilateral coronoidectomy and tempolaris myotomy –
    1. Coronoid process cut from the level of sigmoid notch till the anterior border or ramus
    2. Tempolaris muscle attachment are severed by carrying out tempolaris myotomy à check intraoral opening – if >35mm à no need for C/L procedure. If opening <35mm àthen C/L coronoidectomy and tempolaris myotomy (this can be done by intraoral incision).
  4. Lining of glenoid fossa region with tempolaris
  5. Reconstruction of ramus with costochondral graft.
  6. Early mobilization and aggressive physiotherapy for at least 6months period post-op.
  7. Regular long term follow up
  8. Cosmetic surgery later on when patient grows.

Coronoidectomy – Important to excise rather than just release à otherwise reankylosis will occur.

Temporalis myofascial flap for Lining of glenoid fossa – based on middle and deep temporal arteries. This flap is a versatile flap for glenoid fossa lining because of –

  • Robust blood supply
  • Proximity to TMJ
    ability to alter arc of rotation by basing the flap inferiorly or posteriorly
  • Vague simulation of disc.

El- Sheikh, 1999- Cardinal principles –

  1. Radical resection of ankylosed mass via wide surgical exposure
  2. Release of pterygo-masseteric muscle sling with resection of condylar process
  3. Restoration of vertical ramal height and condylar head by a costochondral graft
  4. Simultaneous correction of jaw bone deformities at the same time as release of ankylosis
  5. Careful selection of patient – who can comply for at least 1 year of follow up.

MC cause of reankylosis –Incomplete removal of the bony or fibrous mass (esp. from medial aspect of joint).

Surgeries –

  1. Gap Arthroplasty (GA) –

Resection –

First described by Abbe, 1880.  Recurrence – 14-100%. Minimum extent of width of bone resection – At least 1cm. The procedure causes – gleno-mandibular dysjunction

Laser & arthroscopy –

Ho:YAG laser can be used to debride fibrous ankylosis through arthroscopy creating a pseudo-arthrosis below the mass.

Described by Salins.

Made subcondylar fracture below the ankylosed mass à through post-op physiotherapy creates a pseudo-arthrosis – resulting in mouth opening.

It does not resects the ankylosed mass.

  1. Interpositioning arthroplasty (IA) –

Various grafts has been used for lining the joint after resection of ankylotic mass.

Glovine, 1898- first used the tempolaris myofascial flap (TMF) for orbital reconstruction.

Topazian, 1966 – compared GA and IA in favor of IA.

Other autogenous interposition grafts –

Dermal graft, Masseter muscle graft, Auricular cartilage, Fascia lata, FTG

Alloplastic material –

Proplast/Teflon, Polyethylene, Christensen metallic fossa implant, Silastic sheets, Acrylic marbles

Modification of TMF –

Feinberg & Larsen – described full thickness, pedicled, tempolaris muscle-pericranial flap that includes periosteum along with muscle.

Pogrel Kaban – flap includes fascia alone or with muscle and is inferiorly rotated over the arch into the joint space.

Omura & Fujito – Folded the flap over itself making fascia face both condylar surface and glenoid fossa and thus reducing the functional friction.

Routes of placing TMF –

  1. Tunnel under zygomatic arch (ZA)
  2. Osteomatize the ZA
  3. Thinning of ZA & pass under it
  4. Over the ZA

CCG (costochondral graft)–

Harvested either from 5th, 6th rib.

Costochondral junction of rib is chosen along with some length of rib.

Length of total graft will depend on the height of ramus to be restored.

A minimum of 1.5cm of costochondral junction should be included in the graft.

Fixation to lateral aspect of ramus with screws or interosseous wire.

Reconstruction of resected joint –

Goals –

  1. Reestablish joint function
  2. Reestablish vertical height of the ramus and occlusion
  3. Provide growth potential in children

Autogenous grafting –

Costochondral graft (CCG) –

First described by Gillies- 1920

Ware & Brown – promoted its use as potential growth center for the mandibular joint.

CCG is forerunner in autogenous graft choice –

Easily adaptable to the site. Remodels over time. Less donor site morbidity

Infection are rare. Harvested rib generally regenerates.

Anatomical similarity to the mandible condyle. Regenerative and growth potential both at host & donor site. Ease in training and adapting the graft.

Disadvantage –

The cost & time for preparation are considerable

Unpredictable growth pattern – progressive dental midline shift, occlusion changes, chin deviation, enlargement of the graft itself.

CCG should be at least 0.5cm to 2cm to diminish the chance of all graft converting to bone.

A minimum gap of 0.5cm to 1cm should be there b/w graft and glenoid fossa so that free movement is possible.

Other autogenous materials –

Metatarsal, Sternoclavicular joint, Fibula, Iliac crest, Ankylotic mass itself after contouring, Free vascularized whole joint transplant to 2nd toe, Preserved costal cartilage

Alloplastic materials –

Advantage –

Ability to begin physiotherapy almost immediately after the surgery.

Avoidance of second surgical site

Ability to mimic normal anatomy

Rationale to use alloplastic Vs autograft –

Placing an autogenous tissue into an area where reactive or hypertrophic bone already formed once is not a good idea.

Previously operated joints has compromised vascular bed that will not take up autogenous tissue predictably

Relatively contraindication for allograft use –

  1. Age
  2. Uncontrolled systemic disease eg. DM
  3. Active infection at implant site
  4. Allergy to implant material

Disadvantages –

  1. Cost of device
  2. Material wear & tear
  3. Questionable long term stability
  4. Lack of growth potential

Total joint prosthesis –

CAD-CAM design are useful.

Distraction –

McCarthy first used distraction technique for mandibular lengthening in microsomia. Papageorge & Apostolicis then used this for TMJ ankylosis

Distractor placed along – ascending ramus and inferior border. A reverse corticotomy performed through sigmoid notch.

Simultaneous arthroplasty is done.

Complications –

During anesthesia –

Difficult intubation and risk a/w it.

During surgery –

  1. Hemorrhage – sources –
    1. Superficial temporal vessels
    2. Transverse facial a
    3. Inferior alveolar vessels
    4. Internal maxillary vessels
    5. Pterygoid plexus of vein
  2. Damage to EAM
  3. Damage to Zygomatic and temporal branch of facial nerve
  4. Damage to Glenoid fossa à leading to perforation of middle cranial fossa
  5. Damage to auricotemporal nerve
  6. Damage to parotid gland
  7. Damage to teeth during jaw opening with stretcher

Post-operative –

  1. Infection
  2. Open bite
  3. Re-ankylosis
  4. Unpredictable growth of costochondral graft
  5. Fracture of graft at costochondral junction à remove cartilage and reshaping the bony part.

Frey’s syndrome –

Pain in auricotemporal region. Gustatory swaeting and occasional erythema. Flushing on the affected side.

Treatment –

Topical agents – Antiperspirants – only for mild symptoms. Anticholinergic – topical glycopyrrolate

Radiation therapy – Dose of 50Gy is used. For very symptomatic patient when other forms of treatment fails.

Surgical procedure –

Skin incision – for localized and small areas

Auricotemporal nerve resection. Tympanic neurectomy. Botulinum toxin A injection

Recurrence of ankylosis –

Causes –

  • Inadequate gap b/w the fragments
  • Missing on medial condylar stump and leaving it behind
  • Fracture of costochondral graft
  • Loosening of costochondral graft due to inadequate fixation
  • Inadequate coverage of glenoid fossa
  • Inadequate post-operative physiotherapy

Two most dreaded complications of TMJ surgery –

  • Perforation into middle cranial fossa
  • Severe bleeding from the medial infra-temporal fossa

Dural exposure through glenoid fossa à if Dural tear present à neurosurgical consult

Internal maxillary artery tear à Embolization.

Steps of surgery –

Safe and secure airways or tracheostomy under GA
Gap arthroplasty – with 1.5 – 2.0 cm gap

Tempolaris fascia flap – interposition in the gap

Costochondral graft placed through Risdon’s incision. CCG fixed with two 2mm diameter and 8-10mm length screw.

I/L or C/L coronoidectomy or both if intraoral mouth opening <35mm

Extended sliding genioplasty to correct retruded chin

Consent –

For GA. For Tracheostomy. For CCG

Incision – Skin – as planned (preauricular with hemicoronal extension)

S/C tissue –> incision stops at level of tempolaris fascia

Blunt stripping with back of scalpel sweeping forward, inferiorly up to inferior point of helical attachment.

Root of zygomatic arch palpated – on which a vertical incision is placed down to the bone. Upper limit of incision is carried up to 2 cm above ZA angulated forward at 45°.

Periosteal dissector is used to tunnel the periosteum over the ZA and anteriorly retracted -> exposing the ankylotic mass.

Periosteum over the ramus is bluntly divided to expose the ankylosed mass up to the anterior border of ramus and coronoid if present separately.

Deeper dissection should not be extended below the inferior limit of the bony EAM (to prevent injury to facial nerve).

Ankylotic mass dissected with a cutting burr.

Initially – inferior cut is placed and completed with an osteotome.

Superior cut usually follows cleavage b/w the supposed glenoid fossa and condyle or a horizontal cut.

In dense ankylosis- 1.5 cm osteotomies are performed in layers to avoid arteriovenous anatomy medial to mandible.

Bleeding at this level is due to –

1). Inferior alveolar vessel, 2). Pterygoid plexus, 3). Middle meningeal vessels

And rarely from internal maxillary a. Pressure and cautery will control bleeding.

Mandible is now opened to achieve 35-40 mm mouth opening –> if not achieved –>C/L coronoidectomy

Coronoid, if identified, separately, is usually hypertrophied and is excised through same incision.

Temporoparietal flap – 2 cm in width, dissected about 6 cm superior to ZA. This flap is freed up to 1 cm from ZA (5 x 2 cm flap) and tucked into gap arthroplasty (sutured to remnant of pterygoid muscle or to medial of ramus).

Harvest of CCG –

5th or 6th rib. Subperiosteal elevation. 4cm of rib with 5mm of cartilaginous cap.

Chest wound closed in layers. Harvested graft placed lateral to ramus of mandible through Risdon incision.

CCG is secured with two 2mm screws of 8-10mm length.

Advancement genioplasty –

Extended genioplasty is done making bone cut inferior to the mental nerve on either side.

Osteotomy is completed using 2mm burr. Osteomized chin is pulled forward and overlapped on body of mandible anteriorly

Total joint replacement technique –

CAD-CAM generated custom made TMJ condyle and fossa prosthesis.

Endaural (Lamport’s) with hockey stick extension.

Ankylotic mass is exposed.

A Steiger burr is used to perform gap arthroplasty & a condylectomy and ankylotic mass removed.

A sialistic block is then contoured and placed in the gap as a temporary spacer.

IMF is done. Pt is discharged.

CT scan done –> CT scan sent to company for manufacturing prosthesis – after CT, IMF can be removed.

2nd stage of surgery –

IMF given – Gap arthroplasty exposed à sialistic spacer removed à I/L coronoidectomy done à prosthesis fitted & fixed (with 2mm screw) à IMF released.

Additional procedure if desired range of motion not achieved à C/L coronoidectomy à B/L masseteric myotomy.

F/b post-op radiation –> 10Gy in 5 fraction.

TMJ disorders –

Intra-articular or intrinsic

Extra-articular or extrinsic

Extrinsic factors –

Masticatory muscle disorder –

Protective muscle splinting

MPD (masticatory muscle spasm) syndrome


Extrinsic trauma –

Fracture, Traumatic arthritis, Myositis, myospasm, Tendonitis, Myofibrotic contracture

Causes of trismus –

  1. Infection –
    1. Acute – odontogenic, or
      1. Around the joint
    2. Chronic – tubercular osteomyelitis of ramus/body
  2. Trauma –
    1. Fracture ZA – impinging on coronoid
    2. Fracture mandible – pain and tenderness or muscel spasm
  3. Inflammation – myositis or muscular atrphy
  4. Myositis ossificans
  5. Tetany
  6. Tetanus
  7. Neurological disorder – epilepsy, brain tumor, bulbar paralysis
  8. Psychosomatic trismus
  9. Drug induced – strychnine
  10. Mechanical blockage – elongation, exostosis, osteoma, osteochondroma
  11. Extrarticular fibrosis
  12. Iatrogenic – hematoma in medial pterygoid (following needle puncture) à leading to fibrosis

Intrinsic factors –

  1. Trauma – dislocation, subluxation, intracapsular fracture, extracapsular fracture, hemarthrosis
  2. Internal disc displacement
  3. Arthritis – OA, RA, JRA, infectious arthritis
  4. Developmental defects –
    1. Agenesis/ aplasia of condyle – B/L or U/L
    2. Hyperplasia/hypoplasia of condyle
    3. Bifid condyle
  5. Ankylosis
  6. Neoplasm

Dislocation, Subluxation, hypermobility of TMJ –

Excursion of condylar head –> normally just under the apices of articular eminence (in some individuals till anterior slope of articular eminence) –> beyond this point is abnormal.

Mandibular dislocation is uncommon in comparison to other joints in body.

Dislocation can be –

Unilateral or Bilateral

Acute (Luxation) or Chronic recurrent (habitual) – subluxation or Long standing

Acute dislocation –

Extrinsic or iatrogenic

Intrinsic or self-inducing forces

Extrinsic or iatrogenic causes –

Blow to chin (while mouth open)

Injudicious use of mouth gag during anesthesia

Excessive pressure on mandible

Intrinsic or self-inducing forces –

Excessive yawning, Vomiting

Singing/blowing wind instruments/laughing loudly

Excessive opening during eating

Hysterical fits

Predisposing factors –

  1. Laxity of ligaments, capsule
  2. Abnormal skeletal form
  3. Previous injuries
  4. Ehler-Danlos Syndrome
  5. Epilepsy
  6. Parkinsons

Clinical factors –

U/L –

Difficulty mastication and swallowing. Profuse drooling of saliva

Deviation of chin to opposite side

Lateral cross and open bite on C/L side

B/L –

Inability to close mouth. Pain, excessive salivation, difficulty speaking

Protruding chin. Anterior open bite

Management –

Assurance. Pain killers. Sedatives.

Pressure and massage of area.

Manipulation – downward force–> and then backward force.

Patient kept on semisolid diet

Long standing dislocation – when dislocation longer than one month.

Chronic recurrent or habitual dislocation or subluxation –

Triad of –

Ligamentous and capsular flaccidity

Eminential erosion


Management –

IMF for 3-4 weeks

Sclerosing agents in joint space –> fibrosis

Surgical options –

  1. Capsule tightening procedure
  2. Creation of mechanical obstacle or block
  3. Creation of new muscle balance
  4. Removal of mechanical obstacle
  5. LeClerck’ procedure – ZA fractured to create eminence
  6. Glenotemporal osteotomy – eminence augmentation

Capsule tightening procedure –

  1. Capsulorrhaphy – shortening the capsule and resuture
  2. Placement of vertical incision – in the capsule and drawing it tight by overlapping the edge and suturing
  3. Reinforcement of the joint capsule – by turning down a strip of temporal fascia and suturing to capsule

Creation of mechanical obstacle –

  1. Eminence osteotomy and turning down in front of condylar head – Lindermann
  2. Mayor- eminence grafting – Bone grafting (taken from zygoma) over the eminence to increase the size and height.
  3. Silastic block or Vitallium mesh implant to add to height of eminence
  4. Dautry – zzygomatic arch osteotomy and depressing it in front og condylar head to prevent abnormal forward translation
  5. Findlay – “L-shpaed” pins anchored in the zygomatic process of temporal bone and projecting it anterior to condyle.
  6. Creation of mechanical obstacle – has certain disadvantage – not used frequently.

Direct restrain of condyle – Questionable results

  1. Tempolaris fascia turned down and sutured to lateral surface of articular capsule.
  2. Piece of fascia lata – threaded through hole in the ZA and then second hole in condyle and then tighten it until half of pre-operative opening existed.

Creation of new muscle balance –

  1. After making vertical intraoral incision –

Tempolaris fascia and periosteum divided – from the tip of coronoid to retromolar area.

At and below the coronoid tip – masseter muscle is also partly elevated from the lateral surface of ramus.

Wound then closed horizontally –> fibrosis –> restricts oral opening.

  1. Medial pterygoid myotomy procedure

Removal of mechanical obstacle –

  1. Removal of torn meniscus or meniscectomy – became popular à but lots of side effects.
  2. High condylectomy –
    1. Excision of the superior portion of condylar head above the attachment of the lateral pterygoid.
    2. This shortened head has now less chance of locking
  3. Eminectomy –
    1. Myrhang, 1951
    2. Eminectomy allows condylar head to move freely forward and backwards.

Indications –

  1. Recurrent episodes of dislocation
  2. Chronic hypermobility a/e severe pain
  3. Irreversible TMJ pain a/w clicking or grating

Eminectomy –

Simple to perform. Can be performed under local anaethesia.

Joint cavity not opened – avoids injury to meniscus and capsule

Steps –

Skin incision – small horizontal incision over the ZA in the region of articular eminence in front of tragus.

Articular eminence is located ⁓1.5 cm anterior to EAM.

Eminence is then exposed with T-incision, the horizontal portion being over and parallel to ZA and vertical portion extending to the apex of the eminence.

Periosteum reflected to expose entire lateral portion of the eminence.

Series of burr hole then created at the base of eminence in a line parallel to ZA

Burr is directed downwards @ 10° to horizontal plane.

These burrs are then connected with fissure burr.

Eminence is then sectioned and separated.

Base is then smoothened.

(Foramen spinosum is just mesial to articular eminence. It contains MMA (middle meningeal artery) – may be source of major hemorrhage after eminectomy).

Area is thoroughly irrigated – wound closed in layers.

Pressure bandage given for 48-72 hrs.

Create a free website or blog at WordPress.com.

Up ↑

Create your website with WordPress.com
Get started